Differential fornix ablations and the circadian rhythmicity of adrenal corticosteroid secretion

Fischette, Christine T.; Komisaruk, Barry R.; Edinger, Henry; Feder, Harvey H.; Siegel, Allan

doi:10.1016/0006-8993(80)90073-6

Cited by 93 publications

(39 citation statements)

References 39 publications

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“…These results contrast with reports of adrenocortical hyperactivity after large nonselective mechanical or electrolytic lesions of the hippocampus (Fendler et al, 1961;Kim and Kim, 1961;Knigge, 1961;Moberg et al, 1971;Murphy et al, 1979;Fischette et al, 1980;Wilson et al, 1980;Sapolsky et al, 1984Sapolsky et al, , 1991Herman et al, 1989). Discrepant effects on corticosterone secretion after hippocampal lesions have previously been attributed to differences in recovery time between surgery and experimentation (Jacobson and Sapolsky, 1991).…”

Section: Discussioncontrasting

confidence: 56%

“…Corticosterone was measured at the nadir of the rat circadian cycle of corticosterone secretion when the hypersecretion is maximal after nonselective lesions (Moberg et al, 1971;Fischette et al, 1980). All animals responded with elevated corticosterone levels after stress, but the concentrations did not increase more in lesioned animals than in control-operated animals at any of the time points tested or with any of the behavioral procedures that we used.…”

Section: Discussionmentioning

confidence: 99%

“…Physiological evidence from various sources indicates that hippocampal activity exerts an inhibitory influence on the HPA axis (Jacobson and , but does normal HPA activity depend on this hippocampal input or can other control systems provide similar inhibition? Several studies have shown that damage to the hippocampus increases basal glucocorticoid secretion (Fendler et al, 1961;Kim and Kim, 1961;Knigge, 1961;Moberg et al, 1971;Fischette et al, 1980;Wilson et al, 1980;Sapolsky et al, 1984Sapolsky et al, , 1991Herman et al, 1989), but these lesions were made either by aspiration or by transection of the fimbria-fornix and caused damage to bypassing fibers as well as adjacent brain systems, including the parahippocampal cortices and several subcortical structures. Other studies failed to identify a hippocampal inhibitory influence on the HPA axis (Coover et al, 1971;Lanier et al, 1975;Conforti and Feldman, 1976;Smotherman et al, 1981;Bradbury et al, 1993;Herman et al, 1995) but there was only incomplete damage to the hippocampus in these studies.…”

Section: Introductionmentioning

confidence: 99%

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Selective Hippocampal Lesions Do Not Increase Adrenocortical Activity

et al. 2003

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It has been proposed that the hippocampus exerts a tonic inhibitory influence on the hypothalamic-pituitary-adrenal (HPA) stress axis. This claim rests, in particular, on the upregulation of corticosterone secretion and other measures of HPA activity after nonselective lesions of the hippocampal formation. We measured plasma corticosterone concentrations after selective neurotoxic damage to the hippocampus and the subiculum in rats. Concentrations were estimated during rest in the rat's home cage and at several time points after varying degrees of stress. Lesions of the hippocampus did not increase the concentration of corticosterone relative to control rats in any condition. Temporary inactivation of the hippocampus or the ventral subiculum by infusion of the GABA A receptor agonist muscimol also failed to induce hypersecretion, although hippocampal infusions did impair spatial memory. These results suggest that the hippocampus is not necessary for tonic inhibition of adrenocortical activity and imply that the HPA axis receives efficient negative feedback inhibition from other brain systems too.

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Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Selective Hippocampal Lesions Do Not Increase Adrenocortical Activity

et al. 2003

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“…Efferents from the subiculum project to the PVN, either directly (Kiss et al, 1983) or via the BNST (Herman et al, 1994). Lesioning of the fimbria-fornix pathway to the BNST has been reported to abolish the circadian rhythm of glucocorticoids (Fischette et al, 1980), although this has been contested (Bradbury et al, 1993). It is therefore possible that changes in subicular 5-HT 2C receptor activity could alter the recognized hippocampal regulation of HPA axis activity (Jacobson and Sapolsky, 1991).…”

Section: Hpa Axis Regulationmentioning

confidence: 99%

Dysregulation of Diurnal Rhythms of Serotonin 5-HT_2Cand Corticosteroid Receptor Gene Expression in the Hippocampus with Food Restriction and Glucocorticoids

Holmes

French

1997

J. Neurosci.

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Both serotonergic dysfunction and glucocorticoid hypersecretion are implicated in affective and eating disorders. The adverse effects of serotonergic (5-HT) 2C receptor activation on mood and food intake, the antidepressant efficacy of 5-HT 2 receptor antagonists, and the hyperphagia observed in 5-HT 2C receptor knockout mice all suggest a key role for increased 5-HT 2C receptor-mediated neurotransmission. Glucocorticoids, however, downregulate 5-HT 2C receptor mRNA in the hippocampus, and it is unclear how increased 5-HT 2C receptor sensitivity is achieved in the presence of elevated glucocorticoid levels in depression. Here we show a monophasic diurnal rhythm of 5-HT 2C receptor mRNA expression in the rat hippocampus that parallels time-dependent variations in 5-HT 2C receptor agonist-induced behaviors in open field tests. Rats entrained to chronic food restriction show marked but intermittent corticosterone hypersecretion and maintain an unaltered 5-HT 2C receptor mRNA rhythm. The 5-HT 2C receptor mRNA rhythm, however, is suppressed by even modest constant elevations of corticosterone (adrenalectomy ϩ pellet) or with elevated corticosterone during the daytime (8 A.M.), whereas a normal rhythm exists in animals that have the same dose of corticosterone in the evening (6 P.M.). Thus, animals showing even a transient daytime corticosterone nadir exhibit normal hippocampal 5-HT 2C receptor mRNA rhythms, even in the presence of overt corticosterone hypersecretion. Chronic food restriction also abolishes the normal diurnal variation in hippocampal glucocorticoid receptor (GR) and mineralocorticoid receptor mRNAs and produces, unusually, both elevated corticosterone and increased GR. The mismatch between elevated glucocorticoids and maintained 5-HT 2C receptor and increased GR gene expression in the hippocampus provides a new model to dissect mechanisms that may underlie affective and eating disorders.

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“…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)(5)(6)(7)(8)(9). Furthermore, stimulation of most parts of the structure inhibits stress-induced HPA activation (10)(11)(12)(13).…”

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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Differential fornix ablations and the circadian rhythmicity of adrenal corticosteroid secretion

Cited by 93 publications

References 39 publications

Selective Hippocampal Lesions Do Not Increase Adrenocortical Activity

Selective Hippocampal Lesions Do Not Increase Adrenocortical Activity

Dysregulation of Diurnal Rhythms of Serotonin 5-HT_2Cand Corticosteroid Receptor Gene Expression in the Hippocampus with Food Restriction and Glucocorticoids

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

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Differential fornix ablations and the circadian rhythmicity of adrenal corticosteroid secretion

Cited by 93 publications

References 39 publications

Selective Hippocampal Lesions Do Not Increase Adrenocortical Activity

Selective Hippocampal Lesions Do Not Increase Adrenocortical Activity

Dysregulation of Diurnal Rhythms of Serotonin 5-HT2Cand Corticosteroid Receptor Gene Expression in the Hippocampus with Food Restriction and Glucocorticoids

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

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Dysregulation of Diurnal Rhythms of Serotonin 5-HT_2Cand Corticosteroid Receptor Gene Expression in the Hippocampus with Food Restriction and Glucocorticoids