John E. Jalowiec

Opiates and play dominance in juvenile rats.

Social play between pairs of individually housed juvenile rats was studied by measuring pinning frequencies occurring during rough-and-tumble play. Low doses of morphine increased play, and opioid blockade with naloxone reduced play. Dominance, as measured by which pinned which most, was markedly reduced by naloxone and slightly increased by morphine. These effects were most apparent when animals were treated with these drugs continuously from the beginning of play testing. Although the respective drugs tended to reverse established dominance patterns (i.e., naloxone made dominant animals more submissive, and morphine made submissive animals more dominant), it was apparent that previously established social learning limited the effectiveness of these manipulations. In general, the results are consistent with the proposition that brain opioids are important in controlling the vigor of social relations.

Effects of growth hormone on sleep-waking patterns in cats.

Abstract Cats given growth hormone in doses from 50–1000 μg, i.p., showed a selective elevation of REM sleep in the first 3 hr postinjection. Bovine thyrotropin control injections did not alter sleep patterns. When the effect of growth hormone on sleep was blocked by REM deprivation for the first 3 hr, the REM elevating effect of growth hormone still occurred in the subsequent sleep period. These results suggest that growth hormone affects the central nervous system, either directly or indirectly. Also, the greatly increased secretion of growth hormone, which has been reported during slow-wave sleep in man, may play a role in the occurrence of REM sleep.

Sodium appetite elicited by furosemide: effects of differential dietary maintenance

Rats were maintained on two diets differing in sodium content and were injected later with the diuretic, furosemide, to induce acute sodium loss. Rats maintained on a sodium deficient diet ingested more sodium following diuretic injection than animals maintained on a sodium replete diet and showed behavioral overcompensation for the deficit established by natriuresis. In contrast, the salt intake of diuretic-injected rats maintained on the sodium replete diet was precisely sufficient to restore sodium balance to control levels. Maintenance on a sodium deficient diet did not reduce sodium balance substantially and furosemide-induced sodium loss produced similar degrees of hypovolemia and hyponatremia when water was available regardless of dietary maintenance. However, marked urine sodium retention accompanied by enhanced excretion of potassium during maintenance on the sodium deficient diet suggested that mineralocorticoid activity was enhanced prior to diuretic treatment. The greater intakes of hypertonic (0.51 M) saline in the diuretic-injected rats maintained on the sodium deficient diet were attributed to potentiation of the sodium appetite elicited by sodium loss by high endogenous mineralocorticoid levels, since maintenance on the sodium deficient diet did not elicit sodium appetite in the absence of sodium depletion.

Noradrenergic pathways and sleep-waking states in cats ☆

Abstract Four female cats were surgically prepared with an array of recording electrodes (cerebral cortex, hippocampus, lateral geniculate nuclei, neck and eye muscles) for electrophysiological recording of sleep-waking patterns. Polygraphic recordings were obtained before and after administration of 6-hydroxydopamine into the region of the ventral noradrenergic pathway at the mesencephalic level. Records were scored in five categories: active awake, quiet awake, light slow wave sleep, deep slow wave sleep and REM (rapid eye movement) sleep. The acute effect of 6-hydroxydopamine was a shift toward electrocortical arousal; this probably reflects release of endogenous amines within ascending noradrenergic systems. The chronic effect was a small increase in deep slow wave sleep and REM sleep. Biochemical analyses of regional norepinephrine and serotonin levels indicated significant depletion of norepinephrine in all parts sampled (occipital cortex, temporal cortex, pyriform lobe, basal forebrain region, striatum, hypothalamus, cerebellum, and brain stem). Serotonin was depleted to a lesser extent in occipital cortex, temporal cortex, pyriform lobe, cerebellum, and brain stem. Since the greatest depletion of norepinephrine was found in the basal forebrain (to 24% of control levels), the ventral noradrenergic pathway was selectively influenced to some extent. The data thus appear to indicate that activation of the ventral pathway induces electrocortical arousal, while depletion of amines within this pathway may induce somnolence.

