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J Herbert

Publications and source records attributed to J Herbert.

At least 91 records · Page 5Linked to original sources
PubMed1996

Central antagonism of atrial natriuretic peptides on behavioral and hormonal responses to angiotensin II: mapping with c-fos.

The expression of the immediate early gene (IEG) c-fos has been used to map the antagonistic effects between atrial natriuretic peptide (ANP) and angiotensin II (Ang II). Intracerebroventricular (i.c.v.) infusions of ANP (100, 250, 1000 or 2000 pmol) did not induce detectable c-fos expression in the forebrain when compared with CSF-treated rats. Neither did C-type natriuretic peptide (CNP, 10, 100, 500 or 1000 pmol), another member of the natriuretic peptide family, which appears to be predominant in the brain. ANP was found to inhibit the water intake and corticosterone release induced by i.c.v. infusions of Ang II. However, ANP could not suppress the c-fos expression in the organum vasculosum of the lamina terminalis (OVLT), medial preoptic nucleus (MNPO), subfornical organ (SFO), supraoptic (SON) and paraventricular (PVN) nuclei of forebrain induced by the same dose of Ang II. The activation of second messenger pathways following i.c.v. infusion of Ang II may result in two different sets of effects: immediate behavioural and physiological responses (presumably through postsynpatic responses in neurons sensitive to Ang II), and the delayed expression of c-fos (and other IEGs proteins) which control the expression of late response genes. Whilst there is considerable, and growing evidence that IEGs mark the pattern of neuronal activity induced by peptides such as Ang II, the precise role played by these gene products is still problematical and awaits clarification by further experiments.

Angiotensin II↗
PubMed1996

Effects of unilateral or bilateral lesions within the anteroventral third ventricular region on c-fos expression induced by dehydration or angiotensin II in the supraoptic and paraventricular nuclei of the hypothalamus.

This paper reports the effects of AV3V lesions on the pattern of c-fos induced by 24 h dehydration. As expected, bilateral electrolytic lesions within the AV3V region (the ventral median preoptic nucleus) suppressed water intake following 24 h water deprivation. C-fos expression was also suppressed in the supraoptic (SON) and (less completely) in the paraventricular (PVN) nuclei, but not in the subfornical organ (SFO). Unilateral lesions of the AV3V region suppressed c-fos expression in the ipsilateral SON, but this selective ipsilateral effect was less in the PVN. The SFO was again unaffected. Unilateral lesions also suppressed c-fos expression in the ipsilateral SON and PVN (to a lesser degree) following intraventricular infusions of angiotensin II (250 pmol). These results suggest that the cellular response of supraoptic neurons to osmotic stimuli require inputs from the AV3V region, but that this is less absolute for the PVN; that the projection from the ventral AV3V area to the SON is ipsilateral, but that to the PVN may be less lateralised. Activation of the SFO by dehydration is not dependent upon the integrity of the ventral AV3V region. These results are closely comparable to the effects of similar lesions on c-fos expression following intraventricular infusions of angiotensin II, and suggest that the effect of dehydration on forebrain c-fos expression may be related to the central actions of angiotensin II.

Angiotensin II↗
PubMed1996

A role for central glucagon-like peptide-1 in temperature regulation.

We have already established that central glucagon-like peptide-1 (GLP-1) has a role in the central control of food intake. In this study, experiments were conducted to establish the effect of acute intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) administration of GLP-1 on temperature. Injection of 10 micrograms GLP-1 i.c.v. caused a significant reduction in temperature over the subsequent 2 h and reduced food intake as expected. Both effects were blocked by prior i.c.v. administration of the GLP-1 antagonist exendin 9-39 at a ratio of 30:1. Administration of 300 micrograms GLP-1 i.p. also reduced temperature over the 2 h following injection but had no effect on food intake. Administration of exendin 9-39 alone by the i.c.v. route had no effect on temperature. These results indicate that GLP-1 is a neuropeptide involved in the regulation of temperature. Furthermore, the mechanisms that mediate the effect on temperature may be different from those regulating food intake given the effect on temperature but not food intake of i.p. GLP-1.

Animals↗
PubMed1996

A role for glucagon-like peptide-1 in the central regulation of feeding.

