The relevance of neuronal substrates of defense in the midbrain tectum to anxiety and stress: empirical and conceptual considerations

The relevance of neuronal substrates of defense in the midbrain tectum to anxiety and stress:... The medial hypothalamus, amygdala, and dorsal periaqueductal gray constitute the main neural substrates for the integration of aversive states in the brain. More recently, some regions of the mesencephalon, such as the superior and inferior colliculi have also been proposed as part of this system. In fact, fear-like behaviors often result when these sites are electrically or chemically stimulated. Both the behavioral and autonomic consequences of electrical stimulation of the mesencephalic tectum have been shown to be attenuated by minor tranquilizers, probably through enhancement of γ-aminobutyric acid (GABA)-mediated neurotransmission, which exerts a tonic inhibitory control on the neural circuits responsible for the so-called defense behavior repertoire. Besides GABA, also 5-hydroxy tryptamine serotonin (5-HT), opioids, neuropeptides, histaminergic and excitatory amino acids have all been implicated in the regulation of anxiety-related behaviors induced by stimulation of midbrain tectum. Efforts have been made to characterize how these neurotransmitters interact with each other in the organization of these reactions to aversive stimulation. In this review, we summarize the evidence linking the brain's defense response systems to the concept of fear–anxiety. Furthermore, a case is made for the consideration of the relevance of this body of data to the search for the physiological underpinnings of depression and its consequences. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Pharmacology Elsevier

The relevance of neuronal substrates of defense in the midbrain tectum to anxiety and stress: empirical and conceptual considerations

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Publisher
Elsevier
Copyright
Copyright © 2003 Elsevier Science B.V.
ISSN
0014-2999
DOI
10.1016/S0014-2999(03)01284-6
Publisher site
See Article on Publisher Site

Abstract

The medial hypothalamus, amygdala, and dorsal periaqueductal gray constitute the main neural substrates for the integration of aversive states in the brain. More recently, some regions of the mesencephalon, such as the superior and inferior colliculi have also been proposed as part of this system. In fact, fear-like behaviors often result when these sites are electrically or chemically stimulated. Both the behavioral and autonomic consequences of electrical stimulation of the mesencephalic tectum have been shown to be attenuated by minor tranquilizers, probably through enhancement of γ-aminobutyric acid (GABA)-mediated neurotransmission, which exerts a tonic inhibitory control on the neural circuits responsible for the so-called defense behavior repertoire. Besides GABA, also 5-hydroxy tryptamine serotonin (5-HT), opioids, neuropeptides, histaminergic and excitatory amino acids have all been implicated in the regulation of anxiety-related behaviors induced by stimulation of midbrain tectum. Efforts have been made to characterize how these neurotransmitters interact with each other in the organization of these reactions to aversive stimulation. In this review, we summarize the evidence linking the brain's defense response systems to the concept of fear–anxiety. Furthermore, a case is made for the consideration of the relevance of this body of data to the search for the physiological underpinnings of depression and its consequences.

Journal

European Journal of PharmacologyElsevier

Published: Feb 28, 2003

References

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