The amygdala and forced immobilization of rats

doi:10.1016/0166-4328(85)90078-6

Behavioural Brain Research

Volume 16, Issue 1, July 1985, Pages 19-24

https://doi.org/10.1016/0166-4328(85)90078-6 Get rights and content

Abstract

Forced immobilization of rats produced changes in the multiple-unit activity in the medial, central and lateral nuclei of the amygdala. Chlordiazepoxide suppressed the activity of these units. Low-level electrical stimulation of the area of these units produced gastric erosions only when the stimulation was applied to the central amygdalar nucleus. It was concluded that these areas of the amygdala respond to the emotional component of immobilization stress.

References (25)

D.T. Chou et al.
Unit activity of amygdala and hippocampal neurons: effects of morphine and benzodiazepines
Brain Res.
(1977)
P.G. Henke
The centromedial amygdala and gastric pathology in rats
Physiol. Behav.
(1980)
P.G. Henke
Facilitation and inhibition of gastric pathology after lesions in the amygdala of rats
Physiol. Behav.
(1980)
P.G. Henke
Unit-activity in the central amygdalar nucleus of rats in response to immobilization-stress
Brain Res. Bull.
(1983)
D.A. Hopkins
Amygdalotegmental projections in the rat, cat and rhesus monkey
Neurosci. Lett.
(1975)
D.L. Innes et al.
Gastric mucosal ulceration associated with electrochemical stimulation of the limbic system
Brain Res. Bull.
(1980)
J. Axelrod et al.
Stress hormones: their interaction and regulation
Science
(1984)
S.E. File et al.
Benzodiazepines reduce gastric ulcers induced in rats by stress
Brit. J. Pharmacol.
(1981)
P. Gloor
Temporal lobe epilepsy: its possible contribution to the understanding of the functional significance of the amygdala and of its interaction with neocortical-temporal mechanisms
P. Gloor et al.
The role of the amygdala in the expression of psychic phenomena in temporal lobe seizures

J. Haot et al.

Action protective du chlordiazepoxide sur l'ulcère de contrainte chez le rat

Arch. Int. Pharmacodyn.

(1964)

P.G. Henke

The amygdala and restraint ulcers in rats

J. comp. physiol. Psychol.

(1980)

Cited by (33)