The sequence of glucagon-like peptide-1 (7-36) amide (GLP-1) is completely conserved in all mammalian species studied, implying that it plays a critical physiological role. We have shown that GLP-1 and its specific receptors are present in the hypothalamus. No physiological role for central GLP-1 has been established. We report here that intracerebroventricular (ICV) GLP-1 powerfully inhibits feeding in fasted rats. ICV injection of the specific GLP-1-receptor antagonist, exendin (9-39), blocked the inhibitory effect of GLP-1 on food intake. Exendin (9-39) alone had no influence on fast-induced feeding but more than doubled food intake in satiated rats, and augmented the feeding response to the appetite stimulant, neuropeptide Y. Induction of c-fos is a marker of neuronal activation. Following ICV GLP-1 injection, c-fos appeared exclusively in the paraventricular nucleus of the hypothalamus and central nucleus of the amygdala, and this was inhibited by prior administration of exendin (9-39). Both of these regions of the brain are of primary importance in the regulation of feeding. These findings suggest that central GLP-1 is a new physiological mediator of satiety.

Animals↗
PubMed1996

Desmopressin in the management of nocturia in patients with multiple sclerosis. A double-blind, crossover trial.

BACKGROUND: Neurogenic bladder affects up to 80% of patients with multiple sclerosis (MS) and, in 50% of these patients, it is a significant cause of disability. The current management of neurogenic bladder, based on fluid restriction, anticholinergic agents, intermittent self-catheterization, and, in some cases, surgical intervention, often fails to relieve all symptoms. Furthermore, anticholinergic drugs have significant adverse effects and may be medically contraindicated. Nocturia is a particularly disabling symptom of neurogenic bladder; by disrupting sleep patterns, it aggravates the chronic fatigue of MS, imposes serious demands on caregivers, and can lead to institutionalization. To evaluate a novel approach to the symptomatic management of nocturia in patients with MS, we have conducted a trial of desmopressin acetate (1-desamino-8-D-arginine vasopressin), a synthetic analogue of antidiuretic hormone. OBJECTIVE: To evaluate the efficacy and short-term safety of desmopressin therapy in the symptomatic treatment of nocturia in patients with MS. METHODS: Seventeen patients were enrolled in a double-blind, crossover trial of desmopressin administered at bedtime. Patients with both relapsing-remitting and chronic-progressive forms of MS were admitted. Night time voiding diaries were maintained for the 6 weeks of the trial; similarly, serum electrolyte levels and plasma osmolality were measured twice weekly and urinalyses and urine cultures were performed weekly during the trial. RESULTS: Desmopressin reduced the percentage of nights with nocturia in patients from 97% to 66%. The average number of episodes of nocturia per night in patients decreased from 2.35 to 1.09 and the maximum hours of sleep uninterrupted by nocturia increased from 3.74 to 5.77. These results were highly significant. Four of the 17 patients discontinued participation in the study after developing asymptomatic or minimally symptomatic hyponatremia. CONCLUSIONS: Desmopressin was found effective; no tolerance and only minimal adverse effects have been observed. Our results suggest that desmopressin, either alone or in combination with other therapeutic modalities, is effective in the symptomatic management of nocturia in patients with MS. The only adverse effect attributed to desmopressin was hyponatremia, which occurred in 4 of 17 patients and appeared to be dose related.

Adult↗
PubMed1996

Behavioural, autonomic and endocrine responses associated with C-fos expression in the forebrain and brainstem after intracerebroventricular infusions of endothelins.

Endothelins are a range of peptides (endothelin-1, endothelin-2, and endothelin-3) well known to act peripherally as powerful cardiovascular-regulating agents. Recently, they have been shown to be localized in CSN, where they may act as central neurotransmitters. A variety of putative roles has been ascribed to them in the CNS. To identify those regions of the brain capable of responding to these peptides, the expression of c-fos (an immediate-early gene), has been used to map patterns of activation following intracerebroventricular (i.c.v.) infusions of endothelins in Lister-hooded rats. This has been correlated with changes in heart rate, core temperature and plasma corticosterone levels. Endothelin-3 i.c.v. (50 pmol) decreased both heart rate and core temperature (both recorded by telemetry). This effect lasted for about 30-45 min. Endothelin-1 (10 pmol) or endothelin-3 (50 pmol) i.c.v. induced c-fos expression in the specific regions in the forebrain and brainstem. Strong expression was found in the septum, bed nucleus of the stria terminalis, parvicellular paraventricular nucleus, the central nucleus of the amygdala, dorsal motor nucleus of the vagus and solitary nucleus. There was less marked c-fos expression in other areas of the basal forebrain, such as the organum vasculosum of the lamina terminals, median preoptic nucleus, supraoptic nucleus and the magnocellular. There are two classes of endothelin receptor (A and B). An endothelin-A receptor antagonist, BQ-123, abolished c-fos expression in all structures in the forebrain and brainstem following endothelin-1 infusions. However, an endothelin-B agonist (TetraAla endothelin-1) did not induce discernible c-fos expression in the forebrain or brainstem. These results suggest that the endothelin-A receptor is responsible for endothelin-dependent c-fos induction in the brain. Interactions between endothelins and angiotensin II were also studied. The pattern of c-fos induced by endothelin-3 and angiotensin II was different (particularly in the anteroventral region of the third ventricle). Furthermore, prior infusions of endothelin-3 interfered with the expression of c-fos induced by subsequent angiotensin II, and also suppressed the latter's dipsogenic effect. These results show that endothelin-3 and angiotensin II interact at both behavioural and cellular levels, and that endothelins may play significant roles in the central control of fluid balance and autonomic activity.

