Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The modifications of rat brain muscarinic acetylcholine receptors induced by chronic immobilization stress lasting 10 min/daily or 2 h/daily for 3, 7 or 21 days were analyzed by quantitative in vitro autoradiography. [3H]N-Methylscopolamine ([3H]NMS) was used as ligand. Chronic immobilization stress for 10 min/day did not produce any significant change in the properties of [3H]NMS binding sites throughout the rat brain. In contrast, 2 h/day immobilization caused a significant increase in the maximal number of muscarinic receptors (Bmax) in several brain areas such as the cortical layers, the CA1 field of the hippocampus and caudate-putamen, among others. Affinity values (Kd) were not modified. These results suggest that chronic immobilization stress induces supersensitivity of muscarinic receptors in certain cholinergic pathways in rat brain, the pattern of response being different to that previously found for acute stress.
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PMID:Modification of muscarinic acetylcholine receptors in the rat brain following chronic immobilization stress: an autoradiographic study. 147 57

We used in-situ hybridization to study the effect of acute stress on induction of the immediate early genes (IEGs), c-fos and zif/268, in the rat brain. After one hour of restraint plus intermittent tail shock, messenger RNA (mRNA) levels for both genes were significantly increased bilaterally in the neocortex, particularly in layers IV, V and VI, and in the CA1 region of the hippocampus. This regionally-specific response suggests that IEGs may have a role in the mediation of acute stress responses in the central nervous system.
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PMID:Activation of immediate early genes after acute stress. 176 44

Glucocorticoids potentiate hippocampal damage induced by various noxious insults in vivo and in vitro and are implicated in age-related loss of neurons in the hippocampus of various species. The cholinergic innervation of the hippocampus appears to be especially prone to the endangering effect of glucocorticoids, since corticosterone, like acute stress or ACTH, induces a rapid activation of the cholinergic septo-hippocampal pathway. We now report the influence of glucocorticoids on the degeneration of this pathway induced by the cholinergic neurotoxin ethylcholine aziridinium (AF64A). The toxic effect of a submaximal dose of AF64A on cholinergic neurons was evaluated in rats during exposure to glucocorticoids or vehicle as well as in adrenalectomized or sham-operated rats. Daily treatment with either corticosterone or dexamethasone, starting 7 d before the bilateral intracerebroventricular injection of AF64A (1 nmol/ventricle), significantly increased the AF64A-induced loss of ChAT activity in the whole hippocampus, whereas bilateral adrenalectomy 7 d prior to AF64A-injection attenuated the effect of AF64A. Short-term exposure to corticosterone starting 24 hr before AF64A was as effective as the 7 d pretreatment. Dexamethasone exacerbated the AF64A-induced cholinergic lesion in the hippocampal subregions CA1, CA3, and dentate gyrus, and adrenalectomy protected all subregions against the action of AF64A. Along the longitudinal axis of the hippocampus a comparable influence was seen in the dorsal and ventral parts. The subregional pattern in the response to glucocorticoid suggests the involvement of mineralocorticoid type I receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of glucocorticoids in the cholinergic degeneration in rat hippocampus induced by ethylcholine aziridinium (AF64A). 768 81

We studied messenger RNA (mRNA) expressions of receptors for glucocorticoid (GR), thyroid hormone (TR), androgen (AR), and estrogen (ER) and their changes with age in the hippocampal subregions in postmortem human brain. In situ hybridization was done with biotin-labeled antisense synthetic oligonucleotide probes. About 80% or more of the pyramidal neurons in the hippocampal subregions expressed mRNAs for individual receptors in the brains of subjects younger than 65. The ratio of mRNA-containing neuron density to total neuron density significantly decreased with age for GR in CA1 and CA3, and for AR in CA1. Non-significant trends in the reduction with age in the ratio of ER mRNA-containing neurons in CA1 and the ratio of GR mRNA-containing neurons in the hilus also were found. Age-related reductions in nuclear receptor protein mRNA expression in neurons in the hippocampal subfields may be important in the impairments of cognition, emotion, and responses to acute stress in the aged.
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PMID:Effects of age on messenger RNA expression of glucocorticoid, thyroid hormone, androgen, and estrogen receptors in postmortem human hippocampus. 862 17