Stress, ethanol, and neuroactive steroids
2007, Pharmacology and Therapeutics
Neurosteroids play a crucial role in stress, alcohol dependence and withdrawal, and other physiological and pharmacological actions by potentiating or inhibiting neurotransmitter action. This review article focuses on data showing that the interaction among stress, ethanol, and neuroactive steroids may result in plastic molecular and functional changes of GABAergic inhibitory neurotransmission. The molecular mechanisms by which stress–ethanol–neuroactive steroids interactions can produce plastic changes in GABA_A receptors have been studied using different experimental models in vivo and in vitro in order to provide useful evidence and new insights into the mechanisms through which acute and chronic ethanol and stress exposure modulate the activity of GABAergic synapses. We show detailed data on a) the effect of acute and chronic stress on peripheral and brain neurosteroid levels and GABA_A receptor gene expression and function; b) ethanol-stimulated brain steroidogenesis; c) plasticity of GABA_A receptor after acute and chronic ethanol exposure. The implications of these new mechanistic insights to our understanding of the effects of ethanol during stress are also discussed. The understanding of these neurochemical and molecular mechanisms may shed new light on the physiopathology of diseases, such as anxiety, in which GABAergic transmission plays a pivotal role. These data may also lead to the need for new anxiolytic, hypnotic and anticonvulsant selective drugs devoid of side effects.
Chronic cold stress alters prefrontal cortical modulation of amygdala neuronal activity in rats
2005, Biological Psychiatry
Recent studies suggest that long-term exposure to stress can sensitize animals to subsequent novel or acute stressors. Stressors affect amygdala activity, and the prefrontal cortex has been implicated in the regulation of responses to stress. Little is known, however, about how the physiology of amygdala neurons is altered by chronic stressors or the role of the prefrontal cortex in these changes.
We used in vivo extracellular recordings from neurons in the rat central and basolateral amygdala nuclei to examine the effects of chronic stress on the basal firing and responses of amygdala neurons to a novel stressor. Additionally, prefrontal cortical afferents were severed to examine its role in the modulation of the response to stressors.
Chronic exposure to cold enhanced the sensitivity of central amygdala neurons to footshock. A portion of this may be due to enhanced basolateral amygdala output. Furthermore, prefrontal cortical regulation of this response is weakened by chronic stress.
The physiology of the amygdala is altered by chronic stress. Furthermore, the prefrontal cortical regulation of these responses may be weakened after chronic stress. This is a potential biological substrate for abnormal affect upon chronic stress and its effect on affective disorders.
Expression of aggression attenuates both stress-induced gastric ulcer formation and increases in noradrenaline release in the rat amygdala assessed by intracerebral microdialysis
1998, Pharmacology Biochemistry and Behavior
The effects of an aggressive biting response on stress-induced noradrenaline (NA) release in the rat amygdala and gastric ulcer formation were studied with an intracerebral microdialysis technique. Rats were exposed to a 60-min period of cold restraint stress with or without being allowed to bite a wooden stick. They were sacrificed 100 min after release from stress to investigate gastric ulcer formation. Cold-restraint stress increased NA release to 304 ± 22.3 and 206 ± 23.8% of basal levels (mean ± SEM) in the nonbiting and biting groups, respectively. The stress-induced increases in NA release in the nonbiting group were significantly higher than those in the biting group. In the nonbiting group, significant increases in NA release continued for 80 min after release from stress; however, NA levels in the biting group recovered to basal levels immediately after the cessation of stress. Although many severe gastric lesions with bleeding were found in the nonbiting group, fewer gastric lesions without bleeding were found in the biting group. The cumulative length of gastric lesions in the nonbiting group and in the biting group was 26.2 ± 7.4 and 6.8 ± 3.9 mm (mean ± SEM), respectively. The mean number of ulcers in the nonbiting group and the biting group was 11.8 ± 1.3 and 1.8 ± 0.7 (mean ± SEM), respectively. Both the cumulative length of ulcers and the number of ulcers were significantly lower than those seen in the nonbiting group. These findings strongly suggest that expression of aggression during stress exposure attenuates not only stress-induced increases in NA release in the rat amygdala but also gastric ulcer formation consequent to stress.
Neuroimmunomodulation via limbic structures - The neuroanatomy of psychoimmunology
1997, Progress in Neurobiology
During the last 20 years, mutual communications between the immune, the endocrine and the nervous systems have been defined on the basis of physiological, cellular, and molecular data. Nevertheless, a major problem in the new discipline “Psychoneuroimmunology” is that controversial data and differences in the interpretation of the results make it difficult to obtain a comprehensive overview of the implications of immunoneuroendocrine interactions in the maintenance of physiological homeostasis, as well as in the initiation and the course of pathological conditions within these systems. In this article, we will first discuss the afferent pathways by which immune cells may affect CNS functions and, conversely, how neural tissues can influence the peripheral immune response. We will then review recent data, which emphasize the (patho)physiological roles of hippocampal-amygdala structures and the nucleus accumbens in neuroimmunomodulation. Neuronal activity within the hippocampal formation, the amygdaloid body, and the ventral parts of the basal ganglia has been examined most thoroughly in studies on neuroendocrine, autonomic and cognitive functions, or at the level of emotional and psychomotor behaviors. The interplay of these limbic structures with components of the immune system and vice versa, however, is still less defined. We will attempt to review and discuss this area of research taking into account recent evidences for neuroendocrine immunoregulation via limbic neuronal systems, as well as the influence of cytokines on synaptic transmission, neuronal growth and survival in these brain regions. Finally, the role of limbic structures in stress responses and conditioning of immune reactivity will be commented. Based on these data, we propose new directions of future research. © 1997 Elsevier Science Ltd. All Rights Reserved.
Stimulation of the lateral septum attenuates immobilization-induced stress ulcers
1996, Physiology and Behavior
Rats with electrodes implanted in their dorsolateral septal area underwent a cold-immobilization restraint procedure during which the experimental group received electrical stimulation while the control group did not. Electrical stimulation of the dorsolateral septal region clearly reduced the number of gastric ulcers formed during the cold-immobilization stress procedure. The pattern of results with septal stimulation contrasts with that seen by other investigators after stimulation of the central amygdaloid nucleus. The mitigation of stress-induced ulceration after lateral septal stimulation is consistent with the proposed function for the lateral septal area in relief from aversive emotional states.
The neurobiology of stress ulcers
1991, Brain Research Reviews
We have reviewed the neurobiology of stress ulcers from animal models to potential pharmacotherapeutic mechanisms. The evidence strongly supports the hypothesis that certain stress-related gastric lesions are ‘braindriven’ events which may be more effectively managed through central manipulations than by altering local, gastric factors. Recent advances in the use of anxiolytic and antidepressant drugs in the management of stress-related gastric mucosal injury further supports the contention that a brain-gut axis, which may have nervous, peptidergic and classic monoaminergic components, modulates the intricate and complicated pattern of communication between the brain and the stomach. Delineation of the precise pathways which make up this communication as well as their manipulation by various pharmacological agents will be the focus of future research endeavour.

View all citing articles on Scopus

View full text

Research paperThe amygdala and forced immobilization of rats

Abstract

Brain Res.

Physiol. Behav.

Physiol. Behav.

Brain Res. Bull.

Neurosci. Lett.

Brain Res. Bull.

Stress hormones: their interaction and regulation

Science

Benzodiazepines reduce gastric ulcers induced in rats by stress

Brit. J. Pharmacol.

Temporal lobe epilepsy: its possible contribution to the understanding of the functional significance of the amygdala and of its interaction with neocortical-temporal mechanisms

The role of the amygdala in the expression of psychic phenomena in temporal lobe seizures

Action protective du chlordiazepoxide sur l'ulcère de contrainte chez le rat

Arch. Int. Pharmacodyn.

The amygdala and restraint ulcers in rats

J. comp. physiol. Psychol.

Research paper
The amygdala and forced immobilization of rats