Angiotensin II↗
PubMed1996

Adrenal secretion during major depression in 8- to 16-year-olds, I. Altered diurnal rhythms in salivary cortisol and dehydroepiandrosterone (DHEA) at presentation.

The association between basal cortisol, dehydroepiandrosterone (DHEA), its sulphate (DHEAS) and major depression was investigated in 8- to 16-year-olds. Eighty-two subjects with major depression, 25 non-depressed psychiatric cases and 40 community controls were systematically assessed for current mental state and hormone levels at 08.00, 12.00 and 20.00 h, assayed from salivary samples collected over a 48 h period. The average mean of the two time points was compared between the three groups. Evening cortisol hypersecretion and morning DHEA hyposecretion were significantly, and independently, associated with major depression. High evening cortisol (> 0.594 ng/mL) and low morning DHEA (< 0.200 ng/mL) identified subgroups of depressives with different types of adrenal hormone dysregulation. The association between high evening cortisol or low morning DHEA and MDD was not affected by either age or gender.

Adolescent↗
PubMed1996

Adrenal secretion and major depression in 8- to 16-year-olds, II. Influence of co-morbidity at presentation.

The association between high evening cortisol and low morning DHEA and the pattern of co-morbid diagnoses in 82 cases of major depressive disorder in 8- to 16-year-olds has been analysed. There was a significant association between the presence of high evening cortisol and co-morbid dysthymia. This was independent of age or sex. No positive association was found between the presence of low morning DHEA and any co-morbid diagnosis. However, co-morbid panic or phobic disorder was significantly associated with the absence of this endocrine abnormality. These findings suggest that specific endocrine disturbances may be associated with different patterns of co-morbidity during an episode of major depression in this age group.

Adolescent↗
PubMed1996

Simvastatin inhibits myointimal hyperplasia following carotid artery injury in cholesterol-fed rabbits.

The effect of simvastatin, a potent inhibitor of 3-hydroxy 3-methylglutaryl coenzyme A reductase (HMG-CoA reductase) was evaluated in an experimental model of myointimal hyperplasia in cholesterol-fed rabbits. Myointimal hyperplasia was induced by an air-drying injury of the left carotid artery followed by a 2%-cholesterol diet for 14 days. A 2-week oral treatment with simvastatin (6 mg/kg/day, p.o.) significantly lowered the circulating levels of cholesterol and triglycerides (41% and 49% inhibition respectively) as well as the low density lipoprotein (LDL)-cholesterol and high density lipoprotein (HDL)-cholesterol levels. Simvastatin also strongly affected the uptake of cholesterol in the arteries occurring as a consequence of vascular injury (44% inhibition, P < 0.001). Morphometric analysis revealed that both the intima and the media areas increased substantially 2 weeks after the lesion and showed a considerable smooth muscle cell accumulation in the neointima together with the presence of numerous foam cells. A 16-day oral treatment with simvastatin strongly reduced smooth muscle cells hyperplasia occurring in both the media and the intima following deendothelialization (19% and 60% inhibition respectively) suggesting that simvastatin may be a useful inhibitor of restenosis which occurs following vascular injury.

Animals↗
PubMed1996

Cortisol, dehydroepiandrosterone (DHEA), and DHEA sulfate in the cerebrospinal fluid of man: relation to blood levels and the effects of age.

