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Results for “Injections, Intraventricular”

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PubMed1988

Characterization of central actions of neuropeptide Y on food and water intake in rabbits.

The effects of a 36-amino acid peptide, neuropeptide Y (NPY), on feeding and drinking behaviors were studied in young and adult rabbits. Intraventricular injection of NPY to adult rabbits induced feeding and drinking in a dose-related manner. While the lowest doses tested (0.2 micrograms) was without effect, other doses (0.5 and 1 microgram) elicited feeding and drinking almost instantaneously. When 1, 5 and 10 microgram doses were injected into young rabbits, immediate increases in feeding and drinking were evident, but differences in the magnitude of responses among these dosages were significant only in water consumption. Unlike studies in rats, in these rabbits NPY elicited a more pronounced response in drinking than in feeding. The drinking response after NPY administration was not a consequence of food intake because it occurred in the absence of food. With ad lib feeding, the majority of enhanced food consumption was confined to the first 30-min after NPY injection; however, an increased motivation to eat was retained for at least 2 hr after NPY when food was withheld and then returned. These observations are consistent with specific stimulatory effects of NPY on food and water intake.

Age Factors↗

PubMed1976

Effects of intracranial injections of 6-OHDA on food and water intakes, body temperature and body weight regulation in the rat.

6-Hydroxydopamine was injected either intraventricularly (320 mug in 10 mul) or intrahypothalamically (64 mug in 2 mul) into rats kept under either free feeding or body weight reduced conditions. Intraventricular injections caused a temporary aphagia and hypodipsia in free feeding rats but daily measurements failed to reveal any long term effects; body weight reduced rats did not display the temporary aphagia but were initially hyperphagic. Injections into the more rostral hypothalamic areas of free feeding rats also showed only minimal short term effects; however, some of the body weight in both body weight reduced group died within several days of injection. Injections made at more posterior loci again showed very little effect in both body weight reduced and free feeding groups; some temporary disruption of feeding occurred from lesions in the proximity of the zone incerta of some free feeding animals.

Animals↗

PubMed1976

The tryptolines: effect of intraventricular administration on spontaneous motor activity of rats.

The pharmacologic properties of the tryptolines, hindered analogues of the tryptamines, were studied behaviorally in rats. Following intraventricular injections, it was found that spontaneous motor activity decreased markedly during the initial 25 mins when compared with saline. Since both the tryptolines and tryptamines have been shown to be inhibitors of 5-hydroxytryptamine uptake, it may be possible that these compounds are acting indirectly throught an effect on the serotonergic system.

Animals↗

PubMed1977

Barrel rotation induced by vasopressin and related peptides in rats.

Intraventricular injection of arginine-8-vasopressin and its analogues vasotocin and lysine-8-vasopressin into rat brain evoked a special rotational behavior resembling somatostatin-induced barrel rotation [1]. Oxytocin and oxypressin were less active while vasopressin fragments had no effect. Vasopressin-induced barrel rotation was accompanied by pathological symptoms indicating a disturbance of muscle tone regulation and is considered to be a non-specific and toxic effect. This rotational behavior was not prevented by atropine, propranolol, phentolamine, methylsergide or haloperidol but was reduced by chlorpromazine, probably due to the latter's muscle relaxing activity.

Animals↗

PubMed1982

Prostaglandin inhibition of apomorphine-induced circling in mice.

The effect of prostaglandins (PGs) on apomorphine (apo)-induced circling was examined in unilaterally lesioned mice. Intraventricularly injected PGD2, PGE2, and PGF2 alpha at a dose of 1.0 nmole/g all inhibited apo-induced circling. When injected directly into the striatum, these same PGs also inhibited circling in a dose range of 0.01-0.1 nmole/g, while the PGE2 metabolite, 13,14-dihydro-15-keto-PGE2, was inactive at 0.1 nmole/g. For both routes of administration, PGF2 alpha appeared to be the most potent of the PGs tested. PGs administered alone by either route to unilaterally lesioned mice did not produce circling. Pretreatment with the PG synthetase inhibitor, indomethacin, caused the apo treated mice to circle at significantly higher rates than control animals. These results are the first report suggesting that within dopamine (DA)-mediated pathways PGs act at sites postsynaptic to the dopaminergic synapse.

Animals↗

PubMedDate not supplied

A study on the release mechanism of vasopressin and oxytocin.

The changes in plasma levels of arginine-vasopressin (AVP) and oxytocin (OXT) of rabbits by intraventricular administration of various drugs and their effects on the release of both hormones from the isolated posterior pituitary of rats were examined. An intraventricular injection of hypertonic saline, carbachol, angiotensin II, prostaglandin E2 or histamine to a rabbit increased the concentrations of plasma AVP and OXT, whereas serotonin decreased their plasma levels. Noradrenaline increased the concentration of OXT, but not that of AVP. Dopamine did not significantly affect the plasma level of either hormone. The release of AVP and OXT from the posterior pituitary fragments of rats was stimulated by changing the osmolality of the perfusion medium in vitro. Perfusion with medium containing dopamine suppressed the release of both hormones. However, the other bioactive amines and the drugs mentioned above did not affect the release of AVP and OXT.

