Emotionally significant experiences tend to be well remembered.1,2 We
know this from personal experiences as well as from extensive research findings. Significant experiences such as birthdays, graduation ceremonies, or the loss of a loved one typically
leave lasting and vivid memories. Findings of experimental studies indicate that people have good recollections of where they were and what they were doing when they experienced
earthquakes3 or witnessed accidents.4 Similarly, a rat remembers the place in an apparatus where
it received a footshock or the location of an escape platform in a tank filled with water.5,6 Such
memory enhancement is not limited to experiences that are unpleasant or aversive. Pleasurable events also tend to be well remembered. Our research focuses on understanding the role of
emotional responses induced by such arousing experiences in enabling the significance of events to regulate their remembrance.
Extensive evidence indicates that stress hormones released from the adrenal glands are critically involved in memory consolidation of emotionally arousing experiences. Epinephrine,
glucocorticoids, and specific agonists for their receptors administered after exposure to emotionally arousing experiences enhance the consolidation of long-term memories of these
Do stress hormones also enhance memories of experiences that are not emotionally arousing? The findings of recent experiments suggest that this may not be the case. As discussed
below, we recently reported that the endogenous glucocorticoid corticosterone enhanced memory consolidation of object recognition training when administered to rats that were
emotionally aroused by an unfamiliar training apparatus. However, the treatment had no effect when administered to rats that had extensive prior habituation to the training context in
order to reduce novelty-induced arousal.11 In studies of human memory, epinephrine or cortisol
treatment also appear to selectively enhance memory for emotionally arousing material.12–15
These findings thus provide some important clues concerning the neurobiological mechanism(s) underlying adrenal hormone effects on memory consolidation and suggest that at least some
degree of training-associated endogenous emotional arousal is essential for enabling their effects on memory consolidation. Our findings indicate that adrenal stress hormones
influence memory consolidation of emotional experiences via interactions with arousal-induced activation of noradrenergic mechanisms within the amygdala.
13.2. STRESS HORMONE EFFECTS ON MEMORY CONSOLIDATION
It is well established that hormones of the adrenal medulla (epinephrine) and adrenal cortex (corticosterone, cortisol in humans) are released during and immediately after stressful
stimulation of the kind used in emotionally arousing learning tasks. The degree to which these hormonal systems are activated depends on the severity as well as type of stressor
employed.16 As removal of endogenous hormones by adrenalectomy impairs
memory consolidation for emotionally arousing experiences,5,17–19 such evidence indicates that stress hormones released by
the training experience may act as endogenous modulators of memory consolidation.
In support of this view, single injections of epinephrine or glucocorticoids administered after training enhance the long-term retention of many different kinds of training
experiences typically used in animal memory studies including inhibitory avoidance, active avoidance, contextual and cued fear conditioning, spatial discrimination, conditioned taste
aversion, object recognition, and appetitively motivated tasks.11,20–23 Further, antagonists of adrenoceptors or adrenal steroid
receptors as well as drugs that disrupt glucocorticoid functioning (i.e., metyrapone) impair memory consolidation.5,17,24,25 Injections of stress hormones at doses that enhance memory
when administered shortly after training are generally ineffective when administered several hours after training.26,27 Such findings indicate that the hormones affect memory by
modulating the storage or “consolidation” phase. Extensive evidence also indicates that epinephrine and glucocorticoids or stressful conditions that stimulate their release enhance
memory consolidation in human subjects when administered shortly before or after learning.12,13,28,29
Although epinephrine and glucocorticoids interact in influencing memory consolidation,24,30,31 their effects are initiated through different mechanisms.
Because epinephrine does not readily cross the blood–brain barrier, a peripheral central pathway must be involved in mediating epinephrine effects on brain activity in modulating
memory consolidation. The findings of many experiments indicate that epinephrine effects on memory consolidation are initiated by activation of peripheral β-adrenoceptors located on
vagal afferents that project to the nucleus of the solitary tract (NTS) in the brain stem. Noradrenergic projections originating in the NTS innervate forebrain structures involved in
learning and memory, including the amygdala,32,33 but
may also influence norepinephrine release via projections to the nucleus paragigantocellularis in the lower medulla, which projects to the locus coeruleus. The locus coeruleus
noradrenergic system is viewed as a broad system with projections to many areas involved in memory processing including the amygdala, hippocampus, and prefrontal cortex.34–36
Glucocorticoids are highly lipophilic and readily enter the brain to bind to mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs). These two receptor types differ in
their affinities for corticosterone and synthetic ligands. MRs have a high affinity for the natural steroids and are almost saturated during basal levels of corticosterone and
cortisol, whereas GRs have a high affinity for synthetic ligands such as dexamethasone and RU 28362.37 In
contrast to MRs, GRs become occupied only during stress and at the circadian peak. Several studies using pharmacological and genetic techniques indicate that the memory–modulatory
effects of glucocorticoids selectively involve activation of GRs.17,38–41 GRs are considered classical intra-somatic receptors
that, after their activation, translocate to the nucleus and regulate gene transcription by binding of receptor homodimers to DNA or other nuclear proteins.42–45 However, glucocorticoids or specific GR agonists also
have rapid (milliseconds to minutes) effects on the brain and behavior, suggesting that they may also produce fast-acting, nongenomic effects, presumably involving an activation of
Stress hormone effects on memory consolidation follow an inverted-U shaped doseresponse effect. Moderate doses of epinephrine or glucocorticoids enhance memory consolidation but lower
or higher doses are less effective or may even impair memory consolidation.49,50 Other
variables such as gender and age may also influence the direction of the effects of stress hormones on memory consolidation due to differences in stress responses and vulnerability
Stress hormone effects on memory consolidation depend further on the level of emotional arousal induced by the training experience. For example, posttraining injections of moderate
doses of corticosterone or dexamethasone, a synthetic ligand, enhance memory consolidation in a water-maze spatial task.54 However, the same glucocorticoid treatment impairs memory
consolidation when the task becomes more aversive by lowering the water temperature.54,55Similarly,
epinephrine and glucocorticoids, as well as drugs affecting many other neurotransmitter systems, are known to enhance memory of inhibitory avoidance training when administered after a
mild, low-arousing foot shock, but to impair memory consolidation when given after a strong, highly aversive foot shock that produces robust memory in control animals.56 Thus, these findings indicate that the efficacy and even
the direction of the effects of exogenous drug administration on memory consolidation depend on the level of endogenous emotional arousal evoked by the training experience.
