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At least 757 records · Page 42Linked to original sources
PubMed1988

Use of antiserum to neurotensin reveals a physiological role for the peptide in rat prolactin release.

Previous studies have indicated that the brain peptide neurotensin can stimulate prolactin release by direct action on the pituitary gland, whereas its action within the hypothalamus is inhibitory. The inhibitory action is mediated by the release of dopamine into the hypophyseal portal veins, which deliver the neurotransmitter to the anterior pituitary gland to inhibit prolactin release. Our experiments were done to evaluate the physiologic significance of these neurotensin actions by injecting the globulin fraction of highly specific neurotensin antiserum either intravenously or intraventricularly. Injection into the third ventricle of either 1 or 3 microliter of neurotensin antiserum significantly increased plasma prolactin concentrations in (i) ovariectomized and (ii) ovariectomized estrogen- and progesterone-primed rats within 1 hr of injection. The response was more pronounced in the ovariectomized than in the ovariectomized estrogen- and progesterone-treated animals and was dose related. Intraventricular injection of these doses of neurotensin antiserum also evoked elevations in plasma prolactin in intact males, which were significant but smaller in magnitude than those seen in female rats. To evaluate the effect of the antiserum on the pituitary directly, the antiserum was injected intravenously at a dose of 40 microliter, which was sufficient to block the blood pressure-lowering effect of neurotensin. After the intravenous injection of antiserum, a highly significant suppression of plasma prolactin occurred, detectable when first measured at 1 hr after injection in both ovariectomized and ovariectomized estrogen- and progesterone-treated animals; however, the intravenous injection of antiserum had no significant effect on the prolactin release in males. These data indicate the physiological significance of the hypothalamic inhibitory actions of neurotensin on prolactin release, which are probably mediated by its stimulation of dopamine release that in turn, inhibits prolactin secretion by the lactotropes. The direct stimulatory effect of the peptide on prolactin release after its presumed release into portal vessels also appears to be physiologically significant in female but not in male rats.

Animals↗
PubMed1992

Intraventricular endothelin-1 uncouples the blood flow: metabolism relationship in periventricular structures of the rat brain: involvement of L-type calcium channels.

Endothelin-1 (ET) produces contraction of cerebral resistance vessels in vitro and in situ, but also is neuroactive causing increases in tissue energy metabolism as measured by [14C]deoxyglucose autoradiography in the intact rat brain. ET may, therefore, disengage the normally tight linkage between cerebral blood flow and tissue metabolism. Using anatomically rigorous autoradiographic and imaging techniques to measure focal blood flow in anesthetized, ventilated rats, we found that intraventricular injection of 9 pmol of ET reduced rates of perfusion by an average of 29% (compared to a saline-injected condition) in 6 individual periventricular structures bordering the injected lateral ventricle. A significant vasoconstrictor effect (41% decrease in blood flow) also occurred in the ipsilateral choroid plexus after ET injection, despite its increased rate of glucose metabolism. We employed a hydrogen clearance method to monitor rates of blood flow serially within the periventricular margin of the caudate nucleus after intraventricular injection of the dihydropyridine calcium-channel antagonist, nimodipine (72 nmol), or 9 pmol ET, alone and in sequence. Nimodipine increased caudate blood flow (by 47%) and prevented the vasoconstriction produced by ET. The results indicate that ET causes vasoconstriction in penventricular brain structures and choroid plexus even in the presence of substantial increases in glucose metabolism. The simultaneous stimulation by intraventricular ET of tissue hypermetabolic and vascular constrictor mechanisms, leading to a net reduction of periventricular blood flow, is mediated, at least in part, by dihydropyridine-sensitive calcium L-channels.

Anesthesia↗
PubMed1991

Interleukin 1 alpha inhibits prostaglandin E2 release to suppress pulsatile release of luteinizing hormone but not follicle-stimulating hormone.

