Effect of antianxiety drugs on fear and stress

Berger, F. M.

doi:10.1002/bs.3830250408

Cited by 9 publications

(5 citation statements)

References 26 publications

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“…The present studies indicate that alterations in circulating corticosteroid levels regulate 5-HT,, receptor mRNA expression within the hippocampal formation, a central anatomical structure in limbic circuitry, thus providing one possible molecular mechanism bv which adrenal steroids mav act to influence circuitrv associated with affective state. This interaction may prove to be highly relevant to the body of evidence indicating abnormalities in HPA axis function in both endogenous depressive illness and anxietv disorders (Berger, 1980;McEwen, 1987).…”

Section: Resultsmentioning

confidence: 92%

Corticosteroids regulate brain hippocampal 5-HT1A receptor mRNA expression

et al. 1993

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Using in situ hybridization techniques, the expression of 5-HT1A receptor mRNA was measured within the hippocampal formation after bilateral adrenalectomy (ADX). After 24 hr ADX, 5-HT1A receptor mRNA expression was significantly increased in all hippocampal subfields in ADX animals relative to sham-operated controls (SHAM). The magnitude of the increase was most pronounced within CA2 (127%) and CA3/4 (94%)-subfields of dorsal hippocampus, intermediate in the dentate gyrus (73%), and least within CA1 (60%). Administration of exogenous corticosterone (CORT) at the time of ADX maintained the level of 5-HT1A receptor mRNA expression within the range of SHAM animals. In vitro receptor autoradiographic analysis of 5-HT1A receptors in adjacent sections from the same animals indicated a simultaneous increase in 5-HT1A binding throughout the hippocampus in response to ADX. 5-HT1A binding increased to a similar extent (approximately 30%) in CA subfields and dentate gyrus but remained within SHAM levels in CORT-replaced animals. 5-HT1A receptor mRNA levels were also increased in hippocampal subregions of 1 week ADX animals relative to SHAM animals. Within both CA1 and CA2 subfields, the increments were approximately double those observed after 1 d ADX. 5-HT1A receptor binding was increased in every hippocampal subfield to a similar extent as that observed after 1 d ADX. Increases in both 5-HT1A receptor mRNA expression and 5-HT1A receptor binding were preventable by administration of exogenous CORT at the time of ADX. Hippocampal 5-HT1C receptor mRNA and D1 receptor mRNA expression were not significantly altered by either acute or chronic ADX treatment. These data indicate that adrenal steroids may selectively regulate hippocampal 5-HT1A receptors at the level of 5-HT1A receptor mRNA expression.

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Section: Resultsmentioning

confidence: 92%

Corticosteroids regulate brain hippocampal 5-HT1A receptor mRNA expression

et al. 1993

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“…However, because the same chronic treatment with sodium valproate does not significantly modify ACTH levels in normal volunteers [I], it is evident that GABA mimetic drugs are effective in counteracting pathological or physiological hypersecretion of the HPA axis. Interestingly, because HPA axis hormones have been shown to be involved in the stress-associated anxiety [5], the anxiolytic effect of diazepam might be related to such in hibitory effect.…”

Section: Discussionmentioning

confidence: 99%

Effects of Sodium Valproate and Diazepam on Beta-Endorphin, Beta-Lipotropin and Cortisol Secretion Induced by Hypoglycemic Stress in Humans

et al. 1986

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Evidence that γ-aminobutyric acid (GABA) and benzodiazepine receptors play a role in the inhibition of ACTH-cortisol secretion in humans has until now been drawn only from data indicating that sodium valproate, a GABA mimetic, and diazepam, a benzodiazepine, decrease hypothalamus-pituitary-adrenal (HPA) axis secretion in patients affected by pathological hypersecretion of the axis. Therefore, the present study investigated the effects, in the same healthy subjects, of sodium valproate or diazepam, on both basal and stress-stimulated concentrations of β-endorphin (β-EP), β-lipotropin (β-LPH) and cortisol. A single maximal dose of sodium valproate (400 mg) or diazepam (10 mg) did not significantly modify basal concentrations of β-EP, β-LPH and cortisol. On the other hand, in the same subjects, pretreatment with sodium valproate (20 mg × 3) or diazepam (10 mg × 2) blocked the increases in these hormones produced by hypoglycemic stress in all patients tested (p< 0.01 vs. placebo at 45, 60 and 90 min after insulin injection), without affecting the decrease in blood glucose levels. The present data show that sodium valproate and diazepam inhibit stress-induced β-EP, β-LPH and cortisol secretion in humans, suggesting that endogenous GABA and benzodiazepine receptors participate in physiological mechanisms regulating the activity of the HPA axis.

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“…The role of glucocorticoids in responses to stressful events is well-known and prolonged glucocorticoid release has been linked to pathological anxiety. Data indicate a positive correlation between anxiety and cortisol (Berger 1980;Levitt et al 1963;Sachar 1970). Increases in circulating cortisol in pathological states such as Cushing's disease, depression or other psychiatric disorders, are often associated with a state of anxiety (Warburton 1974).…”

Section: A Working Hypothesis: Role Of Glucocorticoids In Anxietymentioning

confidence: 99%

Models and mechanisms of anxiety: evidence from startle studies

2007

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Rationale-Preclinical data indicates that threat stimuli elicit two classes of defensive behaviors, those that are associated with imminent danger and are characterized by avoidance or fight (fear), and those that are associated with temporally uncertain danger and are characterized by sustained apprehension and hypervigilance (anxiety).Objective-To 1) review evidence for a distinction between fear and anxiety in animal and human experimental models using the startle reflex as an operational measure of aversive states, 2) describe experimental models of anxiety, as opposed to fear, in humans, 3) examine the relevance of these models to clinical anxiety.Results-The distinction between phasic fear to imminent threat and sustained anxiety to temporally uncertain danger is suggested by psychopharmacological and behavioral evidence from ethological studies and can be traced back to distinct neuroanatomical systems, the amygdala and the bed nucleus of the stria terminalis. Experimental models of anxiety, not fear, are relevant to nonphobic anxiety disorders.Conclusions-Progress in our understanding of normal and abnormal anxiety is critically dependent on our ability to model sustained aversive states to temporally uncertain threat.

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Effect of antianxiety drugs on fear and stress

Cited by 9 publications

References 26 publications

Corticosteroids regulate brain hippocampal 5-HT1A receptor mRNA expression

Corticosteroids regulate brain hippocampal 5-HT1A receptor mRNA expression

Effects of Sodium Valproate and Diazepam on Beta-Endorphin, Beta-Lipotropin and Cortisol Secretion Induced by Hypoglycemic Stress in Humans

Models and mechanisms of anxiety: evidence from startle studies

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