Behavioral Neuroscience

Introduction to the special section on “Hormones and cognition: Perspectives, controversies, and challenges for future research”.
The research of the past two decades has firmly established that hormones modulate numerous aspects of cognitive function, including memory, attention, decision-making, and sensory processing. That such a wide variety of hormones influence cognition mediated by multiple nonhypothalamic brain regions illustrates the critical importance of hormones to neural and cognitive function. The diversity of hormonal effects on cognition is evident in the collection of reviews and original research articles assembled for this special section. Together, these articles provide an overview of recent research on varied topics in hormones and cognition, address controversial issues in the field, and discuss challenges that must be overcome in future research to gain a better understanding of the mechanisms through which hormones modulate cognitive function. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Estrogen effects on the brain: Actions beyond the hypothalamus via novel mechanisms.
From its origins in how the brain controls the endocrine system via the hypothalamus and pituitary gland, neuroendocrinology has evolved into a science that now includes hormone action on many aspects of brain function. These actions involve the whole central nervous system and not just the hypothalamus. Advances in our understanding of cellular and molecular actions of steroid hormones have gone beyond the important cell nuclear actions of steroid hormone receptors to include signaling pathways that intersect with other mediators such as neurotransmitters and neuromodulators. This has, in turn, broadened the search for and identification of steroid receptors to include nonnuclear sites in synapses, dendrites, mitochondria, and glial cells, as well as cell nuclei. The study of estrogen receptors and estrogen actions on processes related to cognition, mood, autonomic regulation, pain, and neuroprotection, among other functions, has led the way in this new view of hormone actions on the brain. In this review, we summarize past and current work in our laboratory on this topic. This exciting and growing field involving many laboratories continues to reshape our ideas and approaches to neuroendocrinology both at the bench and the bedside. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
To modulate and be modulated: Estrogenic influences on auditory processing of communication signals within a socio-neuro-endocrine framework.
Gonadal hormones modulate behavioral responses to sexual stimuli, and communication signals can also modulate circulating hormone levels. In several species, these combined effects appear to underlie a two-way interaction between circulating gonadal hormones and behavioral responses to socially salient stimuli. Recent work in songbirds has shown that manipulating local estradiol levels in the auditory forebrain produces physiological changes that affect discrimination of conspecific vocalizations and can affect behavior. These studies provide new evidence that estrogens can directly alter auditory processing and indirectly alter the behavioral response to a stimulus. These studies show that: 1) Local estradiol action within an auditory area is necessary for socially relevant sounds to induce normal physiological responses in the brains of both sexes; 2) These physiological effects occur much more quickly than predicted by the classical time-frame for genomic effects; 3) Estradiol action within the auditory forebrain enables behavioral discrimination among socially relevant sounds in males; and 4) Estradiol is produced locally in the male brain during exposure to particular social interactions. The accumulating evidence suggests a socio-neuro-endocrinology framework in which estradiol is essential to auditory processing, is increased by a socially relevant stimulus, acts rapidly to shape perception of subsequent stimuli experienced during social interactions, and modulates behavioral responses to these stimuli. Brain estrogens are likely to function similarly in both songbird sexes because aromatase and estrogen receptors are present in both male and female forebrain. Estrogenic modulation of perception in songbirds and perhaps other animals could fine-tune male advertising signals and female ability to discriminate them, facilitating mate selection by modulating behaviors. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Building a better hormone therapy? How understanding the rapid effects of sex steroid hormones could lead to new therapeutics for age-related memory decline.
