The contribution of adrenal and reproductive hormones to the opposing effects of stress on trace conditioning males versus females.

Wood, Gwendolyn E.; Beylin, Anna V.; Shors, Tracey J.

doi:10.1037/0735-7044.115.1.175

Cited by 182 publications

(183 citation statements)

References 87 publications

(127 reference statements)

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“…In rats, exposure to an acute stressful event can facilitate learning in males, but impairs performance in female rats. 311,312 Furthermore, exposure to an elevated plusmaze, a rodent anxiety test, leads to decreased 5-HTergic activity in the dorsal raphe nuclei in female rats, but to decreased 5-HTergic activity in the medial raphe nuclei in males. 101 There is also data to indicate that male rats may adapt better to stress than females.…”

Section: Biopsychological Interactionsmentioning

confidence: 99%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

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Section: Biopsychological Interactionsmentioning

confidence: 99%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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“…Using this paradigm we have found that exposure to an acute stressor of inescapable tailshocks or forced swimming facilitates classical eyeblink conditioning 24 h later in male rats (Beylin & Shors, 1998;Shors, Weiss, & Thompson, 1992). In females, however, exposure to these same stressors impairs eyeblink conditioning (Shors, Lewczyk, Pacynski, Mathew, & Pickett, 1998;Wood, Beylin, & Shors, 2001;Wood & Shors, 1998). In both cases, stress is thought to modulate learning directly, but an alternative interpretation is that prior stressor exposure affects performance during eyeblink conditioning, and not learning, per se.…”

Section: Introductionmentioning

confidence: 97%

“…

AbstractExposure to an acute stressor of inescapable swimming or intermittent tailshocks impairs classical eyeblink conditioning 24 h later in female rats (Wood, Beylin, & Shors, 2001). This effect is often attributed to a deficit in "learning," but since stress has been shown to induce analgesia (Jackson, Maier, & Coon, 1979), an alternative explanation is that stressor exposure reduces conditioning by lessening the perceived intensity of the unconditioned stimulus (US).

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confidence: 99%

Acute stress impairs trace eyeblink conditioning in females without altering the unconditioned response

Bangasser

Shors

2004

Neurobiology of Learning and Memory

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Exposure to an acute stressor of inescapable swimming or intermittent tailshocks impairs classical eyeblink conditioning 24 h later in female rats (Wood, Beylin, & Shors, 2001). This effect is often attributed to a deficit in "learning," but since stress has been shown to induce analgesia (Jackson, Maier, & Coon, 1979), an alternative explanation is that stressor exposure reduces conditioning by lessening the perceived intensity of the unconditioned stimulus (US). To address this possibility we examined the amplitude of the unconditioned response (UR) during training and found that although exposure to the stressor impaired trace conditioning, there was no difference in the UR amplitude. We also found that eyeblink responses to different US intensities (4-12 V) in the absence of training were unaffected by stressor exposure. Taken together, these experiments indicate that the stress-induced impairment of conditioning in females is not due to a decreased perception of US strength. KeywordsSex differences; Estrogen; Analgesia; Hippocampus; Unconditioned stimulus; Performance; Gender Classical eyeblink conditioning is becoming an increasingly important paradigm for the study of learning. In our rat version of eyeblink conditioning, a white noise conditioned stimulus (CS) precedes and predicts an unconditioned stimulus (US), which is a periorbital shock to the eyelid. Through this pairing, the CS comes to elicit an eyeblink, or conditioned response (CR). Using this paradigm we have found that exposure to an acute stressor of inescapable tailshocks or forced swimming facilitates classical eyeblink conditioning 24 h later in male rats (Beylin & Shors, 1998;Shors, Weiss, & Thompson, 1992). In females, however, exposure to these same stressors impairs eyeblink conditioning (Shors, Lewczyk, Pacynski, Mathew, & Pickett, 1998;Wood, Beylin, & Shors, 2001;Wood & Shors, 1998). In both cases, stress is thought to modulate learning directly, but an alternative interpretation is that prior stressor exposure affects performance during eyeblink conditioning, and not learning, per se. In males, several possible performance explanations have been addressed (Servatius, Brennan, Beck, Beldowicz, & Coyle-DiNorcia, 2001;Shors, 2001), but less has been done to rule out performance deficits in females (but see Wood & Shors, 1998). Most notably, acute exposure to inescapable shock has been shown to induce analgesia 24 h after the stress or exposure if animals are "reminded" of the event (Jackson, Maier, & Coon, 1979). So, there remains the possibility that analgesia caused by stressor exposure prior to training reduces the perceived intensity of the training stimuli. If, for example, the US eyelid shock is perceived as less intense-and is therefore less salient-less conditioning would occur in stressed females. NIH Public AccessAuthor Manuscript Neurobiol Learn Mem. Author manuscript; available in PMC 2012 May 30.One way of evaluating the salience of the US is to examine the magnitude of the UR. A more salient US will elicit an ey...

