PubMed Health⌕ Search

Biomedical subjects

J L Meyerhoff

Publications and source records attributed to J L Meyerhoff.

At least 55 records · Page 3Linked to original sources
PubMed1989

Dexamethasone suppresses ACTH release without attenuating pituitary cyclic AMP response to stress in vivo.

Dexamethasone, a synthetic glucocorticoid, has been shown to decrease basal and stress-elevated levels of the pituitary hormone ACTH. Glucocorticoids are known to bind to multiple sites within the brain and pituitary and it is not known which site(s) is most important in mediating the observed inhibition of ACTH release. At the level of the corticotroph, there is contradictory data from in vitro studies regarding whether dexamethasone acts proximal or distal to the formation of the cyclic AMP second messenger that has been shown to be involved in CRF-stimulated ACTH release. In the present report, we have examined the effects of dexamethasone pretreatment on stress-induced elevations in pituitary cyclic AMP and the release of ACTH in vivo. Acute stress (15 min of intermittent footshock) elevated levels of pituitary cyclic AMP and plasma ACTH consistent with previous studies. Dexamethasone administration (0.4 mg/kg 24 hr prior to sacrifice plus 0.2 mg/kg 2 hr prior to sacrifice) inhibited stress-induced elevations in plasma ACTH but did not affect pituitary cyclic AMP response to acute stress. These findings suggest that dexamethasone inhibits the release of ACTH via an action distal to the generation of cyclic AMP.

Adrenocorticotropic Hormone↗
PubMed1989

ACTH, prolactin, corticosterone and pituitary cyclic AMP responses to repeated stress.

The present experiment was conducted to determine whether the plasma hormonal and pituitary cyclic AMP responses observed following a single exposure to an acute stressor would diminish following reexposures to the same stressor. Fifteen-min stress exposures (forced running) were separated by 45-min recovery periods. Separate groups of control and stressed animals were sacrificed before and after each of four 15-min stress periods and after each recovery period. The first exposure to 15 min of forced running raised plasma ACTH, corticosterone and pituitary cyclic AMP levels approximately 6-fold and more than tripled levels of plasma prolactin. Plasma ACTH and pituitary cyclic AMP responses to the second, third and fourth stress exposures were very similar to the responses to the first stress exposure, and levels of these substances returned to prestress levels during each 45-min recovery period. Plasma prolactin responses to the four stress sessions were somewhat variable but no significant trend among the responses was seen. Plasma prolactin levels also returned to prestress levels between stress exposures. Corticosterone levels were similar following each of the four stress sessions but levels remained elevated compared to prestress levels between stress exposures. These data suggest that pituitary responses to acute stress are rapid, that return to prestress levels is also rapid, with the exception of corticosterone, and that repeated responses of the same magnitude may be evoked when stressors are separated by short recovery periods.

Adrenocorticotropic Hormone↗
PubMed1988

Psychological stress increases pituitary cyclic AMP.

Exposure to physical stressors has been shown to produce increases in pituitary cyclic AMP in laboratory rats. In this experiment, the generality of these findings has been extended to include a psychological stressor, defined as returning the animals to a situation in which they had been exposed to footshock for four days. Rats in the psychological stress group exhibited increases in pituitary cyclic AMP and in plasma corticosterone and prolactin which were similar to those seen in animals that received the physical stressor on the test day. At present it is not known whether the effects are due to associative conditioning or to sensitization of the neuroendocrine system following repeated presentations of the physical stressor.

Animals↗
PubMed1987

Atropine sulfate increases pituitary responses to stress.

The effects of atropine sulfate pretreatment on pituitary indices of stress response were examined. Pituitary cyclic AMP and plasma prolactin increases following 15 min of acute stress were used as measures of stress response. Over a range of doses (0, 5, 10, 30 and 60 mg/kg), pretreatment with atropine sulfate increased the measured stress responses to footshock but had little or no effect on resting or non-stressed levels of the substances measured. The effects of atropine on response to immobilization were tested only at 5 mg/kg. At this dose, atropine sulfate, but not methylatropine nitrate, increased pituitary cyclic AMP response to immobilization stress demonstrating that the potentiation of the pituitary cyclic AMP stress response was not limited to footshock stress and suggesting that this effect of atropine was central rather than peripheral. Neither atropine nor methylatropine pretreatment at this dose potentiated prolactin response to immobilization stress.

Animals↗
PubMed1987

The prolonged increase in thyrotropin-releasing hormone in rat limbic forebrain regions following electroconvulsive shock.