The relation between blood and cerebrospinal fluid (CSF) concentrations of cortisol, dehydroepiandrosterone (DHEA), and its sulfate (DHEAS) was measured in 62 subjects aged 3-85 yr old, fitted with ventriculo-peritoneal or lumbar-peritoneal shunts for a variety of diagnoses. There were 36 males and 36 females. Forty-eight subjects were not taking exogenous corticosteroids; the other 14 were receiving either systemic or local steroids. A single sample of blood and CSF was taken from each subject within 10 min for measurement of cortisol, DHEA, and DHEAS. The proportional levels of cortisol (5.8%) and DHEA (5.4%) in the CSF compared with those in the blood were similar in subjects not taking steroids. However, CSF DHEAS levels were only 0.15% of those in the blood. Because DHEAS blood levels were so much greater than DHEA, DHEAS in the CSF was still higher than DHEA despite the reduced penetration of the sulfated steroid. The blood/CSF ratios were similar in subjects taking steroids. There were significant correlations in steroid-free subjects between blood and CSF levels for DHEA (r = 0.65) and DHEAS (r = 0.88) but not for cortisol (r = 0.26). Steroid treatment significantly lowered blood cortisol, DHEA and DHEAS, and CSF DHEA, but not CSF cortisol or DHEAS compared with an age- and sex-matched sample of steroid-free subjects. In steroid-free adults (18 yr and over; n = 37), blood cortisol showed no age-related change. However, CSF cortisol was markedly raised in a proportion of steroid-free subjects over the age of 60 yr. Levels of corticoid-binding globulin in plasma did not alter with age. As expected, there were significant age-related decrements in both blood DHEA and DHEAS. CSF DHEA (r = 0.42) and CSF DHEAS (r = 0.39) were significantly negatively correlated with age. In steroid-free juveniles (n = 11) there were no age-related changes in either blood or CSF cortisol, but significant increases with age in DHEA and DHEAS in both blood and CSF. Calculation of the cortisol/DHEA and cortisol/ DHEAS molar ratios in the CSF showed both to be raised in the very young (3-8 yr) and the elderly (60 yr and over) by a factor of 4-5 compared with young adults aged 18-39. There were no sex differences in any of the parameters measured. These findings show that the relation between levels in the blood and CSF differ for each of these three neuroactive steroids. The brain is exposed to relatively high levels of DHEA and DHEAS during later childhood and early adulthood but to relatively or absolutely high levels of cortisol during infancy and older age. In view of the known antiglucocorticoid action of DHEA and DHEAS, and the direct action of these steroids on membrane-bound transmitter events (such as gamma-aminobutyric acidA receptors), these changes may have important implications for age-related alterations in brain function.

Adolescent↗
PubMed1996

Antenatal assessment using the FECG obtained via abdominal electrodes.

During the past decade a variety of intrapartum fetal monitors have been constructed that process the entire fetal electrocardiogram (FECG), obtained via a scalp electrode. They therefore differ from conventional monitors in aiming to extract relevant timing and magnitude information from the morphology of the FECG rather than simply the RR interval and hence heart rate. An intrapartum monitor such as this has been successfully developed by ourselves. This paper describes the early results obtained whilst attempting to extend this form of monitoring forward into the antenatal period. In order to achieve this the FECG must be acquired via surface electrodes placed on the maternal abdomen, which yields a signal containing the FECG amidst a number of noise sources. Our investigations into the feasibility of "antenatal abdominal FECG analysis" have been on two fronts. The first has been to produce a bedside monitor similar in function to our intrapartum device, whilst the second has been to address the possibility of performing such monitoring in ambulant subjects. At present the antenatal bedside monitor has successfully extracted and processed the FECG in approximately 75% of the cases studied, with subjects ranging from 20 weeks through to term having been monitored. We also have demonstrated the feasibility of the long term monitoring of maternal and fetal heart rate using a portable instrument.

Abdomen↗
PubMed1995

Essence of stress.

Explore the source record for details and available documents.

Adaptation, Psychological↗
PubMed1995

c-fos expression in the paraventricular nucleus of the hypothalamus following intracerebroventricular infusions of neuropeptide Y.