To address the question raised earlier in this chapter of whether stress hormone effects on memory consolidation require emotional arousal, we recently investigated the importance of
emotional arousal in influencing stress hormone effects on memory consolidation in rats trained on an object recognition task.11 Learning tasks in animal experiments are often emotionally
arousing because of the punishment or reward necessary to elicit changes in behavior. It is obvious that with the use of such experimental conditions, it is not possible to determine
whether emotional arousal is a prerequisite in regulating stress hormone influences on memory processes. Although no rewarding or aversive stimulation is used during object
recognition training,57 such training induces modest novelty-induced stress or
arousal. However, extensive habituation of rats to the training apparatus (in the absence of any objects) prior to the training reduces the arousal level induced by object recognition
training. Thus, object recognition training may be performed under two distinct conditions in which rats are either exposed to the objects while in a state of heightened arousal or in
a less aroused state. We found that corticosterone administered systemically immediately after training enhanced 24-hour retention performance of rats that were not previously
habituated to the experimental context (i.e., emotionally aroused rats). In contrast, corticosterone did not affect 24-hour retention of rats that received extensive prior habituation
to the experimental context and thus had decreased novelty-induced emotional arousal during training.11 Clearly, these findings indicate that at least some degree
of training-associated endogenous emotional arousal is essential for enabling stress hormone effects on memory consolidation.
Recent studies of human memory have also investigated interactions of stress hormones with training-associated emotional arousal. Decreasing glucocorticoid levels below baseline with
the cortisol synthesis inhibitor metyrapone impaired long-term memory for both emotionally arousing and emotionally neutral information,58 presumably involving a reduced MR occupancy. However,
cortisol administration selectively enhance long-term memory of emotionally arousing, but not emotionally neutral, pictures.12,15 Consistent with these findings, Abercrombie and
colleagues14reported that levels of endogenous cortisol correlated with
enhanced memory consolidation only in individuals who were emotionally aroused.
The memory-enhancing effects of epinephrine administration or stress exposure immediately after learning also appear to depend on the arousal level.13,29 For
example, Cahill and Alkire13 recorded electrodermal skin responses in human subjects as
they viewed standard nonarousing slides, followed by infusions of epinephrine or saline. They reported that epinephrine-treated subjects showed enhanced memory for the first slides
(i.e., primacy effect). Likewise, electrodermal skin responses to those slides were significantly greater than responses to slides shown at a later time. Therefore, the authors
concluded that epinephrine effects on memory depend on the level of arousal at the time of encoding.
13.4. INVOLVEMENT OF AMYGDALA IN MEDIATING STRESS HORMONE EFFECTS ON MEMORY CONSOLIDATION
Why do stress hormones selectively enhance memory for emotionally arousing experiences? The findings described above suggest that stress hormones must interact with some other
component of emotional arousal in mediating memory enhancement. Our findings indicate that stress hormone effects on memory consolidation require amygdala activity. It is well
established that emotional experiences that induce the release of adrenal stress hormones also activate the amygdala.59
Lesions or temporary inactivation of the amygdala block the memory-modulatory effects induced by posttraining systemic injections of drugs affecting a variety of neuromodulatory
systems including norepinephrine, opioid peptides, GABA, vasopressin, and ACTH.9,60 Furthermore, as noted above, the amygdala mediates
epinephrine as well as glucocorticoid effects on memory consolidation.20,61 Selective NMDA-induced lesions of the amygdala restricted
to the basolateral complex (BLA; consisting of the lateral, basal, and accessory basal nuclei) block inhibitory avoidance memory enhancement induced by posttraining systemic
injections of the synthetic glucocorticoid dexamethasone.39 In contrast, lesions of the adjacent central nucleus (CEA)
do not block the dexamethasone-induced memory enhancement. Moreover, posttraining infusions of the specific GR agonist RU 28362 administered into the BLA, but not the CEA, enhanced
memory consolidation in a dose-dependent fashion, whereas intra-BLA infusions of the GR antagonist RU 38486 impaired memory consolidation.39 Corticotropin-releasing hormone (CRH) is another
neurotransmitter that is released into the amygdala as well as several other brain regions in response to arousing or stressful stimulation. Blockade of endogenous CRH in the BLA with
infusions of a CRH receptor antagonist impaired memory for emotionally arousing training,62 whereas preliminary findings indicate that infusions of CRH
into the BLA dose-dependently enhance memory consolidation. This evidence indicates that BLA activation by emotional arousal is a general gateway in mediating stress hormone and
neurotransmitter effects on memory consolidation.