A wealth of data collected in recent decades has demonstrated that ovarian sex-steroid hormones, particularly 17β-estradiol (E2), are important trophic factors that regulate the function of cognitive regions of the brain such as the hippocampus. The loss of hormone cycling at menopause is associated with cognitive decline and dementia in women, and the onset of memory decline in animal models. However, hormone therapy is not currently recommended to prevent or treat cognitive decline, in part because of its detrimental side effects. In this article, it is proposed that investigations of the rapid effects of E2 on hippocampal function be used to further the design of new drugs that mimic the beneficial effects of E2 on memory without the side effects of current therapies. A conceptual model is presented for elucidating the molecular and biochemical mechanisms through which sex-steroid hormones modulate memory, and a specific hypothesis is proposed to account for the rapid memory-enhancing effects of E2. Empirical support for this hypothesis is discussed as a means of stimulating the consideration of new directions for the development of hormone-based therapies to preserve memory function in menopausal women. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Endocrine substrates of cognitive and affective changes during pregnancy and postpartum.
Pregnancy and motherhood constitute periods of tremendous hormonal variation that orchestrate parturition, lactation, maternal care, maternal aggression, and recognition of offspring, among other functions. Cognitive processing also varies during pregnancy and motherhood and may serve an adaptive function in preparation for parturition and rearing. Additionally, maternal experience may have enduring consequences for the brain, behavior, and cognition long after offspring are mature. However, the early postpartum period also renders women psychologically vulnerable as approximately 15% of women experience postpartum depression, with estimates of 50–80% reporting a milder form of depression termed “maternal blues.” This review will present literature on pregnancy- and parity-related changes in both cognition and affect and how these changes likely involve plastic changes within the hippocampus, a region that is sensitive to reproductive hormones. Further, this review will discuss steroid and peptide hormones that may contribute to affective and cognitive disruptions during pregnancy and postpartum. Research in this area may reveal insight into how pregnancy and motherhood alter the likelihood of developing postpartum depression and related disorders. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Hormones and cognitive functioning during late pregnancy and postpartum: A longitudinal study.
This longitudinal study investigated the possible influence of estradiol (E₂), progesterone (P), testosterone (T), cortisol (CORT), and prolactin (PRL) levels on cognitive functioning during late pregnancy and the early postpartum period. The performance of 55 pregnant women on a battery of neuropsychological tests, tested once during the third trimester of pregnancy and once during the early postpartum period, was compared with that of 21 nonpregnant controls matched for age and education. Women in the pregnancy group had significantly lower scores than the controls during both the pre- and postpartum visits on tasks of verbal recall and processing speed. CORT levels were significantly associated, in an inverted-U function, with verbal recall scores at both the pregnancy and at postpartum periods and with spatial abilities at postpartum only. During pregnancy, PRL levels were associated in both a linear and an inverted-U function with scores on tests of paragraph recall and in a linear function with scores on tests of executive function. At postpartum, E₂ and CORT were negatively associated in a linear fashion with attention scores. These findings provide new evidence that fluctuating hormone levels during late pregnancy and early postpartum may modulate selected cognitive abilities. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Early androgen effects on spatial and mechanical abilities: Evidence from congenital adrenal hyperplasia.
There is considerable controversy about the origins of sex differences in cognitive abilities, particularly the male superiority in spatial abilities. We studied effects of early androgens on spatial and mechanical abilities in adolescents and young adults with congenital adrenal hyperplasia (CAH). On tests of three-dimensional mental rotations, geography, and mechanical knowledge, females with CAH scored higher than their unaffected sisters, and males with CAH scored lower than their unaffected brothers. Exploratory regression analyses suggest that androgens affect spatial ability in females directly and through male-typed activity interests. Findings indicate that early androgens influence spatial and mechanical abilities, and that androgen effects on abilities may occur in part through effects on sex-typed activity interests. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Interplay of oxytocin, vasopressin, and sex hormones in the regulation of social recognition.
