Differential effects of ovarian steroids on anxiety versus fear as measured by open field test and fear-potentiated startle. Behav Brain Res
Department of Psychology, University of Washington, Seattle, WA 98195, USA. Behavioural Brain Research
(Impact Factor: 3.03).
02/2006; 166(1):93-100. DOI: 10.1016/j.bbr.2005.07.021
The ovarian steroids, estrogen (E) and progesterone (P), have been shown to affect anxiety and fear in humans and animals, although with inconsistent results. These ambiguous findings may be due to differential actions of ovarian steroids on anxiety versus fear. To investigate such a role, we used the open field test (OFT) and fear-potentiated startle (FPS). We examined these behaviors between cycling female rats in proestrus (high E and rising P) or diestrus (low E and P), as well as between ovariectomized rats treated for 2 weeks with placebo, E, or E plus P (OVX, OVX/E, OVX/EP, respectively). We found no differences in anxiety-like or fear behaviors in OFT or FPS between proestrus and diestrus rats, perhaps due to the opposing effects of E and P. In contrast, we found that the OVX/E rats spent more time in the center of the OFT compared to the OVX and OVX/EP rats with no difference in overall activity level, suggesting that E reduced anxiety and this was opposed by P. With FPS, the OVX/E rats showed increased startle in the first third of the testing session, followed by a rapid decline in startle magnitude in subsequent trials. The addition of P to E treatment counteracted this effect. In conclusion, E may have differential effects on specific components of anxiety and fear; E may decrease anxiety in a naturalistic environment, but intensify both fear learning and extinction processes. P antagonizes these E effects on anxiety and fear.
Available from: Loretta M Flanagan-Cato
- "For example, ovarian hormones modulate anxiety-related behaviors (Zimmerberg and Farley, 1993); specifically, estradiol exerts anxiolytic actions (Frye and Walf, 2004; Hiroi and Neumaier, 2006; Leret et al., 1994; Nomikos and Spyraki, 1988). Anxiety-like behaviors vary across the estrous cycle in female rats, with the lowest levels of anxiety-like behaviors occurring during proestrus (Frye et al., 2000; Mora et al., 1996). "
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ABSTRACT: Ovarian hormones act in multiple brain regions to modulate specific behaviors and emotional states. For example, ovarian hormones promote female sexual receptivity in the hypothalamic ventromedial nucleus (VMH) and modulate anxiety in the amygdala. Hormone-induced changes within the VMH include structural modifications, such as changes in dendritic spines, dendrite length and the number of synapses. In some situations, dendrite remodeling requires actin polymerization, which depends on phospho-deactivation of the enzyme cofilin, or the ionotropic AMPA-type glutamate receptors, especially the GluA1 and GluA2 subunits. The present experiments used immunohistochemistry to test the hypothesis that ovarian hormone-induced neural plasticity in the VMH and amygdala involves the regulation of phospho-cofilin, GluA1 and GluA2. These proteins were assessed acutely after estradiol administration (0.5, 1.0 and 4.0 h), as well as three days after hormone treatment. Both brain regions displayed rapid (4.0 h or less) and transient estradiol-induced increases in the level of phospho-cofilin. At the behaviorally relevant time point of three days, differential changes in AMPA receptor subunits were observed. Using Golgi impregnation, the effect of estradiol on amygdala dendrites was examined. Three days after estradiol treatment, an increase in the length of dendrites in the central nucleus of the amygdala was observed. Thus, estradiol initiates structural changes in dendrites in both the VMH and amygdala associated with an early phospho-deactivation of cofilin, followed by dynamic, brain region-specific changes in AMPA receptor composition.
Available from: Ziv Ardi
- "However, it is not yet clear if intrusive re-experiencing is only the result or whether it may contribute to the establishment of PTSD following acute stress. Here we analysed the effects of exposure to a trauma reminder by employing behavioural assessments (elevated plus maze and open field) that aim to evaluate the emotional state of the animal (Pellow et al., 1985; Hiroi and Neumaier, 2006). In addition, the effects of trauma reminder on neural activity and plasticity were also evaluated. "
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ABSTRACT: Intrusive re-experiencing is a core symptom in post-traumatic stress disorder (PTSD), often triggered by contextual cues associated with the trauma. It is not yet clear if intrusive re-experiencing is only the result, or whether it may contribute to the establishment of PTSD following acute stress. This study aimed at examining the impact of an underwater trauma (UWT) reminder on anxiety-like behaviour and on neuronal activity and plasticity in the hippocampus and the amygdala. Sprague-Dawley rats were exposed to UWT and 24 h later were re-exposed to the context. The effects on behaviour, activation of the amygdala (BLA) and dentate gyrus (DG), and on long-term potentiation (LTP) and local circuit activity (frequency-dependent inhibition (FDI) and paired-pulse inhibition (PPI)) in the DG were assessed. The exposure to UWT by itself resulted in increased anxiety behaviour in the open field, together with increased PPI. Upon exposure to the UWT reminder, an additional increase in anxiety was also observed in the EPM and in FDI. Moreover, reminder exposure resulted in impaired DG LTP and a significant BLA extracellular-signal-regulated kinases (ERK) 2 activation. In conclusion, these observed effects of exposure to a trauma reminder, following the exposure to the initial trauma, might be associated with the progression of trauma-related pathologies and the development of related disorders.
Available from: Feng Mei
- "The exploratory activity has been linked with both anxiety and schizophrenia phenotypes   . Here, we demonstrated that CPZ-induced demyelination led to a deficit in exploratory activity, and juvenile mice showed the most severe deficit. "
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ABSTRACT: Schizophrenia is a mental disease that mainly affects young individuals (15 to 35 years old) but its etiology remains largely undefined. Recently, accumulating evidence indicated that demyelination and/or dysfunction of oligodendrocytes is an important feature of its pathogenesis. We hypothesized that the vulnerability of young individuals to demyelination may contribute to the onset of schizophrenia. In the present study, three different age cohorts of mice, i.e. juvenile (3 weeks), young-adult (6 weeks) and middle-aged (8 months), were subjected to a 6-week diet containing 0.2% cuprizone (CPZ) to create an animal model of acute demyelination. Then, age-related vulnerability to CPZ-induced demyelination, behavioral outcomes, and myelination-related molecular biological changes were assessed. We demonstrated: (1) CPZ treatment led to more severe demyelination in juvenile and young-adult mice than in middle-aged mice in the corpus callosum, a region closely associated with the pathophysiology of schizophrenia; (2) the higher levels of demyelination in juvenile and young-adult mice were correlated with a greater reduction of myelin basic protein, more loss of CC-1-positive mature oligodendrocytes, and higher levels of astrocyte activation; and (3) CPZ treatment resulted in a more prominent exploratory behavior deficit in juvenile and young-adult mice than in middle-aged mice. Together, our data demonstrate an age-related vulnerability to demyelination with a concurrent behavioral deficit, providing supporting evidence for better understanding the susceptibility of the young to the onset of schizophrenia.
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