13.4.1. Amygdala Interacts With Other Brain Regions
Other evidence indicates that the BLA is not a site of permanent storage of the enhanced memory trace but rather is involved in strengthening consolidation processes in other
brain regions.9,60 The evidence that lesions of the stria terminalis, a
major amygdala input–output pathway, block the memory-modulatory effects of systemic drug infusions and of drugs infused directly into the amygdala63–65 strongly suggests that the amygdala regulates memory
consolidation by influencing the storage of information in efferent brain regions. The BLA interacts with many brain regions, including the hippocampus, caudate nucleus and
insular, entorhinal, and anterior cingulate cortices in regulating the consolidation of different types of information.60 It also interacts with the hippocampus in regulating
stress (hormone) effects on memory consolidation of contextual/spatial components of training. Hippocampal GRs play a role in neuroplasticity66–69 and posttraining activation of hippocampal GRs
enhances memory consolidation for both appetitive and aversive training.40,70,71 However, BLA lesions block the memory enhancement
produced by posttraining intra-hippocampal infusions of a GR agonist.40 Similarly, electrophysiological
findings indicate that BLA lesions or temporary blockade of BLA functioning impair stress- or perforant path stimulation-induced long-term potentiation in the dentate
gyrus.72,73 These findings indicate that BLA neuronal activity is
required for enabling memory modulation induced by local GR activation in the hippocampus. Since the BLA is normally activated by emotional arousal, such evidence may provide an
explanation for the findings that stress hormones selectively influence memory consolidation of emotionally arousing experiences.
Other findings indicate the existence of interactions between the BLA and medial prefrontal cortex (mPFC). The mPFC is implicated in higher cognitive functions such as thought,
decision-making, and working memory74,75 and also plays a role in memory consolidation.76 The BLA interacts with the mPFC via reciprocal
inhibitory connections.77,78 In a recent study, we examined whether the BLA and mPFC
interact in regulating glucocorticoid effects on memory consolidation.79 A GR agonist infused posttraining
into either the mPFC or the BLA enhanced memory consolidation of inhibitory avoidance training. The same GR agonist administered into the mPFC also increased BLA neuronal
activity, as assessed by elevated phosphorylation levels of the transcription factor mitogen-activated protein kinase (MAPK) in the BLA. Importantly, the GR agonist infused into
the mPFCs of animals that had not received inhibitory avoidance training did not increase MAPK levels in the BLA, supporting the hypothesis that glucocorticoid effects on memory
consolidation and brain activity require training-associated emotional arousal. Because the inhibition of this MAPK activation in the BLA with infusions of a MEK inhibitor blocked
the memory enhancement induced by intra-mPFC infusions of the GR agonist,79 these findings further indicate that
BLA activity is essential in regulating stress hormone effects on the consolidation of emotionally arousing memories.
13.4.2. Amygdala Involvement In Human Studies
Considerable evidence from human studies indicates that the enhancing influence of emotional arousal on memory involves activation of the amygdala. Human studies, however, have
not yet investigated a possible selective involvement of the BLA. The evidence that emotionally arousing stimulation does not enhance long-term memory in human subjects with
amygdala lesions supports the view that amygdala activation may be critical for emotionally enhanced memory.80 Interestingly, the reactions of amygdala-damaged
subjects to the emotional material in these studies appeared normal, suggesting that the amygdala in humans may not be as critical for the production of emotional
reactions per se.
The involvement of amygdala activation in emotionally influenced memory has also been investigated in many studies using positron emission tomography (PET) and functional magnetic
resonance imaging (fMRI) in healthy humans.81–84These studies reported that activity of the amygdala
assessed during the presentation of emotionally arousing stimuli correlated highly with memory of the stimuli tested weeks later. Further, the relationship between amygdala
activity during encoding and subsequent long-term memory was greatest for the most emotionally arousing stimuli. Human studies indicate that the enhanced memory for emotionally
arousing events (versus non-arousing events) involves amygdala modulation of the hippocampal formation.85–87 Collectively, these studies of emotionally
influenced memory in human subjects are consistent with findings of animal experiments and indicate that emotional arousal-induced amygdala (BLA) activation may be a critical step
in enabling stress hormone effects in modulating memory processes involving other brain regions including hippocampus-dependent explicit/declarative memory.
