Stress, Synaptic Plasticity, and Psychopathology

García, René

doi:10.1515/revneuro.2002.13.3.195

Cited by 74 publications

(37 citation statements)

References 62 publications

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“…The effect of BMI on Fos expression in the BNST and the LSV, two limbic structures closely associated with emotion and defensive reactions (for reviews, see Koolhaas et al, 1998;Garcia, 2002;Walker et al, 2003;Herman et al, 2005), provide an interesting contrast. A variety of stress paradigms have been reported to increase Fos expression in the BNST (Campeau and Watson, 2000;Greenwood et al, 2003;Ma and Morilak, 2004;Mantella et al, 2004;Bali et al, 2005, Kiyokawa et al, 2005Spencer et al, 2005) and the LSV (Cullinan et al, 1995;Imaki et al, 1995;Lino-de-Oliveira et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

et al. 2008

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Activation of neurons in the dorsomedial hypothalamus (DMH) appears to play an important role in signaling the excitation of brain regions responsible for experimental fever and for many of the physiological and behavioral changes seen in experimental stress or anxiety in rats. Here, we examined the effect of disinhibition of the DMH by unilateral microinjection of bicuculline methiodide (BMI) on Fos expression in selected regions of the brain that have been implicated in anxiety and responses to stress and fever in rats. Disinhibition of the DMH resulted in dramatic increases in local Fos expression and also increased the numbers of Fos-positive neurons in the lateral septal nucleus and in both the parvocellular and magnocellular subdivisions of the paraventricular nucleus, with greater increases ipsilateral to the injection site in the DMH. However, microinjection of BMI had no significant effect on Fos expression in the bed nucleus of the stria terminalis, another forebrain area implicated in stress and anxiety. In the brainstem, disinhibition of the DMH increased Fos expression in the nucleus tractus solitarius and the ventrolateral medulla bilaterally with greater increases again ipsilateral to the site of the microinjection, and also in the midline rostral raphe pallidus. Thus, disinhibition of neurons in the DMH in conscious rats results in increases in Fos expression in selected forebrain and brainstem regions that have been implicated in stress-induced physiological changes, anxiety, and experimental fever.

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Section: Discussionmentioning

confidence: 99%

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

et al. 2008

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“…In addition, BDNF mediates the effects of repeated stress exposure and longterm antidepressant treatment on neurogenesis and neuronal survival in the hippocampus (D'Sa and Duman, 2002;Rasmusson et al, 2002). These findings converge with impaired hippocampal plasticity in depression reflected by a reduced hippocampal volume and hippocampus-related memory deficiency, which supports that BDNF plays a critical role in the pathophysiology of affective and other stress-related disorders (Duman et al, 1997(Duman et al, , 2001Garcia, 2002;Hull, 2002;McEwen and Magarinos, 2001).…”

Section: Introductionmentioning

confidence: 87%

Interaction between BDNF Val66Met and Dopamine Transporter Gene Variation Influences Anxiety-Related Traits

Hünnerkopf

Strobel²,

Gutknecht

et al. 2007

Neuropsychopharmacol

117

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The involvement in neural plasticity and the mediation of effects of repeated stress exposure and long-term antidepressant treatment on hippocampal neurogenesis supports a critical role of brain-derived neurotrophic factor (BDNF) in the pathophysiology of affective and other stress-related disorders. A previously reported valine to methionine substitution at amino-acid position 66 (BDNF Val66Met) seems to account for memory disturbance and hippocampal dysfunction. In the present study, we evaluated the impact of the BDNF Val66Met polymorphism on individual differences in personality traits in a sample of healthy volunteers in relation to other common gene variants thought to be involved in the pathophysiology of affective disorders, such as the serotonin transporter promoter polymorphism (5-HTTLPR) and a variable number of tandem repeat polymorphism of the dopamine transporter gene (DAT VNTR). Personality traits were assessed using the NEO personality inventory (NEO-PI-R) and Tridimensional Personality Questionnaire (TPQ). There was a significant DAT VNTR-dependent association between NEO-PI-R Neuroticism and the BDNF Val66Met polymorphism. Among individuals with at least one copy of the DAT 9-repeat allele, carriers of the BDNF Met allele exhibited significantly lower Neuroticism scores than noncarriers. This interaction was also observed for TPQ Harm Avoidance, a personality dimension related to Neuroticism. Our results support the notion that allelic variation at the BDNF locusFin interaction with other gene variantsFinfluences anxietyand depression-related personality traits.

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“…It has been proposed that long-term synaptic plasticity or its modulation might be disturbed in depressed patients (Garcia, 2002;Stewart and Reid, 2002). Different antidepressants and electroconvulsive therapy have been shown to effectively modulate synaptic plasticity in the dentate gyrus and the CA1 and in the neostriatum (De Murtas et al, 2004;Stewart and Reid, 2000).…”

Section: Cms and Win55212-2 Effects On Plasticitymentioning

confidence: 99%

Cannabinoid Receptor Activation Prevents the Effects of Chronic Mild Stress on Emotional Learning and LTP in a Rat Model of Depression

Segev

Rubin

Abush

et al. 2013

Neuropsychopharmacol

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Most psychiatric disorders are characterized by emotional memory or learning disturbances. Chronic mild stress (CMS) is a common animal model for stress-induced depression. Here we examined whether 3 days of treatment using the CB1/2 receptor agonist WIN55,212-2 could ameliorate the effects of CMS on emotional learning (ie, conditioned avoidance and extinction), long-term potentiation (LTP) in the hippocampal-accumbens pathway, and depression-like symptoms (ie, coping with stress behavior, anhedonia, and weight changes). We also examined whether the ameliorating effects of WIN55,212-2 on behavior and physiology after CMS are mediated by CB1 and glucocorticoid receptors (GRs). Rats were exposed to CMS or handled on days 1-21. The agonist WIN55,212-2 or vehicle were administered on days 19-21 (IP; 0.5 mg/kg) and behavioral and electrophysiological measures were taken on days 23 and 28. The CB1 receptor antagonist AM251 (IP; 0.3 mg/kg) or the GR antagonist RU-38486 (IP; 10 mg/kg) were co-administered with WIN55,212-2. Our results show that CMS significantly modified physiological and behavioral reactions, as observed by the impairment in avoidance extinction and LTP in the hippocampal-accumbens pathway, and the alterations in depression-like symptoms, such as coping with stress behavior, weight gain, and sucrose consumption. The most significant effect observed in this study was that 3 days of WIN55,212-2 administration prevented the CMS-induced alterations in emotional memory (ie, extinction) and plasticity. This effect was mediated by CB1 receptors as the CB1 receptor antagonist AM251 prevented the ameliorating effects of WIN55,212-2 on extinction and LTP. The GR antagonist RU-38486 also prevented the CMS-induced alterations in extinction and plasticity, and when co-administered with WIN55,212-2, the preventive effects after CMS were maintained. The findings suggest that enhancing cannabinoid signaling could represent a novel approach to the treatment of cognitive deficits that accompany stress-related depression.

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Stress, Synaptic Plasticity, and Psychopathology

Cited by 74 publications

References 62 publications

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

Interaction between BDNF Val66Met and Dopamine Transporter Gene Variation Influences Anxiety-Related Traits

Cannabinoid Receptor Activation Prevents the Effects of Chronic Mild Stress on Emotional Learning and LTP in a Rat Model of Depression

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