Changes in single cell responsiveness in the hypothalamus in cats following cortisol administration

doi:10.1016/0006-8993(70)90167-8

Brain Research

Volume 20, Issue 3, 15 June 1970, Pages 369-377

https://doi.org/10.1016/0006-8993(70)90167-8 Get rights and content

Summary

The effects of cortisol on the spontaneous activity of single cells in the anteriortuberal and posterior hypothalamus and their responsiveness to photic, acoustic and sciatic stimulation were studied in cats under pentobarbital anesthesia. It was found that while before hormone administration the sensory stimuli caused a predominant increase in cell firing in the anterior-tuberal hypothalamus, after the hormone administration the effect was mainly inhibitory. On the other hand, in the posterior hypothalamus the hormone caused a further increase in cell firing following sensory stimulation. These results are discussed in view of the role played by the anteriortuberal hypothalamus in adrenocortical regulation and the negative feedback exerted by the glucocorticoids at hypothalamic levels. It is suggested that the present data may possibly demonstrate some electrophysiological correlates of the neuroendocrine effects of the adrenocortical hormones, exerted on the hypothalamus.

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Citation Excerpt :
This pattern of changes suggests that corticosterone inhibits hippocampal responses to single stimulation but increases activity in response to repetitive excitatory stimulations (Zeise et al., 1992). The importance of the input signals on responsiveness of neurons to GCs (cortisol, corticosterone, dexamethasone) is also visible in experiments testing effects of glucocorticoids on resting and sensory-evoked activity (Feldman and Dafny, 1970b, a; Nagler et al., 1973; Mandelbrod et al., 1981; Feldman et al., 1983; Lei et al., 2014). For example, hypothalamic neurons that are not sensitive to locally applied cortisol (with background stimulation with glutamate) become sensitive at the time of distal (sensory and hippocampal) stimulation (Mandelbrod et al., 1981).
The review integrates different experimental approaches including biochemistry, c-Fos expression, microdialysis (glutamate, GABA, noradrenaline and serotonin), electrophysiology and fMRI to better understand the effect of elevated level of glucocorticoids on the brain activity and metabolism. The available data indicate that glucocorticoids alter the dynamics of neuronal activity leading to context-specific changes including both excitation and inhibition and these effects are expected to support the task-related responses. Glucocorticoids also lead to diversification of available sources of energy due to elevated levels of glucose, lactate, pyruvate, mannose and hydroxybutyrate (ketone bodies), which can be used to fuel brain, and facilitate storage and utilization of brain carbohydrate reserves formed by glycogen. However, the mismatch between carbohydrate supply and utilization that is most likely to occur in situations not requiring energy-consuming activities lead to metabolic stress due to elevated brain levels of glucose. Excessive doses of glucocorticoids also impair the production of energy (ATP) and mitochondrial oxidation. Therefore, glucocorticoids have both adaptive and maladaptive effects consistently with the concept of allostatic load and overload.
Rapid corticosteroid actions on behavior: Mechanisms and implications
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Corticosteroid Receptors, 11β-Hydroxysteroid Dehydrogenase, and the Heart
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Mineralocorticoid and glucocorticoid hormones are known as corticosteroid hormones and are synthesized mainly in the adrenal cortex; however, more recently the enzymes involved in their synthesis have been found in a variety of cells and tissues, including the heart. The effects of these hormones are mediated via both cytoplasmic mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs), which act as ligand-inducible transcription factors. In addition, rapid, nongenomically mediated effects of these steroids can occur that may be via novel corticosteroid receptors. The lipophilic nature of these hormones allows them to pass freely through the cell membrane, although the intracellular concentration of mineralocorticoids and glucocorticoids is dependent on several cellular factors. The main regulators of intracellular glucocorticoid levels are 11β-hydroxysteroid dehydrogenase (11βHSD) isoforms. 