13.5. ROLE OF EMOTIONAL AROUSAL-INDUCED NORADRENERGIC ACTIVATION WITHIN AMYGDALA IN ENABLING EPINEPHRINE AND GLUCOCORTICOID EFFECTS ON MEMORY CONSOLIDATION
The enhancing effects of adrenal stress hormones on memory consolidation depend on the integrity of the amygdala noradrenergic system. Infusions of β-adrenoceptor antagonists
administered into the amygdala block the memory-enhancing effects of peripherally administered epinephrine that, as discussed above, are known to be mediated by activation of the
noradrenergic cells of the NTS and locus coeruleus.61 Glucocorticoids also require noradrenergic activation
within the amygdala to influence memory for emotionally arousing training. A β-adrenoceptor antagonist infused into the BLA blocks the memory-enhancing effect of systemically
administered glucocorticoids.88,89Furthermore, a β-adrenoceptor antagonist infused into the BLA
blocked memory enhancement induced by a GR agonist infused into the hippocampus.90
Studies using in vivo microdialysis indicate that stress induced by prolonged immobilization or tail pinch increased amygdala norepinephrine levels.91,92 Even
a single mild foot shock of the kind typically used in inhibitory avoidance training increased amygdala norepinephrine levels93 and the increase in norepinephrine varied with footshock
intensity.94 Furthermore, as shown in Figure 13.1, amygdala norepinephrine levels assessed following inhibitory avoidance training correlated
with retention latencies tested 24 hours later,95 whereas posttraining infusions of norepinephrine or
β-adrenoceptor agonists administered into the BLA enhanced memory consolidation.96,97
Norepinephrine levels in the amygdala are significantly correlated with retention latency scores. Each line represents norepinephrine levels as a percentage of baseline for an
individual rat. Latency to enter the dark compartment on the retention test (more...)
Such findings suggest that systemically administered stress hormones may influence noradrenergic function by altering the synthesis, release, and/or reuptake of norepinephrine. In
accord with this hypothesis, Williams and colleagues33showed that epinephrine administered immediately after inhibitory
avoidance training increased norepinephrine levels in the amygdala.
Brainstem noradrenergic cells in the locus coeruleus and NTS are involved not only in mediating epinephrine effects on memory consolidation but also express high levels of
GRs.98 Posttraining infusions of a GR agonist into the NTS
dose-dependently enhanced memory consolidation of inhibitory avoidance training and the memory enhancement was blocked by intra-BLA infusions of the β-adrenoceptor antagonist
atenolol.50 The findings of a recent in vivomicrodialysis
experiment support the view that glucocorticoids may influence norepinephrine release in the BLA. Corticosterone administration after inhibitory avoidance training increased
norepinephrine levels in the amygdala.99 In contrast, corticosterone did not increase norepinephrine
levels in the amygdala when administered to naive rats that did not receive inhibitory avoidance training, indicating that glucocorticoids facilitate, but cannot initiate, the release
of norepinephrine in the amygdala.
At a postsynaptic level, glucocorticoids may enhance memory consolidation by potentiating β-adrenoceptor-cAMP/PKA efficacy in the BLA.100 Activation of β-adrenoceptors in the BLA enhanced memory
consolidation via stimulation of the cAMP/PKA pathway.101,102 We
found that intra-BLA infusions of a GR antagonist attenuated the dose-response effects of a β-adrenoceptor agonist on retention enhancement for inhibitory avoidance training. The GR
antagonist had no effect on memory enhancement induced by posttraining intra-BLA infusions of the synthetic cAMP analog 8-Br-cAMP.100 These findings suggest that glucocorticoids facilitate the
efficacy of noradrenergic stimulation in the BLA on memory consolidation via an interaction with the β-adrenoceptor-cAMP cascade. A model of this interaction is illustrated
in Figure 13.2.
Summary of interactions of glucocorticoids with the noradrenergic system of the basolateral amygdala at both presynaptic and post-synaptic sites as suggested by the findings
of our experiments. α1 =
13.5.1. Role Of Emotional Arousal-Induced Noradrenergic Activation
The findings summarized above indicate that emotional arousal induces the release of norepinephrine in the BLA and that adrenal stress hormones may facilitate this
training-induced noradrenergic activation. Such findings suggest that emotional arousal-induced noradrenergic activation within the BLA may be essential in enabling stress hormone
effects on memory consolidation.
In a recent experiment we investigated this hypothesis.89 As addressed above, corticosterone enhanced memory
consolidation of object recognition training only in emotionally aroused rats that were not previously habituated to the context. Object recognition training in these rats also
induced marked increases in noradrenergic activity within the BLA, as assessed by immunoreactivity for phosphorylated tyrosine hydroxylase (the rate-limiting enzyme in the
biosynthesis of norepinephrine). As shown in Figure 13.3, a β-adrenoceptor antagonist
administered either systemically or into the BLA blocked this corticosterone-induced memory enhancement. In contrast, infusion of a β-adrenoceptor antagonist into the hippocampus
did not prevent the corticosterone-induced memory enhancement of object recognition training. These findings further indicate that glucocorticoids require noradrenergic activity
in the BLA in regulating memory consolidation.
Glucocorticoid effects on memory consolidation for object recognition training require noradrenergic activation. Data represent discrimination index (%) on a 24-hour
retention trial, expressed as mean ± SEM. (A) Effects of immediate posttraining (more...)