The long-term consequences of acute stress on [3H]phorbol 12,13-dibutyrate ([3H]PDBu) binding, a marker for protein kinase C (PKC) activity, were investigated. In the first experiment, exposure to acute restraint and intermittent tail-shock increased [3H]PDBu binding in the amygdala but not in the hippocampus or cerebral cortex. The increase was persistent, lasting at least 24 h after stressor cessation. In the second experiment, it was determined that the stress-induced increase in binding in the amygdala was dependent on NMDA receptor activation; rats injected with a competitive NMDA receptor antagonist prior to the stressor did not exhibit the increased binding in the amygdala 24 h later. In the third experiment, re-exposure to the stressful context 96 h after stressor cessation reactivated the stress-induced increase the binding of [3H]PDBu in the amygdala. Re-exposure to the context also increased binding in the thalamus and area CA1 of the hippocampus. [3H]PDBu binds preferentially to PKC in the membrane and, therefore, these results suggest that stress induces the translocation of PKC from its resting compartments in the cytosol to the membrane. Its dependence on NMDA receptor activation implicates isoforms of PKC that are sensitive to intracellular calcium, such as PKC gamma. The results further suggest that a "psychological' manipulation, viz. context re-exposure, can reactivate the persistent increase in [3H]PDBu binding in the amygdala.
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PMID:Stress persistently increases NMDA receptor-mediated binding of [3H]PDBu (a marker for protein kinase C) in the amygdala, and re-exposure to the stressful context reactivates the increase. 909 55

Pyramidal cells in the CA1 hippocampal area express both mineralo- and glucocorticoid receptors (MRs and GRs respectively) to which the rat adrenal hormone corticosterone binds effectively. Through activation of these receptors corticosteroids exert a delayed and persistent control over signal transduction in the hippocampus. Many cellular responses are affected by the hormone, including responsiveness to serotonin (5HT) and the cholinergic agent carbachol (CCh). It was found that predominant MR occupation results within hours in small responses to 5HT and to CCh. Concomitant activation of GRs leads to larger transmitter responses. Particularly strong responses to 5HT were observed 1-4 hours after an acute stress; this could be prevented by pretreatment with the antiglucocorticoid RU38486. Steroids also exert a long-term effect on aminergic responses. Chronic exposure to a very high corticosterone dose was found to depress 5HT responses. These data indicate that short-term fluctuations in corticosterone level alter neurotransmitter responses in the hippocampus, a structure involved in mood and cognition. In addition, long-term aberrations in corticosteroid levels, e.g. due to glucocorticoid feedback resistance in association with several stress-related disorders, also change the hippocampal responsiveness to monoamines. Future studies will have to examine the potential of antiglucocorticoids to restore this disturbed neurotransmitter function.
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PMID:Corticosteroid effects on electrical properties of brain cells: temporal aspects and role of antiglucocorticoids. 926 52

The characteristics of short-term potentiation (STP) and long-term potentiation (LTP) in the CA1 region of hippocampal slices were determined at various times following exposure to acute stress produced by restraint and tail-shock in mice. In slices prepared from control animals, theta-burst stimulation resulted in a large increase in evoked field excitatory postsynaptic potentials (EPSPs) amplitude and slope that remained stable at least up to 30 min after stimulation. Slices prepared 1 h after stress exhibited a marked decrease in the extent of both STP and LTP. STP and LTP magnitude were still significantly decreased 24 h after stress exposure and were completely restored to control levels by 48 h. These results provide evidence for a reversible impairment of STP and LTP in CA1 following an acute episode of stress, and suggest that stress activates processes different from those activated by LTP-inducing stimuli.
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PMID:Time-dependent blockade of STP and LTP in hippocampal slices following acute stress in mice. 932 35

In this review, we have described the function of MR and GR in hippocampal neurons. The balance in actions mediated by the two corticosteroid receptor types in these neurons appears critical for neuronal excitability, stress responsiveness, and behavioral adaptation. Dysregulation of this MR/GR balance brings neurons in a vulnerable state with consequences for regulation of the stress response and enhanced vulnerability to disease in genetically predisposed individuals. The following specific inferences can be made on the basis of the currently available facts. 1. Corticosterone binds with high affinity to MRs predominantly localized in limbic brain (hippocampus) and with a 10-fold lower affinity to GRs that are widely distributed in brain. MRs are close to saturated with low basal concentrations of corticosterone, while high corticosterone concentrations during stress occupy both MRs and GRs. 2. The neuronal effects of corticosterone, mediated by MRs and GRs, are long-lasting, site-specific, and conditional. The action depends on cellular context, which is in part determined by other signals that can activate their own transcription factors interacting with MR and GR. These interactions provide an impressive diversity and complexity to corticosteroid modulation of gene expression. 3. Conditions of predominant MR activation, i.e., at the circadian trough at rest, are associated with the maintenance of excitability so that steady excitatory inputs to the hippocampal CA1 area result in considerable excitatory hippocampal output. By contrast, additional GR activation, e.g., after acute stress, generally depresses the CA1 hippocampal output. A similar effect is seen after adrenalectomy, indicating a U-shaped dose-response dependency of these cellular responses after the exposure to corticosterone. 4. Corticosterone through GR blocks the stress-induced HPA activation in hypothalamic CRH neurons and modulates the activity of the excitatory and inhibitory neural inputs to these neurons. Limbic (e.g., hippocampal) MRs mediate the effect of corticosterone on the maintenance of basal HPA activity and are of relevance for the sensitivity or threshold of the central stress response system. How this control occurs is not known, but it probably involves a steady excitatory hippocampal output, which regulates a GABA-ergic inhibitory tone on PVN neurons. Colocalized hippocampal GRs mediate a counteracting (i.e., disinhibitory) influence. Through GRs in ascending aminergic pathways, corticosterone potentiates the effect of stressors and arousal on HPA activation. The functional interaction between these corticosteroid-responsive inputs at the level of the PVN is probably the key to understanding HPA dysregulation associated with stress-related brain disorders. 5. Fine-tuning of HPA regulation occurs through MR- and GR-mediated effects on the processing of information in higher brain structures. Under healthy conditions, hippocampal MRs are involved in processes underlying integration of sensory information, interpretation of environmental information, and execution of appropriate behavioral reactions. Activation of hippocampal GRs facilitates storage of information and promotes elimination of inadequate behavioral responses. These behavioral effects mediated by MR and GR are linked, but how they influence endocrine regulation is not well understood. 6. Dexamethasone preferentially targets the pituitary in the blockade of stress-induced HPA activation. The brain penetration of this synthetic glucocorticoid is hampered by the mdr1a P-glycoprotein in the blood-brain barrier. Administration of moderate amounts of dexamethasone partially depletes the brain of corticosterone, and this has destabilizing consequences for excitability and information processing. 7. The set points of HPA regulation and MR/GR balance are genetically programmed, but can be reset by early life experiences involving mother-infant interaction. 8. (ABSTRACT TRUNCATED)
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PMID:Brain corticosteroid receptor balance in health and disease. 962 55