Social Recognition is a fundamental skill that forms the basis of behaviors essential to the proper functioning of pair or group living in most social species. We review here various neurobiological and genetic studies that point to an interplay of oxytocin (OT), arginine-vasopressin (AVP), and the gonadal hormones, estrogens and testosterone, in the mediation of social recognition. Results of a number of studies have shown that OT and its actions at the medial amygdala seem to be essential for social recognition in both sexes. Estrogens facilitate social recognition, possibly by regulating OT production in the hypothalamus and the OT receptors at the medial amygdala. Estrogens also affect social recognition on a rapid time scale, likely through nongenomic actions. The mechanisms of these rapid effects are currently unknown but available evidence points at the hippocampus as the possible site of action. Male rodents seem to be more dependent on AVP acting at the level of the lateral septum for social recognition than female rodents. Results of various studies suggest that testosterone and its metabolites (including estradiol) influence social recognition in males primarily through the AVP V1a receptor. Overall, it appears that gonadal hormone modulation of OT and AVP regulates and fine tunes social recognition and those behaviors that depend upon it (e.g., social bonds, social hierarchies) in a sex specific manner. This points at an important role for these neuroendocrine systems in the regulation of the sex differences that are evident in social behavior and of sociality as a whole. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Estradiol-dependent modulation of serotonergic markers in auditory areas of a seasonally breeding songbird.
Because no organism lives in an unchanging environment, sensory processes must remain plastic so that in any context, they emphasize the most relevant signals. As the behavioral relevance of sociosexual signals changes along with reproductive state, the perception of those signals is altered by reproductive hormones such as estradiol (E2). We showed previously that in white-throated sparrows, immediate early gene responses in the auditory pathway of females are selective for conspecific male song only when plasma E2 is elevated to breeding-typical levels. In this study, we looked for evidence that E2-dependent modulation of auditory responses is mediated by serotonergic systems. In female nonbreeding white-throated sparrows treated with E2, the density of fibers immunoreactive for serotonin transporter innervating the auditory midbrain and rostral auditory forebrain increased compared with controls. E2 treatment also increased the concentration of the serotonin metabolite 5-HIAA in the caudomedial mesopallium of the auditory forebrain. In a second experiment, females exposed to 30 min of conspecific male song had higher levels of 5-HIAA in the caudomedial nidopallium of the auditory forebrain than birds not exposed to song. Overall, we show that in this seasonal breeder, (a) serotonergic fibers innervate auditory areas; (b) the density of those fibers is higher in females with breeding-typical levels of E2 than in nonbreeding, untreated females; and (c) serotonin is released in the auditory forebrain within minutes in response to conspecific vocalizations. Our results are consistent with the hypothesis that E2 acts via serotonin systems to alter auditory processing. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Estrogen and cognitive functioning in women: Lessons we have learned.
Extant research findings allow several conclusions regarding the relationship between estrogen and cognitive functioning across the female life span. First, performance on tests of verbal memory fluctuates in concert with physiological changes in ovarian hormone production during the menstrual cycle and during pregnancy and the postpartum period. Estrogen therapy (ET) prevents the decrease in verbal memory when administered immediately following the surgical removal of both ovaries in premenopausal women. Some, but relatively little evidence is available to support the idea that ET, initiated at the time of a natural or a surgical menopause for a few years, may protect against cognitive decline 30 years later and more research in this area is urgently needed. Finally, the evidence to date strongly suggests that the initiation of ET decades after the menopause has occurred does not protect against cognitive decline or dementia. Taken together, these findings support the so-called “window of opportunity” hypothesis which holds that ET will be neuroprotective only when administered closely in time to a natural or surgical menopause. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Long-term replacement of estrogen in combination with medroxyprogesterone acetate improves acquisition of an alternation task in middle-aged female rats.