Importantly, training of context-habituated rats on the object recognition task did not induce significant increases in noradrenergic activation within the BLA.89 If the failure of corticosterone to enhance memory
consolidation in context-habituated rats is due selectively to insufficient arousal-induced noradrenergic activation, then posttraining pharmacological augmentation of
noradrenergic activity should provide the activation normally produced by novelty stress and enable glucocorticoid enhancement of memory consolidation. To examine this
implication, a low dose of the α2-adrenoceptor antagonist yohimbine, which
increases norepinephrine levels in the brain, was administered to habituated rats either alone or together with corticosterone immediately after object recognition training.
Yohimbine administered alone did not affect retention performance. However, as shown in Figure 13.3, corticosterone administered concurrently with yohimbine induced dose-dependent
retention enhancement. Posttraining injections of the two drugs separated by a 4-hour delay did not induce a preference for the novel object on the retention. These findings thus
indicate that arousal-induced noradrenergic activation is necessary to mediate glucocorticoid effects on memory consolidation but that pharmacologically stimulated noradrenergic
activity mimics the effects of emotional arousal in enabling glucocorticoid enhancement of memory consolidation under low-arousing training conditions.89 These finding support the notion that the noradrenergic
component of emotional arousal is critical for memory enhancement induced by glucocorticoids and possibly by epinephrine.
13.5.2. Interactions At Cellular Level
Synergistic effects of glucocorticoids and the noradrenergic system in peripheral tissues including the lungs and liver have been implicated in the regulation of several cellular
functions.103 Is there molecular evidence for interactions between
these two systems in regulating memory consolidation? We recently reported that corticoster-one interacts with emotion-induced noradrenergic activation in activating the cAMP
response-element binding (CREB) pathway in the BLA.89 Several findings have implicated CREB phosphorylation
in the BLA in the modulation of memory consolidation.104,105 We found that corticosterone administered immediately
after object recognition training significantly increased the number of pCREB-positive neurons in the BLA. Corticosterone did not alter the number of pCREB-positive BLA neurons in
rats that received prior habituation to the training context. Importantly, however, corticosterone administered together with the noradrenergic stimulant yohimbine after object
recognition training significantly increased pCREB immunoreactivity in the BLA. Thus, these findings are in accord with behavioral studies and indicate that corticosterone
activates the CREB pathway in the BLA only with training conditions that induce sufficient noradrenergic activation.
Other studies have indicated that glucocorticoids may interact with noradrenergic mechanisms in increasing the expression and enzymatic activity of the MAPK pathway, leading to an
increased expression of the immediate early gene Egr1 (early growth response-1).106 Like CREB, phosphorylation
of MAPKs is considered critical for memory consolidation and long-term neuronal plasticity.107,108 Blockade of MAPK signaling in the hippocampus
abolishes the enhancing effect of systemically administered corticosterone on contextual fear conditioning.106 Glucocorticoid effects on MAPK activation may be
modulated by β-adrenoceptor activation. Activation of β-adrenoceptors by epinephrine and norepinephrine leads to the dissociation of G protein subunits β and γ. It has been
demonstrated that β G protein subunits interact with phosphoinositide-3 kinase to stimulate the MAPK pathway.109,110 Further, epinephrine and norepinephrine were found to
potentiate ligand-dependent GR transactivation in cultured hippocampal cells via β2-adrenoceptors.111
The evidence summarized in this chapter indicates that adrenal stress hormones influence memory processes in various animal and human memory tasks. Acutely administered or released
epinephrine or glucocorticoids dose-dependently enhance the consolidation of long-term memory. However, the effects of stress hormones on the storage of long-term memories depend
critically on the arousal state and noradrenergic activation of the BLA. These findings may help to explain why stress hormones do not uniformly modulate memory for all kinds of
information but rather, preferentially influence the consolidation of emotionally arousing information. As adrenal stress hormones also play a critical role in the development of
traumatic memories and posttraumatic stress disorder (PTSD),112–114 these findings may provide some understanding of the
neurobiological processes that underlie the development of PTSD as well as some possible implications for therapeutic intervention (see Reference 115) to ensure that significant events are well remembered, but do
not turn into pathophysiological conditions.
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Men, women in more satisfying relationships have lower testosterone
by Jared Wadley
(Medical Xpress)—Many people assume that the more testosterone, the better, but a new University of Michigan study finds that might not always be the case in romantic
Low testosterone levels may be a
good thing for both men and women, who reported more satisfaction and commitment to their relationships when they had lower levels.
Higher testosterone is generally thought to be associated with attracting sexual partners, but might not be compatible with some kinds of long-term relationships, said Robin
Edelstein, U-M associate professor of psychology and the study's lead author.
"The assumption is generally that high testosterone is good for sexual relationships," she said. "These findings suggest that once people are in a relationship, lower levels of
testosterone may be beneficial—or may reflect better ongoing relationship dynamics."
Previous studies have examined how testosterone levels are associated with the quality of men's relationships, but the U-M research is among the first to demonstrate the
association among women.
