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Biomedical subjects

J L Meyerhoff

Publications and source records attributed to J L Meyerhoff.

At least 37 records · Page 2Linked to original sources
PubMed1995

Stressors, including social conflict, decrease plasma prolactin in male golden hamsters.

Following exposure to a stressor, plasma prolactin (PRL) rises in most species. The purpose of the present study was to examine the effect of social conflict or of footshock stress on PRL responsiveness in male Syrian hamsters. Contrary to expectations, PRL was significantly lower in subordinate hamsters than in their dominant opponents or in controls following one, five, or nine exposures to social conflict. Similarly, PRL was reduced in hamsters subjected to a mild footshock stressor. By contrast, adrenocorticotropin, another stress-responsive hormone, was elevated following exposure to each of these stressors. We also demonstrate that PRL release is inhibited by dopamine as it is in other species by showing that there is a dose-dependent increase in PRL release following treatment with the dopamine receptor blocker, domperidone.

Adrenocorticotropic Hormone↗
PubMed1995

Treadmill exercise training and estradiol differentially modulate hypothalamic-pituitary-adrenal cortical responses to acute running and immobilization.

It is generally believed that physical fitness promotes health by attenuating responsiveness to other stressors. The experimental evidence for this belief is limited and does not extend to interactions between the hypothalamic-pituitary-adrenal cortical (HPA) and hypothalamic-pituitary-gonadal (HPG) axes. We tested the hypothesis that treadmill exercise training would lead to an estrogen-dependent hyporesponsiveness of the HPA axis that would generalize to immobilization stress. Ovariectomized female Sprague-Dawley rats (N = 74) that had been treadmill trained (TT) or sedentary for 6 weeks received intramuscular injections of estradiol benzoate (Eb) or sesame oil on each of 3 days prior to 15 min of acute treadmill running or immobilization. Plasma (adrenocorticotrophin) (ACTH), (corticosterone) (B) and (prolactin) (PRL) were determined from trunk blood by radioimmunoassay and compared in a 2 group (TT vs. sedentary)-by-2 treatment (Eb vs. oil)-by-2 acute stressor (running vs. immobilization) design. Home-cage (HC) animals (N = 24) provided baseline hormone levels. ACTH and B levels were elevated after stressors in animals treated with either Eb or oil compared to HC, but increases in PRL after stressors were dependent on Eb. Treadmill exercise training led to an attenuation of ACTH and prolactin to running, but the attenuation did not generalize to immobilization. In contrast, treadmill exercise training led to a hyperresponsiveness of ACTH. Treadmill training did not modulate prolactin responses to immobilization. The modulating effects of the estradiol treatment are consistent with an interaction of the HPA and HPG axes in response to stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1995

Activity-wheel running attenuates suppression of natural killer cell activity after footshock.

We studied whether voluntary running in an activity wheel moderates splenic natural killer (NK) cell cytotoxicity after footshock. Young (50-day) male Fischer 344 rats were randomly assigned to 1) sedentary (n = 16) or 2) activity-wheel (n = 16) groups that each received controllable or uncontrollable footshock on 2 consecutive days or 3) a sedentary home-cage control group (n = 8). Spleens and trunk blood were collected 30 min after the second footshock session. Cytotoxicity was determined by a standard 4-h 51Cr release assay. Percentages of OX6+ (B), OX8+ [T suppressor/cytotoxic (Ts/c)], W3/25+ (T helper), Thy-1.1 (Pan T cell marker), and 5C6+ (NK) cells were determined by flow cytometry. Plasma adrenocorticotropic hormone, corticosterone, and prolactin concentrations were measured by radioimmunoassay as modulators of NK activity. Percentage of specific lysis after footshock was approximately 52% of control values for sedentary animals compared with approximately 96% of control values for activity-wheel animals. The groups did not differ in percentages of NK or Ts/c cells. We conclude that voluntary activity-wheel running protects against the suppression of splenic NK activity induced by footshock. This protective effect of wheel running is not explained by an elevation in baseline NK activity; increased percentages of splenic NK or Ts/c cells; or plasma levels of adrenocorticotropic hormone, corticosterone, and prolactin.

Adrenocorticotropic Hormone↗
PubMed1994

N-acetyl-aspartyl-glutamate (NAAG) elicits rapid increase in intraneuronal Ca2+ in vitro.