Intracerebroventricular (i.c.v.) infusions of neuropeptide Y (NPY) (2500 pmol) induced c-fos protein in the paraventricular nucleus (PVN) of intact male rats 60 min later. The greatest expression was observed in the dorsal (parvicellular) region of the PVN; there were intermediate levels in the lateral (magnocellular) and lowest ones in the medial (parvicellular) regions. Allowing rats to eat during the post-infusion interval did not modify this pattern of c-fos expression. Depriving rats of food for either 24 or 48 h did not induce recognisable expression of c-fos in the PVN, and allowing 24 h-deprived rats to eat also had no effect on PVN c-fos. Plasma insulin was increased by i.c.v. NPY, and raised still further in rats that were allowed to eat following NPY infusions. However, plasma glucose was not altered by either treatment. Food-deprived rats had low levels of insulin, but unaltered blood glucose, compared to controls. These results show that NPY can induce c-fos expression in both parvicellular and magnocellular areas of the PVN. The pattern of expression within the PVN seems to differ from that induced by other peptides, such as angiotensin II, vasopressin and corticotropin-releasing factor, suggesting that distinct populations of neurons are activated by different peptides within the complex structure of the PVN. Food deprivation does not induce c-fos expression within the PVN, though other studies have shown that NPY levels and release are both increased, so there is no simple relation between current energy state, blood levels of either glucose or insulin and c-fos expression within the PVN.

Animals↗
PubMed1995

Function of the interleukin-2 (IL-2) receptor gamma-chain in biologic responses of X-linked severe combined immunodeficient B cells to IL-2, IL-4, IL-13, and IL-15.

The interleukin-2 (IL-2) receptor gamma-chain is a common component of several members of the cytokine receptor superfamily including those for IL-2, IL-4, IL-7, IL-9, IL-15, and possibly IL-13, and has recently been renamed the common gamma-chain (gamma c-chain). Transfection experiments have shown that the gamma c-chain participates in signal transduction by IL-2, IL-4 and IL-7, but a functional role for the gamma c-chain in biological responses by normal T cells and B cells to these cytokines has not been established. In this study, we have used X-linked severe combined immunodeficiency (X-SCID) as a naturally occurring gamma c-chain gene disruption model to examine the role of the gamma c-chain in human B-cell responses to IL-2, IL-4, IL-13, and IL-15. Our experiments show that B cells from two X-SCID patients with characterized gamma c-chain gene mutations do not respond to IL-2 or IL-15, but respond as well or better than normal B cells to both IL-4 and IL-13 in assays for B-cell activation, proliferation, and IgE secretion. This finding raises important questions about the function of the gamma c-chain in receptors for IL-4 and IL-13, and the nature of the immune defect in X-SCID.

B-Lymphocytes↗
PubMed1995

Immediate-early genes and the neural bases of photic and non-photic entrainment.

The expression of immediate-early genes (IEGs) within the mammalian suprachiasmatic nucleus (SCN) identifies individual light-responsive cells of the circadian system. Cells immunoreactive for products of IEGs form a neurochemically heterogeneous population, of which a few are VIP (vasoactive intestinal peptide)-immunoreactive or GRP (gastrin-releasing peptide)-immunoreactive, although the phenotypes of most of the others have yet to be determined. Dual-labelling experiments with anatomical tracers reveal that only a minority of efferent projection neurons of the SCN are immunoreactive for IEG products, and it is likely that the majority of the immunoreactive cells are interneurons or glia. Photic induction of IEGs is mediated via NMDA (N-methyl-D-aspartate) and non-NMDA glutamatergic receptors, the SCN expressing a topographically specific complement of subtypes of the NMDA receptor. Non-photic cues (arousal) can shift the clock but this is not associated with expression of IEGs, demonstrating that the proteins encoded by IEGs are probably involved in transducing photic cues, rather than shifting the clock per se. Their induction provides an anatomically explicit marker for circadian phase and photic sensitivity and so is useful in analyses of circadian function, for example, in the tau mutant hamster. Non-photic phase shifts are accompanied by adrenocortical activation, confirming the importance of arousal in shifting of the clock. The phase-shifting effect of arousal can be blocked by treatment with the serotonin receptor antagonist ketanserin, suggesting that ascending serotonergic input to the forebrain, possibly directly to the SCN, is an important mediator of entrainment by arousal.

Animals↗
PubMed1995

Alterations in sensitivity to intracerebral vasopressin and the effects of a V1a receptor antagonist on cellular, autonomic and endocrine responses to repeated stress.