Neurocircuit inhibition of hypothalamic paraventricular nucleus (PVN) neurons controlling hypothalamo-pituitary-adrenocortical (HPA) activity prominently involves GABAergic cell groups of the hypothalamus and basal forebrain. In the present study, stress responsiveness of GABAergic regions implicated in HPA inhibition was assessed by in situ hybridization, using probes recognizing the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD65 and GAD67 isoforms). Acute restraint preferentially increased GAD67 mRNA expression in several stress-relevant brain regions, including the arcuate nucleus, dorsomedial hypothalamic nucleus, medial preoptic area, bed nucleus of the stria terminalis (BST) and hippocampus (CA1 and dentate gyrus). In all cases GAD67 mRNA peaked at 1 hr after stress and returned to unstimulated levels by 2 hr. GAD65 mRNA upregulation was only observed in the BST and dentate gyrus. In contrast, chronic intermittent stress increased GAD65 mRNA in the anterior hypothalamic area, dorsomedial nucleus, medial preoptic area, suprachiasmatic nucleus, anterior BST, perifornical nucleus, and periparaventricular nucleus region. GAD67 mRNA increases were only observed in the medial preoptic area, anterior BST, and hippocampus. Acute and chronic stress did not affect GAD65 or GAD67 mRNA expression in the caudate nucleus, reticular thalamus, or parietal cortex. Overall, the results indicate preferential upregulation of GAD in central circuitry responsible for direct (hypothalamus, BST) or multisynaptic (hippocampus) control of HPA activity. The distinct patterns of GAD65 and GAD67 by acute versus chronic stress suggest stimulus duration-dependent control of GAD biosynthesis. Chronic stress-induced increases in GAD65 mRNA expression predict enhanced availability of GAD65 apoenzyme after prolonged stimulation, whereas acute stress-specific GAD67 upregulation is consistent with de novo synthesis of active enzyme by discrete stressful stimuli.
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PMID:Region-specific regulation of glutamic acid decarboxylase (GAD) mRNA expression in central stress circuits. 967 80

Previous studies have shown that corticosteroids affect the changes in membrane potential evoked in CA1 hippocampal neurons by serotonin and the metabolically stable cholinergic analogue carbachol: Low corticosteroid levels induced by steroid administration to adrenalectomized rats or obtained in adrenally intact rats were associated with small transmitter responses. High corticosteroid levels induced by exogenous corticosteroid application or by an acute stress in adrenally intact rats generally evoked large transmitter responses. In the present study we investigated the consequences of this steroid modulation for the main stream of synaptic information in the CA1 hippocampal region, which is carried by amino acids. To this purpose the effect of serotonin and carbachol administration on both extracellularly and intracellularly recorded synaptic responses to Schaffer collateral stimulation were investigated. The data show that the effect of in vivo activation of corticosteroid receptors on the serotonin-induced hyperpolarization of the membrane responses is clearly reflected in the inhibitory effect of serotonin on synaptic responsiveness in the CA1 area. Low circulating levels of corticosterone or selective mineralocorticoid receptor activation reduced the serotonin mediated inhibition of synaptically evoked responses, whereas high corticosterone levels were associated with strong serotonin mediated suppression of synaptic responses. This steroid modulation seems to be specifically aimed at serotonin neurotransmission, as the cholinergic effects on excitatory synaptic transmission were not affected by the hormone treatment.
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PMID:Serotonin and carbachol induced suppression of synaptic responses in rat CA1 hippocampal area: effects of corticosteroid receptor activation in vivo. 978 66


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