N-acetyl-aspartylglutamate (NAAG) is an acidic dipeptide found at high concentrations almost exclusively in the brain and spinal cord. There is evidence that NAAG is an excitatory neurotransmitter/neuromodulator. On the other hand, the identification and characterization of an enzyme in the nervous system which hydrolyzes NAAG to liberate glutamic acid (Glu) has led to an alternative hypothesis that the dipeptide might serve as a precursor of the excitatory amino acid. Using an interactive laser cytometer to quantitate changes in intraneuronal Ca2+ in individual neurons, we demonstrate that NAAG, at the concentrations at which it is found in the brain, promotes a rapid increase in intraneuronal Ca2+. NAAG-induced effects are completely dependent on the presence of Ca2+ in the bathing medium and are inhibited by NMDA receptor and channel antagonists. Several factors have led us to conclude that it is NAAG itself, and not NAAG-derived Glu, which is responsible for the observed effects in this system.

Amino Acid Sequence↗
PubMed1994

Flight-elicited attack and priming of aggression in nonaggressive hamsters.

We report a technique for inducing attack in apparently nonaggressive hamsters that takes advantage of several behavioral effects: (a) the vigorous flight that repeatedly defeated hamsters display in the presence of conspecifics, (b) the potent, attack-eliciting properties of such flight, and (c) attack priming (i.e., aggressive arousal from exposure to an initial stimulus animal carries over to exposure to a second one). Resident hamsters that had consistently failed to attack nonfleeing intruders were found to readily attack intruders that did flee. But repeated exposure to the fleeing intruders alone did not induce long-term changes in aggressiveness. However, flight-elicited attack did successfully prime attack onto nonfleeing intruders presented immediately after the fleeing intruder was removed. Repeating such priming transfer trials induced long-term changes in the formerly nonaggressive subjects. We conclude that this is an effective procedure for inducing aggression that would be preferred when it is important to avoid exposing subjects to aversive stimuli. The changes in behavior that we observed seem to reflect heightened motivational levels.

Aggression↗
PubMed1992

Genetically epilepsy-prone rats have increased brain regional activity of an enzyme which liberates glutamate from N-acetyl-aspartyl-glutamate.

N-Acetylated-alpha-linked acidic dipeptidase (NAALADase) is a membrane-bound peptidase which hydrolyzes the endogenous neuropeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and the excitatory amino acid, glutamate (Glu). Although there is evidence that NAAG might be a neurotransmitter, this dipeptide could also function as a precursor form of Glu, which is liberated by the dipeptidase. We found that the activity of this NAAG hydrolyzing enzyme in genetically epilepsy-prone rats was 11-26% greater than control in brain regions, including the amygdala, hippocampus and cerebellum, as well as the pyriform, entorhinal and frontal cortices. This is consistent with possible increased availability of Glu in certain CNS synapses in these rats, which are reported to have increased susceptibility to audiogenically, electrically and chemically induced convulsions.

Animals↗
PubMed1992

Hormonal responses to fighting in hamsters: separation of physical and psychological causes.

Male Syrian hamsters were paired and allowed to interact with a conspecific for 15 min a day for 4 days. On the fifth day, the animals were again paired, but they were kept physically separated by a mesh partition that allowed visual, olfactory, and auditory contact between the animals. Controls were placed with conspecifics on each of the 5 testing days, but the partition between them was never removed. Hamsters that were submissive on days 1-4 exhibited elevated plasma adrenocorticotropin-like immunoreactivity (ACTH-LI), beta-endorphin-like immunoreactivity (B-EP-LI), and cortisol on day 5 even though no fighting occurred on that day. Dominant hamsters did not differ from controls. These data support the hypothesis that there is an important psychological component to the pituitary-adrenocortical response in defeated hamsters.

Adrenocorticotropic Hormone↗
PubMed1991

Norepinephrine-stimulated phosphatidylinositol metabolism in genetically epilepsy-prone and kindled rats.

Genetically epilepsy-prone rats (GEPR-9) and kindled rats have reduced noradrenergic function. In the present study, norepinephrine-stimulated accumulation of inositol phosphates was reduced in cerebral cortex of GEPR-9 and kindled rats when compared to control and non-kindled rats, respectively. No such reduction was found in amygdala/pyriform cortex and hippocampus. These results support the hypothesis that cortical noradrenergic and associated second messenger systems are impaired in epilepsy.

Animals↗
PubMed1991

Acute and repeated exposure to social conflict in male golden hamsters: increases in plasma POMC-peptides and cortisol and decreases in plasma testosterone.