11βHSD1 acts predominantly as a reductase in vivo, facilitating glucocorticoid action by converting circulating receptor-inactive 11-ketoglucocorticoids to active glucocorticoids. In contrast, 11βHSD2 acts exclusively as an 11β-dehydrogenase and decreases intracellular glucocorticoids by converting them to their receptor-inactive 11-ketometabolites. Furthermore, P-glycoproteins, by actively pumping steroids out of cells, can selectively decrease steroids and local steroid synthesis can increase steroid concentrations. Receptor concentration, receptor modification, and receptor–protein interactions can also significantly impact on the corticosteroid response. This review details the receptors and possible mechanisms involved in both mediating and modulating corticosteroid responses. In addition, direct effects of corticosteroids on the heart are described including a discussion of the corticosteroid receptors and the mechanisms involved in mediating their effects.
Steroids and brain activity. Essential dialogue between body and mind
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Single-cell and multiunit activity in freely moving rats after corticosterone administration
1983, Experimental Neurology
With the purpose of correlating possible electrophysiologic changes in the brain with the negative feedback effect of glucocorticoids on neuroendocrine functions, the effects of corticosterone on multiunit (MUA) and single-cell activity in freely moving rats were studied in the hypothalamus, amygdala, and midbrain reticular formation. The hormone changed the MUA in all regions studied causing mainly an increase in the rate of firing. In the hypothalamus there was a predominance in overall inhibition, when the sensory responsiveness to acoustic stimulation was compared before and after corticosterone administration. No such effect was observed in the amygdala and midbrain reticular formation. The hormonally induced changes in MUA in the hypothalamus were confirmed by analysis of single-cell activity in the freely moving rats which showed also changes in the pattern of firing, as demonstrated by autocorrelations. These findings in the hypothalamus are significant and may represent the electrophysiologic correlates of changes in corticotrophin releasing factor in this region.
Modification of responses to sensory and hippocampal stimuli in neurons of the rat mediobasal hypothalamus in the presence of iontophoretically applied cortisol
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The effects of iontophoretic cortisol on evoked activity was studied in rat tuberal hypothalamic units. Evoked activity from visual, auditory, sciatic nerve and hippocampal stimulation was examined in same neurons both before and during local cortisol administration. Hippocampal stimuli were studied in isolation and as conditioning stimuli for one of the sensory modalities. A constant background glutamate current was frequently used in order to shorten observation periods and to enhance inhibition of firing. Even though the predominant effect of cortisol on spontaneous firing was to reduce the firing rate, the effect of the hormone on evoked responses of all kinds was to reduce the size of the response, independent of sign, and even to reverse the nature of the response, from control facilitation to inhibition or from control inhibition to facilitation. Evoked responses in many units whose spontaneous activity was not affected by cortisol were altered by hormone. Of particular interest are a group of cells which are normally silent and respond to afferent stimulation with inhibition. The responses in these cells are reduced or changed to excitation in the presence of cortisol and they may represent local inhibitory interneurons. The findings are related to the negative feedback of adrenocorticosteroids on CRF and ACTH release.

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Changes in single cell responsiveness in the hypothalamus in cats following cortisol administration

Summary

Electroenceph. clin. Neurophysiol.

Electroenceph. clin. Neurophysiol.

Brain Research

Electroenceph. clin. Neurophysiol.

Brain Research

Brain Research

Effects of corticosteroids on hypothalamic corticotropin releasing factor and pituitary ACTH content

Neuroendocrinology

Cerebral involvement in the inhibition of ACTH secretion by hydrocortisone

Endocrinology

Hormonal ‘feedback’ regulation of pituitaryadrenocortical activity

Acta physiol. Acad. Sci. hung.

Visual projections to the hypothalamus and preoptic area

Ann. N.Y. Acad. Sci.

Inhibitory effect of hypothalamic implants of corticosterone on adrenocortical response to auditory stimulation

Israel J. med. Sci.