Studies have shown that ovarian hormones protect against some of the cognitive deficits associated with aging. Although much of the literature in rodents has focused on hippocampal dependent tasks, studies suggest that tasks dependent on the prefrontal cortex are also influenced by ovarian hormones. The present study investigated the effects of ovarian hormone treatment during aging on a delayed alternation t-maze. Female Long Evans hooded rats were ovariectomized at middle age (11–12 months) and placed in 1 of 5 treatment groups: no replacement, chronic estradiol (E2), cyclic E2, chronic E2 and progesterone, or chronic E2 and medroxyprogesterone acetate (MPA). Following 6 months of hormone treatment, animals were trained to alternate in a t-maze. After reaching criterion, a series of delays from 5 to 90 s were introduced in random order. Rats receiving E2 with MPA reached criterion significantly faster than animals not receiving treatment and those who received chronic or cyclic E2 only. There was a nonsignificant trend for animals receiving E2 and progesterone to reach criterion in fewer sessions than animals receiving E2 only. Mode of administration, cyclic or chronic, did not affect performance. Hormones did not affect performance on the delayed alternation. This study, in combination with previous research, indicates that hormone effects cannot be generalized across tasks, age, or duration, and long-term estrogen in combination with MPA can be beneficial for some tasks. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Once a mother, always a mother: Maternal experience protects females from the negative effects of stress on learning.
Women experience profound hormonal fluctuations throughout their reproductive lives. They are especially susceptible to disturbances in mood and cognition during the transition from pregnancy into postpartum and motherhood (Brummelte & Galea, 2010). Their behavioral and hormonal responses to stressful stimuli are also altered during this time. These changes are not limited to humans but occur in many mammalian species. Virgin female rats express a severe learning deficit in associative eyeblink conditioning after a stressful life event (Wood, Beylin, & Shors, 2001; Wood & Shors, 1998), but lactating females or those that are caring for young learn well even after the stressor (Leuner & Shors, 2006). However, we do not know whether maternal experience persistently alters learning after a stressful event. Here we hypothesized that females that had been maternal at some time in their lives would learn well even after exposure to a stressful event. To test this hypothesis, females that had at least one brood of young and expressed a normal estrous cycle were exposed to an acute stressful event that reliably impairs learning in virgin females. Animals were trained 24 hr later with classical eyeblink conditioning. Exposure to the stressor suppressed learning in virgins but not in females that had been mothers at some time in their lives. These data suggest that maternal experience induces a protective mechanism in mothers, which promotes associative learning long after the offspring have left their care. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Chronic stress and a cyclic regimen of estradiol administration separately facilitate spatial memory: Relationship with hippocampal CA1 spine density and dendritic complexity.
This study investigated the effects of chronic restraint stress and repeated cyclic estradiol pulses on hippocampal CA3 and CA1 dendritic and/or spine morphology and spatial memory in female rats. Sprague-Dawley adult female rats were ovariectomized and then injected over 2 days with 17β-estradiol (10 μg, s.c.), which was repeated every 4–5 days. While all rats received similar estradiol injection histories, half of the rats were chronically restrained and/or given a final cyclic pulse of estradiol prior to testing on a hippocampal-dependent object placement (OP) task to assess spatial memory. OP testing was performed 2 days after the last restraint session, as well as when the last 2 estradiol pulses best captured the maximal effect on hippocampal CA1 spine density. The data revealed several novel findings: (a) chronic stress or estradiol separately facilitated spatial memory, but did not have the same effects when coadministered, (b) CA1 spine densities negatively correlated with spatial memory, and (c) repeated estradiol pulses failed to prevent stress-induced CA3 dendritic retraction. We also corroborated previous studies showing increased CA1 spine density following estradiol, chronic stress, and behavioral manipulations. The present study uniquely combined chronic stress, repeated estradiol pulses, hippocampal morphology, and behavior within the same animals, allowing for correlational analyses to be performed between CA1 spine morphology and spatial memory. We demonstrate novel findings that chronic stress or estradiol pulses independently facilitate spatial memory, but not when coadministered, and that these effects may involve a balance of CA1 apical spine expression that is independent of CA3 dendritic complexity. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Correction to Taylor et al. (2011).