The purpose of the present study was to characterize the hormonal response of dominant and submissive male hamsters to acute and repeated exposure to social conflict. We found that submissive, but not dominant, males exhibited elevated plasma levels of adrenocorticotropin (ACTH), cortisol, and beta-endorphin (beta-EP) following one exposure to an agonistic encounter. After five exposures to a dominant opponent, submissive males showed smaller, but still significant, elevations in these plasma hormones. After nine exposures, submissive hamsters showed significant elevations only in plasma ACTH and beta-EP. Plasma testosterone was significantly suppressed in submissive males that fought nine times. We conclude that hamsters are a useful species with which to study the neuroendocrine correlates of social behavior.

Adrenocorticotropic Hormone↗
PubMed1991

Plasma cyclic AMP increases in hamsters following exposure to a graded footshock stressor.

To assess the utility of plasma cyclic AMP (cAMP) as a sensitive physiological index of an animal's arousal level, we exposed male hamsters to various intensities (0.0-2.0 mA) of a footshock stressor. The plasma cAMP response was directly related to stimulus intensity. Ratings of behavioral arousal were positively correlated with plasma cAMP values. We conclude that plasma cAMP may be a useful index of arousal.

Animals↗
PubMed1990

Elevated TRH levels in pyriform cortex after partial and fully generalized kindled seizures.

In a previous study we reported significant elevations of TRH in neocortex, hippocampus and combined amygdala/pyriform cortex in rats 48 h after the last of a series of stage 5 kindled seizures. In the present study, to determine whether the increases in TRH were proportional to the intensity of the convulsions, and the degree of development of the kindling process, we compared the effects of partially kindled (stage 2) vs fully kindled (stage 5) seizures. As a further refinement, we examined separately the TRH responses in the pyriform, cingulate and frontal cortices. The responses were especially marked in the pyriform cortex, where TRH increased 7-fold after stage 5 kindled convulsions, compared with 2-fold increases after stage 2-3 seizures. Increases were seen in other cortical regions, as well, but only after stage 5 seizures. These findings are consistent with reports suggesting that the increases in brain TRH occurring after convulsions are aftereffects of the seizures, possibly representing homeostatic anticonvulsant responses, and that the pyriform cortex is a site that is uniquely activated by convulsions.

Animals↗
PubMed1990

Neuroendocrine responses to emotional stress: possible interactions between circulating factors and anterior pituitary hormone release.

We have shown that a psychological stressor can elicit increases in plasma AVP levels in normal human subjects. Since AVP can enhance the release of ACTH, and the pituitary gland is outside the blood-brain barrier, AVP present in the general circulation might extend the time course of stress-induced, CRF-mediated release of ACTH from the anterior lobe. Since PRA is involved in the synthesis of angiotensin I, the precursor of AII, and AII is known to enhance CRF-mediated release of ACTH from pituitary cells and to stimulate release of AVP, it is possible that the increase in PRA also contributed to the release of AVP and ACTH in this study. Reports differ as to whether circulating catecholamines can release ACTH in vivo by direct action on the pituitary. Finally, it has been reported that beta-EP enhances the release of PRL, and inhibits release of AVP. Since the increase in beta-EP in the present study was quite robust, it might have extended the PRL release, and truncated the AVP response.

Adrenocorticotropic Hormone↗
PubMed1990

The influence of fitness on neuroendocrine responses to exhaustive treadmill exercise.

Neuroendocrine and sympathoadrenal responses to exhaustive graded treadmill exercise were examined in 17 male subjects of varying degrees of fitness. The mean duration of exercise to exhaustion was 15.2 +/- 0.7 (+/- SE) min. Exercise duration was inversely correlated with baseline heart rate (P less than 0.05). Compared to standing baseline values, mean plasma norepinephrine and epinephrine levels increased 339% and 301%, respectively, in an integrated 2-min blood sample collected immediately after completion of exercise. Mean adrenocorticotrophic hormone (ACTH), beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and prolactin levels increased 282%, 720%, 372%, and 211%, respectively, in an integrated 4-min blood sample beginning 2 min after completion of exercise. Cortisol levels increased 183% in the sample collected 17-21 min after exercise. The magnitude of these neuroendocrine responses to exercise was similar among individuals at the same relative intensity of exhaustive exercise, regardless of the duration of exercise. The exercise-induced increases of the pro-opiomelanocortin (POMC)-derived peptides, ACTH, beta-EP, and beta-LPH, were highly correlated with each other (P values less than 0.001), and were correlated with prolactin increases, (P values less than 0.05). During a 20-min recovery period after exercise, changes in heart rate, ACTH, and beta-LPH levels were correlated with duration of exercise, (P less than 0.01, P less than 0.03, and P less than 0.03, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1990

Effects of social conflict on POMC-derived peptides and glucocorticoids in male golden hamsters.