Interleukin 1 alpha (IL-1 alpha), a powerful endogenous pyrogen released from monocytes and macrophages by bacterial endotoxin, stimulates corticotropin, prolactin, and somatotropin release and inhibits thyrotropin release by hypothalamic action. We injected recombinant human IL-1 alpha into the third cerebral ventricle, to study its effect on the pulsatile release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in conscious, freely moving, ovariectomized rats. Intraventricular injection of 0.25 pmol of IL-1 alpha caused an almost immediate reduction of plasma LH concentration; this decrease was statistically significant 20 min after injection and occurred through a highly significant reduction in the number of LH pulses, with no effect on pulse amplitude. In contrast, there was no change in pulse frequency but a small significant elevation in amplitude of FSH pulses. Intraventricular injection of the diluent had no effect on gonadotropin release. The results provide further evidence for separate hypothalamic control mechanisms for FSH and LH release. To determine the mechanism of the suppression of LH release, mediobasal hypothalamic fragments were incubated in vitro with IL-1 alpha (10 pM) and the release of LH-releasing hormone (LHRH) and prostaglandin E2 into the medium was measured by RIA in the presence or absence of norepinephrine (50 microM). IL-1 alpha reduced basal LHRH release and blocked LHRH release induced by norepinephrine. It had no effect on the basal release of prostaglandin E2; however, it completely inhibited the release of PGE2 evoked by norepinephrine. To evaluate the possibility that IL-1 alpha might also interfere with the epoxygenase pathway of arachidonic acid metabolism, epoxyeicosatrienoic acids were also measured. IL-1 alpha had no effect on the content of epoxyeicosatrienoic acids in the hypothalamic fragments as measured by gas chromatography and mass spectrometry. In conclusion, IL-1 alpha suppresses LH but not FSH release by an almost complete cessation of pulsatile release of LH in the castrated rat. The mechanism of this effect appears to be by inhibition of prostaglandin E2-mediated release of LHRH.

Animals↗
PubMed1986

Influence of cerebroventricular injection of dopamine on plasma prolactin and LH levels of postlaying and broody turkey hens.

Dopamine (DA), a well-known inhibitor of prolactin secretion in mammals, was injected into the third cerebroventricle of turkey hens in two distinct physiological states. Nonbroody postlaying turkeys had preinjection plasma prolactin (Prl) levels of about 68 ng/ml. Prolactin levels were significantly elevated 20 and 40 min after intraventricular injection of 10 micrograms of dopamine and then returned to basal levels. Incubating turkey hens, in contrast, showed the typical hyperprolactinemia characteristic of this physiological state. Mean preinjection Prl levels ranged from about 1290 to 1860 ng/ml. Injection of 10 or 30 micrograms of dopamine neither increased nor decreased plasma Prl levels over the 120-min time course of this experiment. Plasma luteinizing hormone (LH) levels were increased in nonbroody postlaying hens within 40 min after intraventricular injection of 10 micrograms of DA and then declined. Levels in vehicle-injected hens did not change significantly up to 120 min after injection. Dopamine injection had no effect on LH levels of broody turkey hens. These data clearly show that DA is not an inhibitor of Prl secretion in nonlaying turkeys with moderate Prl levels and in fact it appears to stimulate its release.

Animals↗
PubMed1988

Depletion of central catecholamines reduces pressor responses to arginine vasopressin.

Previous reports that central administration of arginine vasopressin (AVP) increases turnover of brain catecholamines raise the possibility that the pressor responses which follow central administration of AVP may be mediated, in part, by central catecholamines. To test this hypothesis, rats were given intraventricular injections of vehicle, or of the neurotoxin, 6-hydroxydopamine, which resulted in significant depletions of hypothalamic and medulla oblongata noradrenalin and hypothalamic dopamine, but not of medullary dopamine or of hypothalamic and medullary 5-hydroxytryptamine. Following a one week recovery, these conscious rats, fitted with indwelling arterial catheters, were given intraventricular injections of AVP; the increases in arterial pressure and heart rate were significantly reduced in the catecholamine-depleted animals. These data support the hypothesis that the pressor and tachycardia responses to intraventricular AVP are mediated, in part, by central catecholamine-containing neurons.

Animals↗
PubMed1984

Prolactin and luteinizing hormone levels of prelaying, laying and postlaying turkey hens following central administration of serotonin and peripheral administration of quipazine maleate.

The influence of serotonin (5-HT) on plasma prolactin and LH levels in female turkeys was studied by systemic injection of quipazine maleate, at 5-HT agonist, or by cerebroventricular injection of 5-HT itself. Within 30 min after injection, quipazine maleate (20 mg administered i.p.) elicited a significant increase in plasma prolactin in hens approaching sexual maturity as well as in laying hens. A 5-mg dose. had no effect on prolactin levels of either prelaying or laying hens. Intraventricular injection of 5 and 25 micrograms of 5-HT caused an increase in plasma prolactin of prelaying hens. A 5-micrograms dose of 5-HT was also effective in increasing prolactin levels in laying hens and in hens that had stopped laying due to ventricular cannula implantation. Neither quipazine maleate nor intraventricularly injected 5-HT had an effect on LH levels in any experiment.