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“…Notably, E 2 increases 3α,5α-THP in the hippocampus [8,9,21], which is an important area for affective processes [17]. Further, stressful or challenging environmental experiences increase biosynthesis of E 2 and 3α,5α-THP [22][23][24][25]. As such, we were interested in the effects of E 2 and/or 3α,5α-THP on behaviors that may promote sexual interactions (exploration, anxiety, social behaviors) and whether actions of E 2 and/or 3α,5α-THP in the VTA are sufficient to modulates these behaviors.…”

Section: Introductionmentioning

confidence: 99%

Infusions of 3α,5α-THP to the VTA enhance exploratory, anti-anxiety, social, and sexual behavior and increase levels of 3α,5α-THP in midbrain, hippocampus, diencephalon, and cortex of female rats

Frye

Rhodes

2008

Behavioural Brain Research

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Abstract17β-Estradiol (E 2 ) and progesterone (P 4 ) influence the onset and duration of sexual behavior and are also associated with changes in behaviors that may contribute to mating, such as exploration, anxiety, and social behaviors (socio-sexual behaviors). In the midbrain ventral tegmental area (VTA), the P 4 metabolite, 5α-pregnan-3α-ol-20-one (3α,5α-THP), modulates lordosis of E 2 -primed rodents; 3α,5α-THP can also influence anxiety and social behaviors. To examine if 3α,5α-THP in the VTA mediates socio-sexual behaviors, we infused 3α,5α-THP to the VTA of diestrous and proestrous rats. As expected, proestrous, compared to diestrous, rats showed more exploratory (open field), anxiolytic (elevated plus maze), pro-social (partner preference, social interaction), and sexual (paced mating) behavior and had increased E 2 , P 4 , dihydroprogesterone (DHP), and 3α,5α-THP in serum, midbrain, hippocampus, diencephalon, and cortex. Infusions of 3α,5α-THP to the VTA, but not control sites, such as the substantia nigra (SN) or central grey (CG), of diestrous rats produced behavioral and endocrine effects akin to that of proestrous rats and increased DHP and 3α,5α-THP levels in midbrain, hippocampus, and diencephalon. Levels of DHP and 3α,5α-THP, but neither E 2 nor P 4 concentrations, in midbrain, hippocampus, diencephalon, and/or cortex were positively correlated with socio-sexual behaviors. Thus, 3α,5α-THP infusions to the VTA, but not SN or CG, can enhance socio-sexual behaviors and increase levels in midbrain, hippocampus, and diencephalon.

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The contribution of adrenal and reproductive hormones to the opposing effects of stress on trace conditioning males versus females.

Cited by 182 publications

References 87 publications

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Acute stress impairs trace eyeblink conditioning in females without altering the unconditioned response

Infusions of 3α,5α-THP to the VTA enhance exploratory, anti-anxiety, social, and sexual behavior and increase levels of 3α,5α-THP in midbrain, hippocampus, diencephalon, and cortex of female rats

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