The effects of fighting and footshock on circulating adrenocorticotropin-like immunoreactivity (ACTH-LI), cortisol, corticosterone, beta-endorphin-like immunoreactivity (beta-EP-LI), and beta-lipotropin-like immunoreactivity (beta-LPH-LI) were examined. In the first experiment, catheterized males were paired with large, ovariectomized females for 15 min. Submissive males exhibited significant increases in plasma ACTH-LI, cortisol, corticosterone, and beta-EP-LI. In the second experiment, two males were paired to determine whether the hormonal response in submissive animals was different from that in dominant hamsters. The pattern and magnitude of the hormonal response was also compared to that following a commonly used stressor-footshock. Footshock was associated with large increases in each of the plasma hormones measured. Submission, but not dominance, was associated with smaller, but still significant, increases in ACTH-LI, cortisol, beta-EP-LI and beta-LPH-LI. The data indicate that fighting is not a generalized stressor. "Losing," in particular, appears to be an example of a biologically relevant stressor.

Adrenocorticotropic Hormone↗
PubMed1990

Hyperresponsiveness of the rat neuroendocrine system due to repeated exposure to stress.

Sequential exposure to stressors may elicit a period of endocrine hyperresponsiveness during which plasma hormone concentrations reach higher levels after repeated exposure to a stressor compared to levels after initial exposure. The present study was designed to further characterize hyperresponsiveness to repeated stress and determine if hyperresponsiveness is dependent upon repeated exposure to the same stressful stimuli. In Experiment 1, rats were stressed by inescapable tailshock, immobilization or exposure to shock chamber without shock for one, two, three, four or five consecutive days (15 min/day). In rats exposed to tailshock, corticosterone (CS) levels in plasma collected on days 2, 3, 4 and 5 were higher than CS levels following acute tailshock on day 1, demonstrating hyperresponsiveness to repeated tailshock. Hyperresponsiveness of CS secretion also occurred in groups of rats restrained for four or five days. No changes occurred in the CS response of animals repeatedly exposed to immobilization. Prolactin (PRL) levels were not affected by repeated exposure to the stressors. However, PRL values were different between the stress conditions and indicated that the order of stressor severity was tailshock greater than immobilization greater than exposure to shock chamber without shock. In Experiment 2, rats were exposed to either one or two consecutive days of tailshock or immobilization. Other rats were exposed to either tailshock or immobilization on the first day, then switched to the other stressor on the next day. Hyperresponsiveness to repeated tailshock, but not immobilization, was reflected in plasma levels of CS and adrenocorticotropic hormone (ACTH), but not PRL. Hyperresponsiveness of CS and ACTH secretion also was found in rats first stressed by immobilization then switched to tailshock, demonstrating that hyperresponsiveness is not dependent upon reexposure to familiar stressful stimuli. However, hyperresponsiveness did not occur in rats first exposed to tailshock then switched to immobilization. The data suggest that both immobilization and tailshock primed the organism to hyperrespond, but only the more severe stressor (tailshock) elicited hyperresponsiveness of the neuroendocrine system.

Adrenocorticotropic Hormone↗
PubMed1989

Seizures decrease regional enzymatic hydrolysis of N-acetyl-aspartylglutamate in rat brain.

Previous results have shown that kindled seizures increase N-acetyl-aspartylglutamate (NAAG) levels in the entorhinal cortex, while non-kindled convulsions have no effect. To further explore possible relationships between epilepsy and the physiology of NAAG, the effect of amygdaloid kindling on the activity of a NAAG-hydrolyzing enzyme was examined in specific brain regions associated with limbic seizures. NAAG is hydrolyzed into glutamate (Glu) and N-acetyl-aspartate (NAA) by N-acetylated-alpha-linked acidic dipeptidase (NAALADase), a membrane-bound peptidase. We found that convulsions decreased NAALADase activity and these effects were generalized to several brain regions. While small decreases in the hippocampus were specific to kindling, the decreases in other limbic regions were larger, non-specific, and appear to be aftereffects of convulsions; i.e. not specific to kindling. Although there is evidence that NAAG may be an excitatory neurotransmitter, it could also function as a storage form of Glu. Thus, a reduction in NAALADase activity could reduce the availability of Glu at certain synapses, which might be a homeostatic mechanism for lessening susceptibility to further seizures.

Animals↗