Effects of growth hormone on brain biogenic amine levels

The effects of IP administered bovine growth hormone (GH) on regional brain serotonin, 5-hydroxyindoleacetic acid (5-HIAA) and norepinephrine levels in rats were examined. GH decreased the levels of both monoamines and 5-HIAA in the diencephalon and brainstem while not affecting telencephalic concentrations. In hypophysectomized rats, however GH produced significant elevations of monoamine and 5-HIAA levels in all brain regions. In normal rats the decreases in norepinephrine content produced by GH were correlated with a reduction in the stimulatory action of d-amphetamine on general activity levels. These results demonstrate that GH can affect brain biogenic amines and that these effects have behavioral consequences.

Suppression of feeding in cats following 2-deoxy-D-glucose ☆

Abstract The glucose utilization hypothesis for the control of food intake postulates that decreases in cellular glucose metabolism initiate feeding. In contrast to findings reported with other species, inhibition of glycolysis with 2-deoxy-D-glucose does not increase feeding in cats, but produces dose-dependent decreases in food intake. Accordingly, glucostatic control of feeding may be qualitatively different in cats than in other species.

Sleep-waking patterns in cats after administration of fenfluramine and other monoaminergic modulating drugs ☆

Abstract Fenfluramine produced a dose-dependent, biphasic effect on sleep-waking patterns in cats. At low doses (0.4 mg/kg) fenfluramine elicited an increase in total waking time and a marked reduction in REM sleep, similar to that seen after administration of amphetamine, without affecting SWS. At anorectic doses (5.0 mg/kg) fenfluramine almost completely suppressed REM sleep, reduced waking time and increased SWS, an effect similar to that seen after administration of 5-HTP, the precursor of serotonin. The fenfluramine-induced increase in SWS was facilitated by 5-HTP and blocked by LSD, a serotonin antagonist. Serotonin was significantly reduced in the neocortex, pyriform lobe, cerebellum and hindbrain at the time of the drugs peak effect on SWS suggesting that the fenfluramine-induced increase in SWS is mediated via serotonin dependent mechanisms.

Inhibition of glycolytic metabolism and sleep-waking states in cats

Abstract In cats, injections of 2-deoxy-D-glucose, a glucose antimetabolite, produces dose-dependent increases of slow wave sleep and decreases of REM sleep. Accordingly, variations of glycolytic metabolism may participate in the control of sleep-waking behavior.

Effects of midbrain tegmental lesions on sleep and regional brain serotonin and norepinephrine levels in cats

Abstract A variety of experimental evidence has implicated the mesencephalic raphe complex of nuclei and the locus coeruleus in the regulation of slow-wave sleep and REM sleep, respectively, and in the maintenance of diencephalic and telencephalic levels of serotonin and norepinephrine. The present study defines further the critical loci subserving brain stem control of fore-brain monoamine levels and electrographic indicators of these two states of sleep. After baseline sleep profiles were determined, lesions were placed in the dorsal and ventral tegmentum of the medbrain in cats. Following these lesions, fluorometric assay of various brain regions revealed widespread depletion of serotonin and norepinephrine although few differences in the pattern of regional reduction of monoamines were noted between the cats with dorsal and ventral tegmental lesions. However, comparison of sleep-waking profiles of the animals taken 2 wk after the lesion with profiles taken before yielded no consistent alterations in waking, slow-wave sleep of REM sleep. These results indicate no clear-cut correlation between regional levels of brain amines and sleep-waking profiles.

Feeding and drinking in rats maintained on a low protein diet.

Male and female rats born of protein malnourished mothers were fed a low-protein diet (8% casein) for 150 days after weaning and daily food and water intakes and body weights were monitored. Although daily intakes of diet throughout the study were significantly lower than those of rats maintained on a normal protein diet (25% casein) or stock diet, intakes/100 g body weight were significantly greater. Daily increments in body weight, as percent of previous days weight, were consistently higher in rats fed the low-protein diet in comparison to rats fed the normal protein diet. Marked retardation of body growth was evident throughout the study although feeding efficiency ratios (daily body wt. increment per g daily food intake) were comparable among the various dietary groups. Compensation for reduction of the protein component of the diet by increased daily food intake/100 g body weight did not alleviate growth retardation.