Animals↗
PubMed1994

Determination of the structural requirements for the inhibitory action of gastrin-releasing peptide on growth hormone release.

We have previously determined that gastrin-releasing peptide (GRP) suppresses plasma growth hormone (GH) levels and blocks the response to growth hormone releasing factor (GRF) following its injection into the third ventricle (3V) of conscious male rats. To determine the portion of the peptide required for this action, fragments of the peptide were injected at various doses to determine their effect on plasma growth hormone and the response to a test dose of GRF (1 microgram/kg IV). The GRP 1-16 lowered plasma GH and blocked the response to GRF following an intraventricular injection of 2 micrograms but not 0.2 microgram of the peptide. Carboxy-terminal fragments were more effective. AcGRP20-27 was partially effective at a 100 times lower dose of 2.0 ng, a result similar to that obtained with the related peptide, bombesin. Even the C-terminal heptapeptide AcGRP-27 was effective at a dose of 2 ng. The results indicate that the C-terminal heptapeptide is the minimal requirement for intraventricularly injected GRP to suppress plasma GH levels and block the response to GRF.

Amino Acid Sequence↗
PubMed1977

Role of transmitters in mediating hypothalamic control of electrolyte excretion.

Changes in urinary volume and electrolyte excretion were monitored after the injection of cholinergic and monoaminergic drugs into the third cerebral ventricle of conscious male rats made diuretic by an intravenous infusion of 5% dextrose. A natriuretic and kaliuretic response was induced by the intraventricular injection of norephrine (NE) or carbachol, whereas dopamine (DA) had no effect. The beta-receptor stimulator isoproterenol (ISO) induced an antinatriuretic and antikaliuretic effect. Intraventricular injection of the alpha-adrenergic blocker phentolamine abolished the natriuretic response to NE and carbachol and to intraventricular hypertonic saline (HS). By contrast, the beta-adrenergic blocker propranolol induced a natriuresis and kaliuresis when injected alone and an additive effect when its injection was followed by NE or HS. Propranolol potentiated the natriuretic response to carbachol. Cholinergic blockade with atropine diminished the response to NE and blocked the natriuretic response to HS. It is suggested that sodium receptors in the ventricular wall can modify renal sodium excretion via a stimulatory pathway involving cholinergic and alpha-adrenergic receptors and can inhibit sodium excretion via a tonically active beta-receptor pathway.

Animals↗
PubMed1993

Essential role of hypothalamic muscarinic and alpha-adrenergic receptors in atrial natriuretic peptide release induced by blood volume expansion.

Expansion of the blood volume induces natriuresis, which tends to return the blood volume to normal. This response is mediated at least in part by the release of atrial natriuretic peptide (ANP) into the circulation. Previous experiments have shown the participation of the anterior ventral third ventricular (AV3V) region of the hypothalamus in the ANP release that follows volume expansion. When injected into the AV3V region, the cholinergic drug carbachol induces natriuresis and the release of ANP. In the present experiments, microinjection of norepinephrine into the AV3V region induced natriuresis and an increase in plasma ANP. To determine whether cholinergic and alpha-adrenergic pathways are crucial to the volume expansion-induced release of ANP, certain receptor-blocking drugs were injected into the AV3V region of conscious rats. Thirty minutes later blood volume was expanded by intravenous injection of 2.0 ml/100 g of body weight of hypertonic saline (0.3 M NaCl). Microinjection of isotonic saline (2 microliters) into AV3V region of control animals 30 min prior to volume expansion had no effect on the 3-fold increase in plasma ANP concentrations measured 5 min after volume expansion. In contrast, although the receptor-blocking drugs did not alter the initial concentrations of plasma ANP 30 min later, just prior to volume expansion, blockade of muscarinic cholinergic receptors by intraventricular injection of 5 nmol (2 microliters) of atropine sulfate or methylatropine markedly reduced the response to volume expansion but did not obliterate it. Microinjection of the alpha receptor blocker phentolamine (5 nmol) into the AV3V 30 min prior to volume expansion also markedly suppressed the ANP response. Intraperitoneal (i.p.) injection of methylatropine (0.01 mmol/100 g of body weight), which does not cross the blood-brain barrier, also did not affect the basal levels of ANP 30 min after i.p. injection. But, in striking contrast with the blockade of the response to volume expansion induced by intraventricular injection of methylatropine, the response to volume expansion was markedly enhanced by i.p. injection of methylatropine. The results therefore indicate that hypothalamic muscarinic and alpha-adrenergic synapses are essential to release of ANP in response to volume expansion. These results are consistent with a hypothetical pathway for physiological control of ANP release which involves distension of baroreceptors within the right atria, carotid and aortic sinuses, and kidney which alters afferent input to brain stem noradrenergic neurons with axons projecting to the AV3V region. There they activate cholinergic interneurons by an alpha 1-adrenergic synapse. The cholinergic neurons in turn stimulate ANP neurons in this brain region via muscarinic receptors. The stimulation of these neurons activates efferent pathways which induce the release of ANP.

