Neuroendocrine Aspects of Learning and Memory Processes

Wied, D de

doi:10.1152/physiologyonline.1989.4.1.32

Physiology

1989

DOI: 10.1152/physiologyonline.1989.4.1.32

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Neuroendocrine Aspects of Learning and Memory Processes

D de Wied¹

Abstract: Limbic structures are involved in learning and memory processes. These structures are richly innervated by fibers containing neurotransmitters and neuropeptides. Corticosteroids and adrenomedullary hormones and peptides related to acetylcholine, corticotrophin-releasing hormone, melanophore-stimulating hormone, oxytocin, vasopressin, and several others modulate learning and memory processes and limbic system activity.

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“…Glucocorticoids (GCs) stimulate a number of biochemical and genomic processes in hippocampal neurons (3)(4)(5) and have been found by extracellular recording to alter brain neuronal excitability (6)(7)(8). Further, stress-related hormones substantially influence memory and other cognitive functions (9,10). In addition to these normal functions, moreover, chronic exposure to GCs can exert neurotoxic actions on hippocampal pyramidal cells, particularly in conjunction with the brain aging process (11)(12)(13)(14)(15).…”

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Hippocampal glucocorticoid receptor activation enhances voltage-dependent Ca2+ conductances: relevance to brain aging.

Kerr

Campbell

Thibault

et al. 1992

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

212

128

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Glucocorticoids (GCs) activate several biochemical/molecular processes in the hippocampus through two receptor types. In addition, GCs influence cognitive behaviors and hippocampal neural activity and can also increase the rate of aging-dependent cell loss in the hippocampus. However, the ionic mechanisms through which Although it has been recognized for >20 yr that the brain, and in particular the hippocampus, is rich in specific corticosteroid receptors (1, 2), the cellular effects of activating these receptors are still poorly understood (3). Glucocorticoids (GCs) stimulate a number of biochemical and genomic processes in hippocampal neurons (3-5) and have been found by extracellular recording to alter brain neuronal excitability (6-8). Further, stress-related hormones substantially influence memory and other cognitive functions (9, 10). In addition to these normal functions, moreover, chronic exposure to GCs can exert neurotoxic actions on hippocampal pyramidal cells, particularly in conjunction with the brain aging process (11-15). Long-term adrenalectomy protects (12) Recent intracellular electrophysiological studies have provided insights into how brain GCRs may act to modify ionic conductances and neuronal function. Two studies (24,25) found that Cort increases the well-defined (26) Ca2+-dependent, K+-mediated afterhyperpolarization (AHP) that normally follows Na+ action potentials in CA1 hippocampal neurons. This effect of Cort on the AHP likely accounts for inhibitory actions of GCs on hippocampal neurons (24,25) and is mediated by the GCR because it can be mimicked by the highly specific GCR agonist RU 28362 (24). Conversely, further studies have indicated that MCR activation increases hippocampal excitability by suppressing neurotransmittermediated hyperpolarization (for review, see ref. 27). These MCR and GCR effects on hippocampal excitability can be blocked by inhibition of protein synthesis (28).However, it is still not clear how GCs modulate the AHP. Although the effect of GCs on the AHP was suggested to be mediated by an increase in voltage-activated Ca2+ conductance (25), the GC effect could also be mediated by actions on Ca2+ buffering/extrusion or K* channels, among others. Steroids have been shown to influence a number of K+ and Cl-conductances, through actions on membrane receptors (29-31), but to date there has been no evidence that steroids can also influence voltage-sensitive Ca2+ conductance.A clear answer to the question of a putative GC-Ca2+ channel linkage is also of particular relevance to present concepts on mechanisms of brain aging. Elevated intracellular Ca2+ can be neurotoxic, and there is increasing evidence of neuronal Ca2+ dysregulation in brain aging (see refs. 32-37). Because the AHP is increased with aging (25,37), the recent findings that GCs modulate the Ca2+-dependent AHP (24, 25) and, moreover, exert an increased impact in aged neurons (25) suggest that there may be a link between the GC and the Ca2+ dysregulation hypotheses of brain aging. That is, it has b...

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mentioning

confidence: 99%

Hippocampal glucocorticoid receptor activation enhances voltage-dependent Ca2+ conductances: relevance to brain aging.

Kerr

Campbell

Thibault

et al. 1992

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

212

128

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“…That is, many of the studies have utilized surgical ADX or stress (or both) to produce variations in serum CORT, without providing sufficient control of ADX-and stress-induced variations in adrenal catecholamines, adrenal opioids, and ACTH. The latter factors have also been implicated in the modulation of LTP (Gold, Delanoy, & Merrin, 1984;Shors, Levine, & Thompson, 199Oa, 199Ob) and memory and learning processes (de Wied, 1989;Gold & van Buskirk, 1975, 1976, and they should be considered as possible experimental confounds (or cofactors; cf. Axelrod & Reisine, 1984) in at least some of the glucocorticoid studies cited above.…”

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confidence: 99%

Modulation of hippocampal long-term potentiation and long-term depression by corticosteroid receptor activation

1994

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Long-term potentiation (LTP) and long-term depression (LTD) are lasting changes in synaptic efficacy which may underlie memory and learning processes. Hippocampal LTP has been shown to vary inversely with the degree of stress or adrenal activity, and adrenal corticosteroids (CORT) have been strongly implicated in this process. The present in vitro study was undertaken to further examine the role of glucocorticoids in LTP, and to extend this analysis to heterosynaptic LTD. Animals were injected twice daily (s.c.) for 2 days prior to sacrifice with either the corticosteroid biosynthesis inhibitor metyrapone (200 mg/kg/day) or CORT (20 mg/kg/day). Noninjected and saline-injected controls were also examined. CAl population spike amplitudes and field EPSP slopes were assessed in response to activation of two separate stratum radiatum inputs. One input received tetanic stimulation and both inputs were monitored for 30 min following tetanization to determine long-term changes in synaptic efficacy (homosynaptic LTP of tetanized synapses; heterosynaptic LTD of nontetanized synapses). Animals exhibiting low and high serum CORT titers exhibited significantly less LTP and LTD than did animals exhibiting moderate levels of CORT. In addition, in vitro perfusion of RU-28362, a Type II glucocorticoid receptor agonist, markedly reduced both LTP and LTD. There was no correlation between serum CORT and serum glucose titers, nor was there any correlation between serum glucose and either LTP or LTD. These results are consistent with recent reports of an inverted-U function for CORT levels versus primedburst LTP (Bennett, Diamond, Fleshner, & Rose, 1991;Diamond, Bennett, Fleshner, & Rose, 1992) and further demonstrate that manipulation of corticosterone in adrenal-intact animals affects LTP and LTD in a similar fashion.It is well established that the hippocampus and related brain structures are rich in specific corticosteroid receptors (CSRs) (

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Neuroendocrine Aspects of Learning and Memory Processes

Cited by 2 publications

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Hippocampal glucocorticoid receptor activation enhances voltage-dependent Ca2+ conductances: relevance to brain aging.

Hippocampal glucocorticoid receptor activation enhances voltage-dependent Ca2+ conductances: relevance to brain aging.

Modulation of hippocampal long-term potentiation and long-term depression by corticosteroid receptor activation

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