Effect of Hippocampal Stimulation on the Plasma Thyrotropin (THS) and Corticosterone Responses to Acute Cold Exposure in the Rat

Dupont, André; Bastarache, Edouard; Endröczi, E; Fortier, Claude

doi:10.1139/y72-054

Cited by 27 publications

(18 citation statements)

References 2 publications

(2 reference statements)

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“…Destruction of the hippocampus, for example, leads to hypersecretion of glucocorticoids under basal and stressed conditions (4)(5)(6)(7)(8)(9). Furthermore, stimulation of most parts of the structure inhibits stress-induced HPA activation (10)(11)(12)(13). At least some of this inhibitory influence of the hippocampus represents mediation of feedback inhibition by glucocorticoids.…”

mentioning

confidence: 99%

Glucocorticoid-sensitive hippocampal neurons are involved in terminating the adrenocortical stress response.

Sapolsky¹,

Krey²,

McEwen³

1984

Proc. Natl. Acad. Sci. U.S.A.

615

333

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The hippocampus is the principal target site in the brain for adrenocortical steroids, as it has the highest concentration of receptor sites for glucocorticoids. The aged rat has a specific deficit in hippocampal glucocorticoid receptors, owing in large part to a loss of corticoid-sensitive neurons. This deficit may be the cause for the failure of aged rats to terminate corticosterone secretion at the end of stress, because extensive lesion and electrical stimulation studies have shown that the hippocampus exerts an inhibitory influence over adrenocortical activity and participates in glucocorticoid feedback. We have studied whether it is the loss of hippocampal neurons or of hippocampal glucocorticoid receptors in the aged rat that contributes most to this syndrome of corticosterone hypersecretion. To do this, we used two model systems for producing reversible glucocorticoid receptor depletion in the hippocampus, and we found that depletion of receptors without inducing cell loss results in corticosterone hypersecretion. Furthermore, correction of the receptor deficit results in normalization of corticosterone secretion. These results focus attention on the hippocampus as an important glucocorticoid sensor in relation to the stress response. They also provide important new physiological correlates for the remarkable plasticity of the hippocampal glucocorticoid receptor system, which is under independent control by corticosterone and by vasopressin.In the mammalian brain, the hippocampus contains the highest concentration of glucocorticoid receptors and retains the highest concentration of [3H]corticosterone after in vivo injection (1). This phenomenon was initially reported in 1968 (2), and considerable speculation still remains regarding the physiological and behavioral significance of the hippocampal uptake system (1, 3). However, the hippocampus has been persistently implicated as an inhibitory influence on the hypothalamic-pituitary-adrenocortical (HPA) axis. Destruction of the hippocampus, for example, leads to hypersecretion of glucocorticoids under basal and stressed conditions (4-9). Furthermore, stimulation of most parts of the structure inhibits stress-induced HPA activation (10-13). At least some of this inhibitory influence of the hippocampus represents mediation of feedback inhibition by glucocorticoids. For example, hippocampectomized subjects are less sensitive to the suppressive effects of exogenous glucocorticoids on HPA secretion (6). Moreover, corticotropin (ACTH) is increased after hippocampectomy and the difference in corticotropin levels between lesioned and sham-lesioned animals is abolished by adrenalectomy, suggesting that the relative increase in corticotropin due to the lesion resulted from lesion-induced disinhibition from corticoid-feedback suppression (5). This evidence that circulating glucocorticoids exert some of their feedback effects via the hippocampus suggests that such actions are mediated by the hippocampal glucocorticoid receptor. Thus, one can postulate that decr...

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mentioning

confidence: 99%

Glucocorticoid-sensitive hippocampal neurons are involved in terminating the adrenocortical stress response.

Sapolsky¹,

Krey²,

McEwen³

1984

Proc. Natl. Acad. Sci. U.S.A.

615

333

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“…While a number of authors have claimed that fornix section or hippocampal lesions abolish the normal diurnal rhythm of plasma corticosteroids * (Mason 1958, Nakadate and de Groot 1963, Moberg et al 1971, Endroczi 1972, there have been many negative reports (Galicich, et al 1965, Endroczi and Nyakas 1971, Wilson and Critchlow 1973/4, Kearley, Van Hartesveldt, and Woodruff 1974. Some of the confusion could relate to the time of testing after operation.…”

Section: 43(a) Physiological Functionsmentioning

confidence: 99%

“…Lengvari and Halasz (1973) have shown a disruption of the diurnal cycle with fornix lesions at 1 week, but not 3 week, postoperative testing. Most of the positive reports indicate that the effect consists of a smoothing out of the normal cyclic rhythm such that lesioned animals have abnormally high levels in the morning and abnormally low levels in the evening, though one study (Endroczi 1972) reported an absolute increase throughout the day. In most of these studies no attempt was made to correlate corticosteroid levels with behavioural activity, in spite of the known relationship between the two, and the fact that hippocampal damage usually alters activity levels, in particular attenuating cyclic activity changes (e.g.…”