Animals↗
PubMed1990

Cholinergic cell loss and cognitive impairments following intraventricular or intradentate injection of colchicine.

Bilateral injections of colchicine (3.5 or 7.0 micrograms/0.5 microliters/site) into either the dentate gyrus or the lateral cerebroventricles (i.c.v.) of Sprague-Dawley rats produced specific behavioral, histopathological and neurochemical alterations. Colchicine, administered via either route, produced impairments in the performance of a radial-arm maze task which did not subside during 8 weeks of testing. Intradentate colchicine decreased (1) the thickness of both blades of the dentate granule cell layer, (2) the size of the overlying molecular layer, (3) hippocampal volume, and (4) the number of cholinergic neurons in the medial septum/vertical limb of the diagonal band (MS/VLDB). I.c.v. administration of colchicine did not alter any index of hippocampal morphology but did significantly decrease the number of cholinergic neurons in the MS/VLDB. An analysis of the time course of cholinotoxicity revealed that both intradentate and i.c.v. colchicine decreased choline acetyltransferase (ChAT) activity and high affinity choline uptake (HAChU) in the hippocampus at 1 and 3, but not 9, weeks following surgery. Furthermore, i.c.v. colchicine decreased ChAT activity in the septum at both 3 and 9 weeks following surgery. Neither route of administration altered ChAT or HAChU in the frontal cortex, olfactory bulb or striatum. The decreases in presynaptic cholinergic parameters were paralleled by a reduction in acetylcholinesterase staining in the hippocampus which appeared to recover within 9 weeks. These data suggest that intradentate colchicine produces either (i) transsynaptic degeneration of cholinergic neurons due to a loss of their target sites (granule cells in the dentate gyrus), (ii) a direct cholinotoxic effect, or (iii) a combination of these mechanisms. The i.c.v. injection of colchicine appears to exert a direct toxic effect on cholinergic neurons and/or nerve terminals that results in the death of these neurons. Colchicine may be a useful tool for investigating the behavioral and neurobiological properties of the septohippocampal cholinergic pathway and its response to injury.

Animals↗
PubMed1989

Arachidonic acid metabolism and cerebral blood flow in the normal, ischemic, and reperfused gerbil brain. Inhibition of ischemia-reperfusion-induced cerebral injury by a platelet-activating factor antagonist (BN 52021).

Cerebral ischemia and ischemia-reperfusion induced cerebral injury results in the accumulation of free fatty acids and diacylglycerols as a result of increased activity of phospholipases A and C. We have evaluated the incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomes, the effect of cerebral ischemia on 14C incorporation, and the effect of a PAF antagonist (BN 52021) on cerebral blood flow, free fatty acids, diacylglycerols, and polyphosphoinositides. Peak incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomal fractions occurred 30 minutes following intraventricular injection. Peak incorporation into cerebellar synaptoneurosomal fractions was at 60 minutes following intraventricular injection. Turnover in phospholipid pools was similar in the whole brain and synaptoneurosomes (PI greater than PC greater than PE). Considering phosphatidylinositol content in the gerbil brain, the specific activity of 14C arachidonic acid was 22 times greater in PI than PC. Five minutes of bilateral carotid artery ligation resulted in decreased phosphatidylinositol and polyphosphoinositols. Bilateral carotid artery ligation resulted in systemic arterial hypertension, complete forebrain ischemia (CBF less than 7 ml/100 gm/min) and a 20% to 50% reduction in midbrain CBF. Reperfusion resulted in cerebral reactive hyperemia and systemic hypotension. BN 52021 inhibited the maturation of ischemia-reperfusion induced cerebral injury. Cerebral blood flow was improved. Free fatty acids were decreased, suggesting inhibition of phospholipase A activity. Decreased DAG pools with increased PIP2 pools suggest a possible coinhibition of phospholipase C.