Reports an error in "Differential brain-derived neurotrophic factor expression in limbic brain regions following social defeat or territorial aggression" by Stacie L. Taylor, Lisa M. Stanek, Kerry J. Ressler and Kim L. Huhman ( Behavioral Neuroscience , 2011[Dec], Vol 125[6], 911-920). This article contains several production-related errors. The title of the article was incorrectly set as “Differential Brain-Derived Neurotrophic Factor Expression in Limbic Brain Regions Following Social Defeat of Territorial Aggression.” In addition, the publication year for Fiore et al. (2003) on p. 912 was listed as 2004. Also on p. 916, the publication year for Xu et al. (2000) was listed as 2004 and on p. 918 Razzoli et al. (2011b), the b was omitted. (The following abstract of the original article appeared in record 2011-27519-008.) Syrian hamsters readily form dominant-subordinate relationships under laboratory conditions. Winning or losing in agonistic encounters can have striking, long-term effects on social behavior, but the mechanisms underlying this experience-induced behavioral plasticity are unclear. The present study tested the hypothesis that changes in brain-derived neurotrophic factor (BDNF) may at least in part mediate this plasticity. Male hamsters were paired for 15-min using a resident-intruder model, and individuals were identified as winners or losers on the basis of their behavior. BDNF was examined with in situ hybridization 2 hr after treatment during the consolidation period of emotional learning. Losing animals had significantly more BDNF mRNA in the basolateral (BLA) and medial (MeA) nuclei of the amygdala when compared with winning animals as well as novel cage and home cage controls. Interestingly, winning animals had significantly more BDNF mRNA in the dentate gyrus of the dorsal hippocampus than did losing animals, novel, and home cage controls. No conflict-related changes in BDNF mRNA were observed in several other regions including the bed nucleus of the stria terminalis and central amygdala. Next, we demonstrated that K252a, a Trk receptor antagonist, significantly reduced the acquisition of conditioned defeat when administered within the BLA. These data support a model in which BDNF-mediated plasticity within the BLA supports learning of submission or subordinate social status in losing animals, whereas BDNF-mediated plasticity within the hippocampus may instantiate aspects of winning such as control of a territory in dominant animals. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The relationship between cortisol, salivary alpha-amylase, and cognitive bias in young women.
Both animal and human studies suggest that cognitive bias toward negative information, such as that observed in major depression, may arise through the interaction of cortisol (CORT) and norepinephrine (NE) within the amygdala. To date, there is no published account of the relationship between endogenous NE and CORT levels and cognitive bias. The present study examined salivary CORT and salivary alpha-amylase (sAA), an indirect measure of NE, in relation to masked affective priming of words in young female participants. Women with higher salivary CORT showed increased priming to negative word pairs only when sAA was also high; when sAA was low, no effect of CORT on priming was observed. These results are in line with previous research indicating that increased CORT is linked to enhanced processing of negative information. However, our findings extend this literature in providing evidence that CORT predicts enhanced processing of negatively valenced information only in the presence of higher sAA. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Stress-induced cortisol facilitates threat-related decision making among police officers.
Previous research suggests that cortisol can affect cognitive functions such as memory, decision making, and attentiveness to threat-related cues. Here, we examine whether increases in cortisol, brought on by an acute social stressor, influence threat-related decision making. Eighty-one police officers completed a standardized laboratory stressor and then immediately completed a computer simulated decision-making task designed to examine decisions to accurately shoot or not shoot armed and unarmed Black and White targets. Results indicated that police officers who had larger cortisol increases to the social-stress task subsequently made fewer errors when deciding to shoot armed Black targets relative to armed White targets, suggesting that hypothalamic pituitary adrenal (HPA) activation may exacerbate vigilance for threat cues. We conclude with a discussion of the implications of threat-initiated decision making. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Bisphenol-A impairs memory and reduces dendritic spine density in adult male rats.