We have shown previously that repeated restraint stress results in differential adaptation at both macrophysiological and cellular levels. Chronic stress accentuates vasopressinergic control of adrenocorticotropic hormone secretion in the pituitary. The present work determined whether endogenous vasopressin plays a role in response to repeated restraint. The first experiment explored changes in the response of repeatedly stressed animals to intracerebral vasopressin infusions. The second determined the effect of pretreating rats with a vasopressin V1a receptor antagonist on the way that they adapted to repeated restraint. Experiment 1: rats were subjected either to daily 60-min restraint for 10 days or transferred to the testing room where restraint sessions took place (controls). On the 11th day, they were infused with either artificial cerebrospinal fluid or 250 pmol vasopressin. The behavioural response to vasopressin was unaltered by previous stress. Plasma corticosterone was lowered in vasopressin-treated rats only after previous stress. Sixty minutes after vasopressin infusion, the central amygdala, locus coeruleus, the nucleus of the solitary tract and the dorsal vagal nucleus expressed increased levels of c-fos, and there were significant two-way interactions between stress and infusion for dorsal paraventricular nucleus, locus coeruleus and dorsal vagal nucleus. One-way analysis suggested that previous stress also reduced the c-fos response to vasopressin in the nucleus of the solitary tract. These results show that previous stress causes differential alterations in behavioural, endocrine and cellular responses to vasopressin. Experiment 2: rats were implanted with a transmitter which monitored heart rate and core temperature and a lateral cerebroventricular cannula. For 10 days, either artificial cerebrospinal fluid or 2500 pmol V1a antagonist, [d(CH2)1(5)-O-Me-Tyr2-Arg8]-vasopressin were infused i.c.v. 10 min prior to a 60-min restraint session. On the 11th day, no infusions were carried out, but rats received the usual period of restraint. The vasopressin antagonist was followed by motor responses (freezing, grooming and burrowing), more evident during the third and fifth days of stress. Core temperature responses were altered by the antagonist: stress-induced hypothermia was greatly reduced. Reduced baseline core temperatures, observed in controls as successive stress proceeded, were absent in antagonist-treated rats. By contrast, there were no significant effects of vasopressin antagonism on stress-induced tachycardia, nor in the way that this adapted to repeated restraint. On the 11th day (no i.c.v. infusions), hypothermic responses were no different in rats previously receiving either antagonist or control vehicle, but secondary hyperthermia was greater in the first group. Corticosterone levels were not altered by previous i.c.v. infusions.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed1995

Regional changes in c-fos expression in the basal forebrain and brainstem during adaptation to repeated stress: correlations with cardiovascular, hypothermic and endocrine responses.

Acute stress is known to evoke a discrete pattern of c-fos expression in the brain. The work reported here shows that this pattern is modified in regionally specific ways following repeated stress, and that this can be correlated with changes in telemetered heart rate, core temperature and corticosterone output that occur during adaptation. Intact male rats were restrained for 60 min daily for one or 10 days. Stress-induced tachycardia was maximal 10 min following the onset of restraint, and decreased thereafter. The peak value was not altered by repeated restraint, but levels fell towards baseline values more rapidly with increasing bouts of stress. Core temperature showed marked reduction during the first 10 min of the initial stress, followed by a minor (and not very consistent) overshoot during the remainder of the stress period. In contrast to heart rate, stress-induced hypothermia did not alter during repeated restraint. Corticosterone was raised dramatically immediately following the first 60-min session of restraint, and this was attenuated by repeated stress. Sixty minutes after the end of the first stress session, there was pronounced c-fos expression in the lateral septum, lateral preoptic area, lateral hypothalamic area, all divisions of the hypothalamic paraventricular nucleus, the medial (but not central) amygdala, the locus ceruleus and a brainstem structure (thought to be Barrington's nucleus), compared to rats transferred to the testing room but not restrained. Sixty minutes after the 10th stress session, c-fos expression was markedly decreased in some of these areas compared with the pattern observed after the first stress, especially in the paraventricular nucleus (dorsal and medial parvicellular regions) and in medial amygdala. However, all other areas measured demonstrated a sustained response even after repeated stress. There were no significant differences in c-fos expression in rats repeatedly transferred to the testing room (but not stressed) compared to singly transferred counterparts. These results show that both neuronal and physiological responses adapt to a repeated stress, but that in both cases this has highly specific components. It seems likely that adaptive changes in c-fos expression are associated with those in some features of autonomic and endocrine reactions. It is noteworthy that there is evidence that the lateral septum, in which c-fos expression did not diminish after repeated stress, may be involved in temperature control, whereas the paraventricular nucleus, in which c-fos did alter, has been linked with both cardiac and corticoid regulation.

Adaptation, Physiological↗