Animals↗
PubMed1986

Stress-induced inhibition of reproductive functions: role of endogenous corticotropin-releasing factor.

In the adult castrated male rat, exposure to inescapable, intermittent electroshocks inhibited the pulsatile pattern of luteinizing hormone release and markedly lowered its plasma concentrations. The central administration of the corticotropin-releasing factor (CRF) antagonist alpha-helical ovine CRF residues 9 to 41 reversed the inhibitory action of stress. Neither its peripheral injection, nor the intraventricular injection of the inactive CRF analog des-Glu to Arg ovine CRF was effective. These results suggest that endogenous CRF may mediate some deleterious effects of noxious stimuli on reproduction.

Adrenocorticotropic Hormone↗
PubMed1981

Evidence that a serotonergic mechanism stimulates the secretion of pituitary beta-endorphin-like immunoreactivity in the rat.

A pharmacological approach was used to investigate serotonergic control of the secretion of pituitary beta-endorphin-like immunoreactivity (beta-END-LI) in the rat. The administration of 75 or 200 mg/kg L-tryptophan (ip, over 30 min) increased brain serotonin by 17% and 19%, respectively, and increased circulating beta-END-LI from 0.30 +/- .06 to 0.56 +/- 0.7 and 0.64 +/- 0.8 ng/ml, respectively. D,L,5-Hydroxytryptophan (30 mg/kg, ip, over 30 min) produced a 4.9-fold increase in brain serotonin content and a 3.4-fold rise in plasma beta-END-LI. The administration of a serotonin reuptake blocker, fluoxetine (10 mg/kg, ip, over 15 min), elevated basal levels of plasma beta-END-LI from a control value of 0.38 +/- 0.02 to 1.21 +/- 0.32 ng/ml. Exposure to ether increased circulating beta-END-LI to 1.08 +/- 0.18 ng/ml, and fluoxetine treatment further increased this rise to 1.69 +/- 0.09 ng/ml (P less than 0.05). Quipazine, a serotonin receptor agonist, evoked a dose-related (2.5-5.0 mg/kg, ip) increase in circulating beta-END-LI levels by 15-45 min post injection. By contrast, intraventricular injection of the neurotoxin 5,7-dihydroxytryptamine (75 microgram free base, for 10 days) caused a 77% depletion of brain serotonin and attenuated the rise in beta-END-LI levels in response to immobilization (3.28 +/- 0.20 vs. 1.83 +/- 0.25 ng/ml). A higher dose of 5,7-dihydroxytryptamine (200 microgram free base, for 10 days) significantly decreased resting levels of beta-END-LI from 0.65 +/- 0.14 to 0.36 +/- 0.08 ng/ml. We conclude that brain serotonin neurons exert a stimulatory influence over the basal secretion of pituitary beta-END-LI and mediate, in part, the stress-induced release of this hormone.

Animals↗
PubMed1975

Effects of antipyretics on normothermic rabbits.

The effects of antipyretics on the ear skin and rectal temperature (Te and Tre) were investigated in non-febrile rabbits placed in a cold environment or when they were cooled locally in the hypothalamus. Intravenous injections of sulpyrin (25-500 mg/kg) or sodium salicylate (25-100 mg/kg) produced the dose-related increase in Te and slight fall in Tre. Decrease in Te induced by hypothalamic cooling was also reversed by the intravenous injection of antipyretics. Intraventricular injections of sulpyrin and salicylate (0.5-5.0 mg/kg) also caused the vasodilatation of the pinna skin and the fall in Tre. Bilateral microinjections of sulpyrin were made into various areas of the brain stem in order to locate the site of action. The injection sites where the vasodilatatory effect was elicited were the anterior hypothalamus, ventromedial nucleus of hypothalamus and the midbrain reticular formation. The responses elicited from the ventromedial nucleus were usually accompanied by restless and violent struggling. Injection of antipyretics into the mammillary body had no effect on Te. Intrahypothalamic injection of procaine depressed the sulpyrin-induced vasodilatation. These findings suggest that action of antipyretics on the normal body temperature is mediated through anterior hypothalamus and midbrain reticular formation.