The study used data from 39 heterosexual couples whose ages ranged from 18 to 31 and were in relationships from two months to seven years. They answered questions about their
satisfaction ("My relationship is close to ideal"), commitment ("I want our relationship to last forever") and investment ("I have invested a great deal into our relationship that
I would lose if the relationship were to end"). Participants also provided their saliva for analysis.
Researchers concluded that the quality of a person's relationship was associated with his/her own and his/her partner's testosterone levels. Both men's and women'stestosterone was negatively correlated with their
own and their partner's satisfaction and commitment. The couples were more satisfied and committed when they or their partner had low testosterone levels, the research
The findings appear in the April issue of Hormones and Behavior.
Relationship satisfaction linked with changing use of contraception
Women's sexual satisfaction in long-term heterosexual relationships may be influenced by changes in hormonal contraceptive use, research from the University of Stirling shows.
The study, published in Psychological Science, a journal of the Association for Psychological Science, was carried out by researchers from the
universities of Stirling, Glasgow, Newcastle, Northumbria and Charles University in Prague.
The team looked at a sample of 365 couples, and investigated how satisfaction levels – in both sexual and non-sexual aspects of long-term relationships – were influenced by women's current and
historical use of hormonal contraception.
"Our findings showed women who had met their partner while taking the pill and were still currently taking it – as well as those who had never used the pill at any point – reported greater sexual
satisfaction than those women who had begun or stopped using the pill during the course of the relationship," says lead researcher Craig Roberts from Stirling's Division of Psychology.
"In other words, the congruence of women's pill use throughout the relationship had a greater influence on sexual satisfaction levels than either simply being on the pill or not being on the pill."
The team found there was no difference in the non-sexual aspects of relationship satisfaction between the groups of women. Additionally, women's history of pill use was also found to make no
difference to their male partners' relationship satisfaction in both sexual and non-sexual contexts.
"Previous research has shown that hormonal contraceptives, such as the pill, subtly alter women's ideal partner preferences and that often women who are using the pill when they meet their
partner find the same partner less physically attractive when they come off the pill," says Roberts.
"Our new results support these earlier findings but, crucially, they also point to the impact a change in hormonal contraceptive use during a relationship – either starting or stopping – can have on a woman's sexual
satisfaction with her partner."
According to Roberts, "The pill has been a tremendously positive social force, empowering women and giving them greater control over their lives, but there is also a lot of controversy surrounding the
question of whether hormonal contraceptives alter women's libido and sexual satisfaction."
"These results show that examining current use is not enough to answer this question. What seems to be important is whether a woman's current use matches her use when she began the relationship with her partner. We hope our results
will help womenunderstand why they might feel the way
they do about their partner when they change use," Roberts concludes.
Do women perceive other women in red as more sexually receptive?
Previous research has shown that men perceive the color red on a woman to be a signal of sexual receptivity. Women are more likely to wear a red shirt when they are expecting to
meet an attractive man, relative to an unattractive man or a woman. But do women view other women in red as being more sexually receptive? And would that result in a woman
guarding her mate against a woman in red? A study published inPersonality and Social Psychology Bulletin sought to answer these
Perceptions of Sexual Receptivity
Nonverbal communication via body language, facial expressions and clothing conveys information to others, occasionally with unintended social consequences. Researchers from the
University of Rochester, Trnava University, and the Slovak Academy of Sciences collaborated to study what information the color red conveys to women.
Three experiments were involved in the study. The first experiment asked individuals to compare a digital image of a woman wearing red versus a woman wearing white. Participants
were asked questions about the woman's sexual receptivity, such as "This person is interested in sex," which required moving a bar along a sliding scale from "No, not at all" to
"Yes, definitely." Participants rated the woman in red as more sexually receptive than the woman in white. Sixty-nine percent of participants reported they were in a committed
relationship, and the results of the experiment showed that participant's relationship status did not have a significant effect on their perceptions of women in white versus red.
Derogation and Mate-Guarding
The researchers tested whether participants would derogate a woman in red and the likelihood of guarding their mate from a woman in red in subsequent experiments. "Derogation
[involves] speaking poorly of another person to make them seem inferior, undesirable, or unlikeable, while making oneself seem superior and more likable by
contrast," lead researcher Adam Pazda explains. "Mate-guarding is the act of protecting one's own romantic partner from romantic or sexual encounters with others." The researchers
specifically tested whether women would derogate on the topics of fidelity ("I would guess that this women cheats on men"), and financial resources ("I would guess that this woman
has no money").
The third and final experiment altered the conditions slightly. Instead of comparing white and red, the researchers chose to compare green and red in an effort to eliminate the
possible bias of associating white and purity. "Using green allowed us to equate both hues on lightness and chroma, which allowed for a more rigorous, controlled test of the red
effect," Pazda said. The participants were located in an Eastern European country, rather than the U.S. as in the two prior experiments. To determine intent to mate-guard,
participants were asked: "How likely would you be to introduce this person to your boyfriend?" and "How likely would you be to let your boyfriend spend time alone with this
Results from the last two experiments confirmed that women found another woman in red to be more sexually receptive, versus white or green. In terms of derogation, participants
who viewed a woman in red were more likely to derogate the woman's sexual fidelity, but not financial resources. Participants did not show any difference between sexual fidelity
derogation and financial resource derogation in relation to a woman in white. Women were more likely to guard their partner from a woman dressed in red if they are in a committed
relationship, relative to a woman in green.