[Correction Notice: An erratum for this article was reported in Vol 126(1) of Behavioral Neuroscience (see record 2011-27126-001). The Online First version of the article contained several production-related errors. In the second paragraph of the section “Western blot analysis,” “PKMΦ” should be “PKMζ.” In Figure 4A, an asterisk should be above PSD95-PSD. In Figure 5, an asterisk should be above pCREB-cyto and a caret above pCRB-Nuc. In the caption for Figure 5, “ ∗ p ∗ p <0.05, ˆp = 0.051.” All versions of this article have been corrected.] Exposure to Bisphenol-A (BPA), an endocrine disruptor used in plastics, occurs in the United States on a daily basis. Recent studies suggest exposure during development causes memory deficits later in life; however, the ramifications of exposure in adulthood are unclear. We examined the effects of acute BPA administration (40 μg/kg) on memory and synaptic plasticity in adult male rats. BPA significantly impaired both visual and spatial memory and decreased dendritic spine density on pyramidal cells in CA1 and the medial prefrontal cortex (mPFC). Additionally, BPA significantly decreased PSD-95, a synaptic marker, in the hippocampus and increased cytosolic pCREB, a transcription factor, in mPFC. Together, these findings show that a single dose of BPA, below the USEPA reference safe daily limit of 50 μg/kg/day, may block the formation of new memories by interfering with neural plasticity processes in the adult brain. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
An NMDA antagonist in the MPOA impairs copulation and stimulus sensitization in male rats.
Systemic injections of an NMDA antagonist have been shown to impair mating in male rats. One site where glutamate and its NMDA receptors may contribute to mating is the medial preoptic area (MPOA), which is vital for male sexual behavior. Glutamate is released in the MPOA during copulation, and especially at the time of ejaculation. We report here that the NMDA antagonist MK-801, microinjected into the MPOA, impaired copulatory behavior in sexually naïve as well as experienced males. In rats tested both as naïve and after sexual experience, drug treatment produced more profound impairment in naïve males. In addition, MK-801, microinjected into the MPOA before each of 7 noncopulatory exposures to receptive female rats, resulted in copulatory impairments on a drug-free test on Day 8, relative to aCSF-treated rats; their behavior was similar to that of males that had not been preexposed to females. Therefore, NMDA receptors in the MPOA contribute to the control of copulation and stimulus sensitization. Glutamate, acting via NMDA receptors, regulates many neural functions, including neuronal plasticity. This is the first demonstration that a similar mechanism in the MPOA sensitizes male rats to the stimuli from a receptive female, and thereby enhances their behavior. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Correction to Eilam-Stock et al. (2011).
Reports an error in "Bisphenol-A impairs memory and reduces dendritic spine density in adult male rats" by Tehila Eilam-Stock, Peter Serrano, Maya Frankfurt and Victoria Luine ( Behavioral Neuroscience , Advanced Online Publication, Oct 17, 2011, np). The Online First version of the article contained several production-related errors. In the second paragraph of the section “Western blot analysis,” “PKMΦ” should be “PKMζ.” In Figure 4A, an asterisk should be above PSD95-PSD. In Figure 5, an asterisk should be above pCREB-cyto and a caret above pCRB-Nuc. In the caption for Figure 5, “ ∗ p ∗ p 2011-23882-001.) Exposure to Bisphenol-A (BPA), an endocrine disruptor used in plastics, occurs in the United States on a daily basis. Recent studies suggest exposure during development causes memory deficits later in life; however, the ramifications of exposure in adulthood are unclear. We examined the effects of acute BPA administration (40 μg/kg) on memory and synaptic plasticity in adult male rats. BPA significantly impaired both visual and spatial memory and decreased dendritic spine density on pyramidal cells in CA1 and the medial prefrontal cortex (mPFC). Additionally, BPA significantly decreased PSD-95, a synaptic marker, in the hippocampus and increased cytosolic pCREB, a transcription factor, in mPFC. Together, these findings show that a single dose of BPA, below the USEPA reference safe daily limit of 50 μg/kg/day, may block the formation of new memories by interfering with neural plasticity processes in the adult brain. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Effects of prior light exposure on early evening performance, subjective sleepiness, and hormonal secretion.