We have previously demonstrated substantial increases in thyrotropin-releasing hormone (TRH) in specific regions of rat forebrain two days after single or repeated alternate-day electroconvulsive shock (ECS). To determine longer term effects of ECS-induced seizures on forebrain TRH content, we extended the time of the post-ECS observations to 6 and 12 days following 1 (ECS x 1) or 3 (ECS x 3) alternate-day ECS. Previous observations at 2 days post-ECS were confirmed except that hippocampal content of TRH was higher after ECS x 1. In pyriform cortex TRH remained elevated for 6 days after ECS x 1 and 3, and for 12 days after ECS x 3. In hippocampus TRH was elevated for 6 days after ECS x 1 and tended to remain elevated beyond 2 days after ECS x 3. In anterior cortex the increase persisted 6 days after ECS x 1 and 12 days after ECS x 3. These data show that convulsive seizures can induce sustained elevations of TRH beyond 48 h. This finding may be especially important in pyriform cortex and hippocampus where TRH may function as an endogenous anti-epileptic. Our data are also consistent with a possible role for TRH in affective regulation in the hippocampus, amygdala, pyriform and other cortical regions. Moreover, the present results further advance the analogy of the time-course of the TRH changes in rat to the course of the antidepressant response to electroconvulsive treatment in humans.

Animals↗
PubMed1987

Paraventricular lesions abolish the stress-induced rise in pituitary cyclic adenosine monophosphate and attenuate the increases in plasma levels of proopiomelanocortin-derived peptides and prolactin.

Acute exposure to footshock stress increased the pituitary level of cyclic adenosine monophosphate (AMP) in vivo and sharply increased plasma levels of adrenocorticotropic hormone, beta-endorphin and beta-lipotrophic hormone, as well as prolactin. Seven days after bilateral lesions of the paraventricular nucleus of the hypothalamus, the pituitary cyclic AMP response to stress was totally eliminated and the increases in plasma levels of these pituitary hormones were blunted. We conclude that while the pituitary hormonal responses to stress might be mediated by several neurohumoral factors, the stress-induced increases in pituitary levels of cyclic AMP in vivo are mediated largely via corticotropin-releasing factor, released from neurons which project from the paraventricular nucleus to the median eminence.

Adrenocorticotropic Hormone↗
PubMed1987

Repeated electroconvulsive shock: effect on sodium dependency and regional distribution of opioid-binding sites.

The effects of single and repeated electroconvulsive shock (ECS) on the binding of [3H]diprenorphine to rat brain membranes was studied. Repeated but not single ECS significantly increased the Bmax of [3H]diprenorphine binding when measured in the absence but not in the presence of NaCl. On a regional basis the effect of ECS was greatest in the olfactory bulb, nucleus accumbens, and striatum. More modest increases were found in the hippocampus, amygdala, septum, hypothalamus, and pyriform cortex. No significant effect was found in the brainstem and frontal cortex. Although the regional rank order of receptor increase does not match the receptor distribution of brain enkephalins, the receptor increase does parallel the regional increases in brain enkephalins following ECS.

Animals↗
PubMed1986

Pituitary cyclic AMP and plasma hormone responses to epinephrine administration in vivo.

The present study was conducted to characterize the in vivo effects of epinephrine administration on levels of pituitary cyclic AMP and plasma hormones. Rats were injected with saline or epinephrine bitartrate (1 mg/kg lP) and sacrificed by decapitation 1, 5, 15, 30 or 60 min post-injection. Levels of pituitary cyclic AMP and plasma ACTH, beta-endorphin, beta-LPH, corticosterone and prolactin were determined by radioimmunoassays. The injection procedure itself was somewhat stressful as demonstrated by increased levels of plasma prolactin and ACTH 5 min following either saline or epinephrine injection. This "stress" response was rapid and short-lasting for the pituitary hormones. The response of the adrenal hormone, corticosterone, to saline injection was slower in onset and longer in duration. Pituitary cyclic AMP levels did not increase following saline injection. Epinephrine-injected animals displayed markedly elevated plasma levels of ACTH, beta-endorphin and beta-LPH at 15, 30 and 60 min as compared to control or saline-injected rats. In addition, levels of pituitary cyclic AMP were increased over 10 fold at these times. Levels of plasma prolactin, a stress-responsive hormone, were not significantly increased in epinephrine-injected animals as compared to saline-injected rats indicating that these later responses seem to be specific to epinephrine rather than to stress.

Adrenocorticotropic Hormone↗
PubMed1986

Electroconvulsive shock activates endogenous opioid systems: behavioral and biochemical correlates.

From the evidence reviewed above, there is little doubt that ECS activates endogenous opioids and modifies their receptors. Thus, this form of SIA is accompanied by many other corollaries of opioid-like actions, including catalepsy, similar EEG patterns, common autonomic effects, and increases in opioid receptor binding sites. Investigations have further indicated that the amnestic effects of ECS can also be attenuated by naloxone, and that pituitary-derived opioids may play an important role as a predominant source of opioids that contribute to these opioid-like effects following ECS. It is hoped that these many attempts to correlate SIA with other behavioral and physiological endpoints following ECS will provide a more global perspective on the role of endogenous opioid systems in ECS. From these results, it is suggested that other forms of SIA may also share many of these properties in common with ECS-induced SIA. Nonetheless, ECS and other forms of SIA, such as cold water exposure and restraint, share with ECS a common history of clinical use in the treatment of human depression. It is possible that the common thread linking these experimental observations to endogenous opioid systems may provide new insights into the cause and treatment of mental disorders as well as the perception of pain.

Analgesia↗
PubMed1986

Diurnal variation in neuroendocrine response to stress in rats: plasma ACTH, beta-endorphin, beta-LPH, corticosterone, prolactin and pituitary cyclic AMP responses.