More information: Pazda, A.D., Prokop, P., and Elliot, A.J. (2014). Red and Romantic Rivalry: Viewing Another Woman in Red Increases
Perceptions of Sexual Receptivity, Derogation and Intentions to Mate-Guard. Personality and Social Psychology Bulletin,
Guarding your girl linked to sperm quality in humans
ПОЛОВОГО ПАРТНЕРА (MATE GUARDING)
Men who perform "mate guarding" behaviours such as staying close to their wife or girlfriend at a party are likely to have poorer-quality sperm than men who do not, research suggests.
A UWA study surveyed 45 WA men in committed heterosexual
relationships about their mate guarding actions and analysed their ejaculate samples.
It found men who performed fewer mate guarding behaviours had a greater concentration of sperm, a higher percentage of motile sperm and sperm that swam faster and less erratically than men who performed more.
Samantha Leivers, who conducted the UWA PhD research, says there is evidence mate guarding behaviour is linked to sperm quality in birds and fish but the study is the first to investigate the
relationship in people.
She says mate guarding in humans is quite broad and can include anything from physically defending a partner to giving flowers, jewellery or an engagement ring.
"Some of the behaviours can be not leaving your partner's side at a party or you can give a guy the stink eye if he's looking at your girlfriend or you can actually physically attack another man
if you think that he's at your girlfriend," Ms Leivers says.
"There's also subtle ways, so giving gifts signals to other men that 'this woman's in a relationship'.
"Even the more negative things that you think of, like moaning about your partner to your friends, because that makes her look like a less desirable mate to them."
Situational factors considered
Ms Leivers says it is unclear from the study whether sperm quality is plastic (dependent on situational factors) or fixed
when it comes to mate guarding.
She says men who are unable to mate guard due to circumstances such as long distance relationships or a partner that does
not allow mate guarding, may experience a plastic effect that improves his sperm quality.
"Once he's able to start mate guarding more, maybe the sperm quality would
"Another idea is that it's actually fixed, in that men who naturally have lower quality sperm basically increase their
chances of paternity through the mate guarding.
"So if they have low quality sperm there is just this innate response that they have to increase their mate guarding
Ms Leivers says the question is very difficult to answer in humans because it would be unethical to manipulate peoples'
behaviour in relationships.
"My guess would probably be that it's plastic but we don't know," she says.
Researchers call for coordinated care to address risks – NIH-funded study
• Press Release
Many patients with psychosis develop health risks associated with premature death early in the course of their mental illness, researchers have found.
Patients with schizophrenia are already known to have higher rates of premature death than the general population. The study found that elevated risks of heart disease and metabolic issues
such as high blood sugar in people with first episode psychosis are due to an interaction of mental illness, unhealthy lifestyle behaviors and antipsychotic medications that may accelerate
Patients entered treatment with significant health concerns – including excess weight, smoking, and metabolic issues – despite an average age of only 24 years. The study identifies key
opportunities for health care systems to improve the treatment of such patients with first episode psychosis. The research was funded by the National Institute of Mental Health (NIMH), part
of the National Institutes of Health.
Christoph Correll, M.D., of The Zucker Hillside Hospital, Hofstra North Shore-Long Island Jewish School of Medicine, New York, and colleagues, report their findings on Oct. 8, 2014
in JAMA Psychiatry.
The study is among the
first of several to report results from the Recovery After an Initial Schizophrenia Episode (RAISE) project, which was developed by NIMH to examine first
episode psychosis before and after specialized treatment was offered in community settings.
The researchers studied nearly 400 individuals between the ages of 15 and 40 with first episode psychosis, who presented for treatment at 34 community-based clinics across 21 states.
The frequency of obesity was similar to the same age group in the general population. However, smoking and metabolic syndrome (a combination of conditions including obesity, high blood
pressure, high blood sugar, and abnormal blood fats, such as cholesterol and triglycerides) were much more common. Frequencies of dyslipidemia (an abnormal amount of blood fats, such as
cholesterol and triglycerides) and pre-hypertension in this relatively young group of study participants were at least as high as rates typically found in people 15-20 years older.
Notably, treatment with antipsychotic medication, even after brief exposure (participants’ average exposure was 47 days), was associated with an increased risk of metabolic syndrome, which is
a major risk for future cardiovascular illness.
Researchers concluded that people with first episode psychosis need a team-based health care approach that combines psychiatric and general medical care to address the full range of needs.
Patients need early interventions for psychiatric illness, lower-risk antipsychotic medications, routine monitoring, and smoking cessation programs to improve health and reduce healthcare
“Our results strongly suggest that clinicians need to pay much more attention to promoting physical health in people with severe mental illness,” said lead author Christoph Correll, M.D. “We
need to routinely educate patients about healthy lifestyle behaviors, monitor physical health, choose lower risk treatments whenever possible, and manage issues as they arise. Without a
combined physical and mental health care approach, we miss major opportunities to improve psychiatric as well as medical health in patients with schizophrenia and other severe conditions.”