Analgesics↗
PubMed1976

Effect of ACTH and its fragment on brain catecholamines in intact and adrenalectomized rats.

Brain catecholamine metabolism was monitored by distribution of labelled noradrenaline (3H-NA) after intraventricular injection to intact and adrenalectomized rats. The adrenalectomy produced an increased disappearance rate of the labelled pool in the hypothalamus, hippocampus and neocortex. These changes could be prevented by hydrocortisone pretreatment. Painful stimuli resulted in an increased disappearance of the labelled pool in both intact and adrenalectomized rats. The implantation of hydrocortisone into the tuberoinfundibular region prevented the stress-induced changes of the catecholamine metabolism. Intraventricular administration of ACTH1-24 and ACTH4-10 produced a significant increase of the disappearance rate in different brain regions of adrenalectomized rats. The blocking of catecholamine synthesis by intraventricular injection of alpha-methyl-m-tyrosine resulted in a marked decrease of the labelled pool but did not prevent the ACTH-induced decrease of the tracer pool. On the other hand, the blocking of monoamine-oxydase activity by Pargyline led to a marked increase of the labelled pool but intraventricular administration of ACTH led to an increase of the disappearance rate. The mechanism of ACTH action on brain catecholamine metabolism is still obscure, however, an increased release of the NA to ACTH peptides is very likely in the light of the present observations.

Adrenal Glands↗
PubMed1982

Dissociation of the inhibitory and facilitatory effects of norepinephrine on the release of LH by premammillary lesions.

A dual action of the adrenergic system on the release of LH has been demonstrated: facilitation mediated by alpha-adrenergic receptors and inhibition mediated by beta-adrenergic receptors. These two actions can be dissociated either by treatment with agents which block-specific adrenergic receptors or by cuts placed just in front of the mammillary bodies (PM cuts) interrupting caudal afferents to the medial basal hypothalamus. These cuts affected the release of luteinizing hormone (LH) in a way similar to that of treatment with the beta-adrenoblocker, propranolol. Thus, in animals with PM cuts (1) the release of LH following the injection of norepinephrine into the third ventricle was enhanced and (2) the blocking action of intraventricular injection of isoproterenol on the release of LH was suppressed whereas the facilitatory effect of clonidine was not changed. Furthermore, whereas the release of LH induced by intraventricular injection of norepinephrine in intact rats was enhanced by treatment with propranolol, in rats with PM cuts the already enhanced induced release was no further raised by propranolol treatment. On the other hand, PM cuts did not affect the suppressive action of the alpha-adrenoblocker phenoxybenzamine on the norepinephrine-induced release of LH. It is concluded that adrenergic mechanisms inhibiting the release of LH were suppressed by PM cuts whereas those facilitating the release were not affected by these cuts.

Animals↗
PubMed1986

Vasoactive intestinal polypeptide (VIP) and cerebrospinal fluid (CSF) of sleep-deprived cats restores REM sleep in insomniac recipients.

In the past few years a steadily increasing number of substances have been suggested to qualify as sleep-inducing factors. Most 'sleep factors' appear to exert their effects on slow-wave sleep. Recently, however, it has been shown that the cerebrospinal fluid (CSF) of sleep-deprived cats may contain a rapid eye movement (REM) sleep factor, and that vasoactive intestinal peptide (VIP) may be a specific REM sleep inducer. The purpose of this study is to determine whether the CSF of sleep-deprived cats and VIP can reverse insomnia produced by parachlorophenylalanine (PCPA). Donor cats were sleep-deprived for 24 h and their CSF extracted. Some donor cats were additionally pre-treated with chloramphenicol, and some extracted CSF was heated. Recipient cats were injected with 400 mg/kg i.p. of PCPA on two consecutive days. Twenty-four h after the second injection, the recipient cats were intraventricularly injected with a 100-microliters of the various CSF types or 200 ng of VIP. The results showed that only CSF from sleep-deprived cats and VIP were capable of restoring REM sleep in the otherwise PCPA insomniac cats. Since the return of REM sleep was through an increase in its frequency, it is suggested that the CSF of sleep-deprived cats contains a VIP-like sleep factor possibly involved in triggering REM sleep.

Animals↗