The effects of restraint stress applied at different times of the day on levels of five stress-responsive plasma hormones (ACTH, beta-endorphin, beta-LPH, corticosterone and prolactin) and pituitary cyclic AMP levels were assessed. Different groups of rats were subjected to 15 min of restraint stress at 2-hour intervals over a 24-hour period. Rats were sacrificed immediately upon removal from their home cage (controls) or immediately following restraint (stressed). The time of day of stress exposure markedly affected the stress responses measured. Generally, responses to stress applied at the beginning of the dark cycle (18:00) were less than those seen following stress applied at the beginning of the light cycle (06:00). Stress at 06:00 increased levels of pituitary cyclic AMP 10-fold, while stress applied at 18:00 did not significantly increase pituitary cyclic AMP levels. In stressed rats, high correlations were seen among levels of hormones derived from the common precursor, proopiomelanocortin (ACTH, beta-endorphin, beta-LPH) and between these hormones and levels of pituitary cyclic AMP. These findings support the hypothesis that pituitary cyclic AMP is involved in the stress-induced release or synthesis of the pituitary hormones ACTH, beta-endorphin, and beta-LPH.

Adrenocorticotropic Hormone↗
PubMed1985

Regional brain levels of N-acetyl-aspartyl-glutamate: the effect of kindled seizures.

Rats were subjected to daily amygdaloid-kindling stimulation and sacrificed 48 h after their fifth stage-5 kindled seizure. Regional brain dissection was performed and the regions assayed for levels of N-acetyl-aspartyl-glutamate, an endogenous dipeptide specific to the brain and a putative excitatory neurotransmitter. Kindling produced significant increases in this dipeptide in the entorhinal cortex.

Amygdala↗
PubMed1985

Subsensitive pituitary cyclic AMP response to stress following adrenalectomy is not caused by loss of adrenal epinephrine.

We have previously reported that various stressors acutely elevate levels of pituitary cyclic AMP in vivo and that this stress response is not seen in animals tested 7 or 30 days post-adrenalectomy. In this report we present data that demonstrate that the loss of the pituitary cyclic AMP stress response following adrenalectomy is not the result of the loss of stress-induced adrenal epinephrine release. These data show that (1) although administration of epinephrine to intact rats does not elevate levels of pituitary cyclic AMP, administration of epinephrine to adrenalectomized animals does not elevate pituitary cyclic AMP levels in vivo; (2) splanchnic denervation prevents stress-induced adrenal epinephrine release but does not abolish stress-induced increases in pituitary cyclic AMP; and (3) the time course of the developing subsensitive pituitary cyclic AMP response to stress following adrenalectomy is much slower (2 to 3 days) than the loss of circulating epinephrine.

Adrenalectomy↗
PubMed1985

Effects of subconvulsive and repeated electroconvulsive shock on thyrotropin-releasing hormone in rat brain.

Male Sprague-Dawley rats were given a single electroconvulsive shock (ECS) on alternate days and sacrificed 48 hrs after 1, 3, or 5 seizures. The content of TRH in hippocampus, pyriform cortex and amygdala was increased 2.5-fold, 5.4-fold and 4.3-fold respectively, 48 hrs. after 3 alternate-day electroconvulsive shocks (ECS) and remained unchanged after 2 additional shocks. Pyriform cortex exhibited a significant intermediate increase (1.7-fold) after only 1 ECS. In a second study, rats were sacrificed 48 hrs after a series of 5 alternate-day ECS vs. subconvulsive shocks (SCS). SCS had no significant effect in these same regions, but was seen to alter TRH in striatum. These results provide an interesting parallel to several aspects of clinical electroconvulsive treatment (ECT) of depression. Together with other findings, these data suggest also, that endogenous TRH may play a role in the modulation of convulsive seizures.

Animals↗
PubMed1985

Habituation to repeated stress is stressor specific.

Rats were exposed to 15 min of restraint or footshock or forced running in an activity wheel once a day for 10 days. Control groups were handled only. On the 11th day, rats from each stressor group and controls were exposed to 15 min of one stressor in a crossed design such that all combinations of one chronic stressor and one acute stressor were performed. Rats were sacrificed immediately following removal from their home cage or after 15 min stressor exposure on the 11th day and plasma corticosterone and prolactin and pituitary cyclic AMP levels were determined. There were no measured differences in these stress indices among groups of rats sacrificed immediately upon removal from their home cage on day 11 regardless of previous history on days 1 through 10. Plasma corticosterone and plasma prolactin and pituitary cyclic AMP levels were elevated in all rats exposed to any of the three stressors immediately prior to sacrifice as compared to all rats not exposed to stress immediately before sacrifice. However, plasma prolactin and pituitary cyclic AMP responses to each of the 3 stressors were attenuated in rats which had previous exposure to that specific stressor as compared to rats which had previous experience with a different or no stressor. We conclude that habituation results from behavioral experience with a particular stressor rather than biochemical adaptation resulting from repeated challenge to hormonal and neurochemical systems responsive to stress.

Animals↗