1Correll CU, Robinson DG, Schooler NR, Brunette MF, Mueser KT,
Rosenheck RA, Marcy P, Addington J, Estroff SE, Robinson J, Penn D, Azrin S, Goldstein A, Severe J, Heinssen R, Kane JM. Cardiometabolic Risk in First Episode Schizophrenia-Spectrum Disorder
Patients: Baseline Results from the RAISE-ETP Study,JAMA Psychiatry, Oct. 8, 2014
False memories could be a side-effect of human ability to learn rules
Our tendency to create false memories could be related to our ability to learn rules according to research from Queen Mary University of London (QMUL).
Errors in memory range from misremembering minor details of events to generating illusory memories of entire episodes. These inaccuracies have wide-ranging implications in crime-witness accounts
and in the courtroom but the researchers believe that they could be an inevitable side-effect of our brains' ability to learn trends, and process objects into categories useful for our survival.
The wiring in our brains is generally well-designed to capture the world around us, but the computations it uses have certain quirks as shown in well-known optical illusions. The new research
suggests that we could also createfalse memories for the
Professor Lars Chittka, from the School of Biological and Chemical Sciences, at QMUL and co-author of the paper, said:
"Our memory is often surprisingly inaccurate, even though we typically feel that we can recall events as they really occurred. For example, witnesses of a nocturnal street robbery might describe
the perpetrator as a hooded teenager, when it later turns out that the assailant was middle-aged and balding."
Participants in the study were given two tests, one to measure their ability to identify associations within groups of words and the other which was designed to elicit false memories of words
appearing in a list. The peer-reviewed results, published in the journal 'F1000Research', showed that people who were better at grouping words into categories were also more likely develop false
memories, leading researchers to believe the two may be linked.
According to Professor Chittka:
"On the surface creating false memories would seem to be bad for our survival, but historical research suggests that false memories are often those that fall in with previously learned rules and
cultural norms which can be useful.
"Our research suggests that individuals who are particularly good at learning rules and classifying objects by common properties are also particularly prone to false memory illusions. So,
like optical illusions, it might be that false memories
are a by-product of the clever ways our brains monitor the world around us."
More information: Hunt K and Chittka L. False memory susceptibility is correlated with categorisation ability in humans [v1; ref status: indexed,
http://f1000r.es/3ty] F1000Research 2014, 3:154 DOI:
Study finds that learning by repetition impairs recall of details
practice doesn't always make perfect.
UC Irvine neurobiologists Zachariah Reagh and Michael Yassa have found that whilerepetition enhances the factual
content of memories, it can reduce the amount of detail stored with those memories. This means that with repeated recall, nuanced aspects may fade away.
In the study, which appears this month in Learning & Memory, student participants were asked to look
at pictures either once or three times. They were then tested on their memories of those images. The researchers found that multiple views increased factualrecall but actually hindered subjects' ability to reject similar "imposter" pictures. This suggests that the details of those memories may have been
shaken loose by repetition.
This discovery supports Reagh's and Yassa's Competitive Trace Theory – published last year in Frontiers in Behavioral Neuroscience – which posits that the details of a memorybecome more subjective the more they're recalled and can compete with bits of other similar memories. The scientists hypothesize that this may even lead
to false memories, akin to a brain version of the telephone game.
Yassa, an assistant professor of neurobiology & behavior, said that these findings do not discredit the practice of repetitive learning. However,
he noted, pure repetition alone has limitations. For a more enriching and lasting learning experience through which nuance and detail are readily recalled, other mnemonic techniques should be
used to complement repetition.
Study creates new memories by directly changing the brain
By studying how memories are made, UC Irvine neurobiologists created new, specific memories by direct manipulation of the brain, which could prove key to understanding and potentially resolving
learning and memory disorders.
Research led by senior author Norman M. Weinberger, a research professor of neurobiology & behavior at UC Irvine, and colleagues has shown that specific memories can be made by directly
altering brain cells in the cerebral cortex,
which produces the predicted specific memory. The researchers say this is the first evidence that memories can be created by direct cortical manipulation. Study results appeared in the August 29
issue of Neuroscience.
During the research, Weinberger and colleagues played a specific tone to test rodents then stimulated the nucleus basalis deep within their brains, releasing acetylcholine (ACh), a chemical
involved in memory formation. This procedure increased the number of brain cells responding to the specific tone. The following day, the scientists played many sounds to the animals and found
that their respiration spiked when they recognized the particular tone, showing that specific memory content was created by brain changes directly induced during the experiment. Created memories
have the same features as natural memories including long-term retention.
"Disorders of learning and
memory are a major issue facing many people and since we've found not only a way that the brain makes memories, but how to create new memories with specific content, our hope is that our
research will pave the way to prevent or resolve this global issue," said Weinberger, who is also a fellow with the Center for the Neurobiology of Learning & Memory and the Center for Hearing
Research at UC Irvine.
The creation of new memories by directly changing the cortex is the culmination of several years of research in Weinberger's lab implicating the nucleus basalis and ACh in brain plasticity and
specific memory formation. Previously, the authors had also shown that the strength of memory is controlled by the number of cells in the auditory cortex that process a sound.