Section: 43(a) Physiological Functionsmentioning

confidence: 99%

“…Resting levels Mason 1958Mason 1959 Endroczi and Lissak 1960 Van Wimersma Griedanus and de Wied 1969Knigge 1961 Endroczi and Nyakas 1971Slusher and Hyde 1961Moberg et al 1971 Endroczi and Lissak 1962Coover et al 1971bMandell et al 1963 Endroczi 1972 Nakadate and de Groot 1963 Kawakami et al 1973Galicich et al 1965 Lengvari and Halasz Slusher 1966 Wilson and Critchlow 1973Rubin et al 1966Kearley et al 1974Fendler et al 1961Jackson and Regenstein 1974Bohus et al 1968 III. Behavioural studies Porter 1954 Bohus 1971 Endroczi et al 1959Dupont et al 1972Knigge 1961 Endroczi 1972 Kim and Kim 1961 Wilson and Critchlow 1973 Endroczi and Lissak 1962Kearley et al 1974Knigge and Hays 1963Lovely 1975Davidson and Feldman 1967Iuvone and Van Hartesveldt 1976 Coover et al 19716 Andy et al 1962 Bland and Vanderwolf 1972b Votaw and Lauer 1963bLevitt and O'Hearn 1972Ursin et al 1966 Brown and Feldman et al 1967 Oliver et al 1974Coury 1967Jackson and Gardner 1974Musty et al 1967Nagy and Decsi 1974Grant and Jarrard 1968Lico et al 1974Siegel and Flynn 1968Rogozea et al 1969Siegfried et al 1975Mountford 1969…”

Section: Acknowledgementsmentioning

confidence: 99%

“…Thus, Mason (1959) showed that endocrine mobilization occurred in 'first-experience' situations, even when these did not involve pain or an obvious threat to the animal. Endroczi (1972) has shown that the pituituary-adrenal system responds strongly to unmet expectancies, such as the withdrawal of expected rewards or closing down an alley normally used to get to water in a maze. Similarly, Bohus (1973), Coover et al (1971a) and Coover, Ursin, and Levine (1973) have all provided evidence that 'one of the conditions which will activate the neuroendocrine mechanisms leading to subsequent release of ACTH is a change in expectancies' (Coover el al.…”

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confidence: 99%

See 2 more Smart Citations

The Hippocampus as a Cognitive Map

Routtenberg¹,

O’Keefe²,

Nadel³

1980

The American Journal of Psychology

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Ventral subicular interaction with the hypothalamic paraventricular nucleus: Evidence for a relay in the bed nucleus of the stria terminalis

Cullinan

Herman

Watson

1993

J of Comparative Neurology

462

332

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The axonal projections of the ventral subiculum to the bed nucleus of the stria terminalis (BST) were examined in the rat with the anterograde neuronal tracer Phaseolus vulgaris-leucoagglutinin (PHA-L). Axons originating in the ventral subiculum coursed to the BST through either the fimbria-fornix, or a pathway involving the stria terminalis via the amygdala. Ventral subicular axons gave rise to dense terminal networks that were preferentially distributed in medial and ventral subregions of the BST. The distribution of subicular fibers and terminals was examined in relation to BST neurons that project to the hypothalamic paraventricular nucleus (PVN). In these cases, discrete iontophoretic injections of the retrograde tracer Fluoro-gold were made in the PVN, with PHA-L delivered to the ipsilateral ventral subiculum. An immunocytochemical double-labeling protocol was then employed for the simultaneous detection of PHA-L and Fluoro-gold, and provided light microscopic evidence for subicular input to PVN-projecting cells located within the BST. In a second series of experiments, the gamma-amino butyric acid (GABA)ergic nature of the BST was examined by in situ hybridization histochemistry for detection of transcripts encoding GAD67 mRNA. The studies revealed that a high proportion of BST neurons express GAD67 transcripts. Also, experiments combining Fluoro-gold tracing with GAD67 in situ hybridization suggested that a proportion of PVN-projecting neurons in the BST are GABAergic. Taken together, the results of these sets of studies suggest that the inhibitory influences of the hippocampus on the PVN might be relayed through specific portions of the BST. These findings may have important implications for our understanding of the neural regulation of the hypothalamic-pituitary-adrenal axis.

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Effect of Hippocampal Stimulation on the Plasma Thyrotropin (THS) and Corticosterone Responses to Acute Cold Exposure in the Rat

Cited by 27 publications

References 2 publications

Glucocorticoid-sensitive hippocampal neurons are involved in terminating the adrenocortical stress response.

Glucocorticoid-sensitive hippocampal neurons are involved in terminating the adrenocortical stress response.

The Hippocampus as a Cognitive Map

Ventral subicular interaction with the hypothalamic paraventricular nucleus: Evidence for a relay in the bed nucleus of the stria terminalis

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