In sighted humans, light intensity, timing, exposure duration, and spectral composition of light are important to entrain the endogenous circadian pacemaker to the 24-h day-night cycle. We tested the impact of two realistic office lighting conditions during the afternoon on subjective sleepiness, hormonal secretion, and cognitive performance in the early evening hours. Twenty-nine young subjects came twice and spent 8 h (12:00–20:00) in our laboratory, where they were exposed for 6 h to either artificial light (AL) or to mainly daylight (DL). In the early evening, we assessed their salivary cortisol and melatonin secretion, subjective sleepiness, and cognitive performance (n-back test) under dim light conditions. Subjects felt significantly more alert at the beginning of the evening after the DL condition, and they became sleepier at the end of the evening after the AL condition. For cognitive performance we found a significant interaction between light conditions, mental load (2- or 3-back task) and the order of light administration. On their first evening, subjects performed with similar accuracy after both light conditions, but on their second evening, subjects performed significantly more accurately after the DL in both n-back versions and committed fewer false alarms in the 2-back task compared to the AL group. Lower sleepiness in the evening was significantly correlated with better cognitive performance (p <.05). In summary, even short-term lighting conditions during the afternoon had an impact on cognitive task performance in the evening. This rapid effect was only distinguishable on the second day of training, when a difficult task had been sufficiently practiced. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Event-specific enhancement of memory via brief electrical stimulation to the basolateral complex of the amygdala in rats.
The basolateral complex of the amygdala (BLA) modulates memory for emotional events, and direct activation of the BLA following a learning session can enhance subsequent memory. Yet optimal enhancement of episodic memory during emotional events would likely require that BLA activation occur close in time to the event and to be brief enough to target specific memories if some events are to be remembered better than others. In the present study, rats were given a novel object recognition memory task in which initial encounters with some of the objects were immediately followed by brief electrical stimulation of the BLA, and these objects were remembered better one day later as compared to objects for which the initial encounter was not followed by stimulation. The results indicated that BLA stimulation can enhance memory for individual events, a necessary ability for the BLA to modulate episodic memory effectively. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Effects of the val(158)met catechol-o-methyltransferase gene polymorphism on olfactory processing in schizophrenia.
The catechol-O-methyltransferase (COMT) val158met polymorphism has received attention in schizophrenia due to its role in prefrontal dopamine catabolism. Given the rich dopaminergic innervations of the olfactory bulb and the influence of dopamine on the transmission of olfactory signals, the authors examined the influence of COMT genotype status on the olfactory processing impairment observed in schizophrenia. The University of Pennsylvania Smell Identification Test was administered unirhinally to individuals with schizophrenia (n = 42) and a demographically matched sample of healthy controls (n = 30). Individuals were genotyped for the COMT val158met polymorphism. A statistically significant interaction of diagnosis and COMT genotype was observed, such that schizophrenia heterozygotes and Met homozygotes showed impaired odor identification accuracy relative to Val158 homozygotes. These findings could not be explained by factors such as antipsychotic medication status, clinical symptomatology, or demographic and illness characteristics. Notably, the schizophrenia Val158 homozygotes' odor identification performance was comparable to that of the control group. These data indicate that odor identification impairments observed in schizophrenia are influenced by the COMT val158met polymorphism. This relationship is consistent with specific dopaminergic modulation of primary olfactory sensory afferents, rather than a broader effect on cognitive processes. Future studies that examine the olfactory processing deficit in schizophrenia with respect to other olfactory measures and COMT haplotypes is warranted. (PsycINFO Database Record (c) 2012 APA, all rights reserved)

Behavioral Neuroscience - Vol 126, Iss 1