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Biomedical subjects

A J Schlosberg

Publications and source records attributed to A J Schlosberg.

12 recordsLinked to original sources
PubMed1984

Acute and chronic effects of caffeine on brain monoamine levels and endocrine function in the rat.

Caffeine was given to rats either acutely (1 injection) or chronically (28 daily injections). Both treatments increased brain levels of tryptophan (Trp), serotonin (5-HT) and 5-hydroxyindoleacetic acid in a dose-related fashion, but the apparent stimulatory actions of acute caffeine on the rates of 5-HT synthesis and turnover appeared to have been reduced by repeated exposure to the drug. Acute caffeine increased the blood levels of nonesterified fatty acids (NEFA), glucose and insulin, and reduced the levels of tyrosine (Tyr). Except for Tyr, chronic caffeine substantially reduced the NEFA and glucose responses in magnitude and duration; moreover, daily caffeine significantly lowered serum insulin levels. Chronically caffeinated rats, however, were able to display positive insulin and glucose responses when challenged with an oral glucose load and epinephrine, s.c., respectively. Those events possibly mediating the acute and chronic effects of caffeine on brain Trp and thus 5-HT levels may include, on the one hand, enhanced insulin secretion and increases in the serum Trp ratio, and, on the other hand, lipolysis and the release of plasma Trp from protein binding.

Animals↗
PubMed1983

Temperature responses in rats after acute and chronic administrations of caffeine.

Acute administrations (IP) of caffeine produced dose-dependent changes in the body temperature of rats. Low doses (12.5 and 25 mg/kg) induced hyperthermia soon after drug administration, while high doses (50 and 100 mg/kg) produced maximal hypothermia approximately 2 hr later. The acute effects of caffeine were also dependent on ambient temperature. The hyperthermic and hypothermic responses were attenuated and blocked, respectively, in rats maintained at 32 degrees C. At 4 degrees C, the hypothermic response was exacerbated, and the hyperthermic response was absent. Tolerance rapidly developed to the hypothermic actions of caffeine when rats were administered the drug over 28 days. Following the emergence of tolerance, hyperthermia was observed in rats given 50 mg/kg of caffeine. The hyperthermic responses to the low doses of caffeine were not altered by the frequency of drug administration. Both the acute and chronic effects of caffeine on thermoregulation are not unlike those found for morphine. Possible mechanisms of action underlying the thermoregulatory effects of caffeine are discussed.

Animals↗
PubMed1981

The pineal does not concentrate arginine vasotocin from biological fluids in vivo.

The ability of the pineal gland to concentrate circulating arginine vasotocin (AVT) from biological fluids in vivo was examined in rats. Intraventricular and intracisternal injections of AVT failed to elevate net pineal AVT content, even though CSF AVT levels were greatly increased by these treatments. Intravenous injection of AVT did elicit a light increase in pineal AVT, but plasma peptide levels wee elevated enormously. Thus, it seems unlikely that an active uptake process for AVT functions in this gland.

Animals↗
PubMed1979

Serotonin neurons project to small blood vessels in the brain.

Electrolytic lesions of the nucleus raphe dorsalis and medianus reduce the concentration of serotonin (5-hydroxytryptamine) within rat brain intraparenchymal blood vessels. The concentration of serotonin within these vessels increases or decreases after the administration of drugs that modify the biosynthesis and degradation of serotonin or destroy nerve terminals by an uptake-dependent mechanism. These studies provide evidence for the existence of a serotonin-containing pathway seemingly analogous to the neuronal projection that terminates on small parenchymal blood vessels from noradrenergic neurons of the locus coeruleus.

Animals↗
PubMed1979

Influence of PCPA, shock level, and home-cage conditions on shock-induced aggression.

In a series of experiments, the effect of parachlorophenylalanine (PCPA) on shock-induced fighting was assessed rats raised and maintained under either a 12-hr alternating light-dark cycle (LD) or constant light conditions (LL). PCPA increased shock-induced aggression only in LL groups when testing was accomplished using a 2 mA shock; PCPA resulted in increased aggression in groups from the LD condition only when testing was done at 1 mA. A procedure that used castrated and intact cagemates to manipulate home-cage social experience provided evidence for a role for social experience in determining differences between LL and LD reared rats in shock-induced aggression. However, these data also suggested that home-cage social experience was not a factor in the lighting condition influence on the effect of PCPA on shock-induced aggression. Finally, a separate experiment demonstrated that diurnal rhythms in shock-induced aggression were disrupted by handling and vehicle injection in the control procedures, so the possible role of serotonin in diurnal rhythms of aggression behavior could not be assessed.

Aggression↗
PubMed1977

Olfactory system damage and brain catecholamines in the rat.

Although a number of studies have reported that bulbectomy results in a fall in telencephalic norepinephrine (NE) content, the present study is the first to examine the relationship between the locus and extent of olfactory system damage and the depletion of telencephalic catecholamines after olfactory system surgery. Our findings indicate that the often reported depletion of telencephalic NE after olfactory bulb ablation is not due to removal of the olfactory bulbs per se, but instead is the result of incidentally produced destruction of tissue, caudal to the bulbs, through which noradrenergic fibers ascend on their way to various regions of the telencephalon.

Animals↗
PubMed1975

Behavioral correlates of serotonin depletion.

Depletion of telencephalic serotonin (5-HT) content by medical forebrain bundle lesions, which interrupt the ascending serotonergic pathways or by DL-p-chlorophenylalanine produces an increased sensitivity to pain as measured by the flinch-jump, stabilimetric, or hot-plate methods. Examination of the effects of a number of other lesions and drugs indicated that dopamine, norepinephrine and acetylcholine are not involved in pain sensitivity. Dosages of 75 mg/kg DL-5-hydroxytryptophan(5-HTP), 37.5 mg/kg L-5-HTP or 50 mg/kg Ro 4-4602 (NI-(DL-seryl)-N2-(2,3,4-trihydroxybenzyl)hydrazine) plus 37.5 mg/kg L-5-HTP administered to medical forebrain bundle lesioned rats returned both the telencephalic content of 5-HT and the pain threshold to normal values. Injection of 37.5 mg/kg of D-5-HTP or an equimolar dose of L-dopa had no effect on pain threshold. Normal animals display increased sensitivity to pain and decreased 5-HT contents in frontal pole, hippocampus, and amygdala during dark as compared to light hours. All three of these telencephalic areas are innervated by the ascending serotonergic pathways, and cells in these areas show inhibition of firing following the iontophoretic application of 5-HT. Taken together these data suggest that the serotonergic system normally acts to inhibit the effects of painful stimuli. A review of a variety of behavioral effects of 5-HT depletion including an enhanced response to lysergic acid diethylamide and amphetamine suggests that the ascending serotonergic system may have a general role in the inhibition of arousal, rather than a specific role with respect to various categories of behavior.

5-Hydroxytryptophan↗