Angiotensin II↗

PubMed1993

Rapid alterations in cAMP accumulation in brain nuclei of rats following microinjections of vasoactive intestinal polypeptide (VIP) into the lateral ventricle.

The in vivo effect of exogenous vasoactive intestinal polypeptide (VIP) on the accumulation of cAMP in 21 microdissected brain nuclei was investigated 3 and 7 min after intraventricular injections in rats. VIP elicited significant (up to 20-fold) increases in cAMP levels. This effect is region specific varying considerably among the brain regions investigated. VIP dramatically increased the cAMP content of the lateral septal nucleus, several hypothalamic nuclei, the habenula, the midbrain central gray and the locus coeruleus. Smaller increases were observed elsewhere including some VIP-rich brain areas such as the cerebral cortex and the hippocampus.

Animals↗

PubMed1981

A pharmacologically pertinent animal model of mania.

Intraventricular injection of 6-hydroxydopamine (HDA) produces rats which are irritable and hyperresponsive to environmental stimuli. Chronic administration of lithium was found to prevent the development of hyperreactivity to mild footshock, while chronic electroconvulsive shock effected a return toward normal behavior. HDA-induced hyperreactivity is proposed as a pharmacological model of mania.

Affective Disorders, Psychotic↗

PubMed1995

Effects of substance P on cardiovascular regulation in the rabbit.

The effect of substance P on blood pressure and aortic reflex was investigated in rabbits. Microinjections of substance P and Sar9, Met(O2)11-SP (a selective NK1-receptor agonist) into the floor of the fourth ventricle led to a dose-dependent increase of blood pressure and a sharp enhancement of the baroreflex. These effects were abolished by pretreatment with SR 140333 (a selective NK1-receptor antagonist). Intraventricular injection of the antagonist alone significantly decreased the amplitude of the aortic reflex. After bivagotomy, the amplitude of the parasympathetic component of the baroreflex decreased dramatically and substance P injections were no longer effective. Our results demonstrate that substance P activation of NK1 receptors plays a major role in the modulation of the parasympathetic component of the baroceptor reflex.

Animals↗

PubMed1996

192 IgG-saporin lesion of basal forebrain cholinergic neurons in neonatal rats.

Seven day old rats received bilateral intraventricular injections (200 ng) of the immunotoxin 192 IgG-saporin. When assayed in adulthood, these rats showed an 84% loss of hippocampal and a 52% loss of cortical choline acetyltransferase (ChAT) activity. ChAT was unaffected in the caudate. Cholinergic neurons immunoreactive (IR) for the low affinity neurotrophin receptor (P75NTR) were severely reduced throughout the basal forebrain nuclei. Cortical and hippocampal norepinephrine were increased and these areas showed ingrowth of ectopic, P75NTR and dopamine beta-hydroxylase IR varicosities. These were probably sympathetic axons. No obvious forebrain dysmorphogenesis was observed and cortical thickness was unaffected. These rats showed no evidence of impaired spatial learning/memory as assessed by the Morris water maze and delayed spatial alternation. However, they were less active on the elevated plus apparatus and spent less time on the open arms, suggestive of increased timidity. 192 IgG-saporin appears to be a powerful tool to selectively lesion basal forebrain cholinergic neurons in the neonatal rat. Surprisingly, the neuromorphological and behavioral sequelae seem minimal. It may be necessary to achieve near-total neonatal destruction of forebrain cholinergic neurons before severe, lasting mnemonic effects are evident.

Acetylcholine↗

PubMed1981

Exploration and motor activity after intraventricular ACTH, morphine and naloxone.

Intraventricular injection of morphine (5 microgram) and ACTH (2.5 microgram) reduced the time spent head-dipping and the number of head-dips made by rats during a 10-min trial in a holeboard. These effects were reversed by naloxone (2.0 mg/kg, i.p.), in spite of the fact that naloxone alone also reduced these measures of exploration. None of the drugs or drug combinations tested significantly reduced locomotor activity. The results are discussed in relation to the action of ACTH on opiate receptors.

Adrenocorticotropic Hormone↗

PubMed1985

Physostigmine reverses memory deficits produced by pretraining electrical stimulation of the dorsal hippocampus in mice.

The aim of the present experiments was to test the validity of the hypothesis that presynaptic cholinergic activity has a functional significance for memory formation. The results show that electrical stimulation of the dorsal hippocampus delivered before learning in BALB/c mice which induces a decrease of about 40% in hippocampal choline acetyltransferase (ChAT) activity at the time of learning results in deficits in retention scores in two appetitive learning tasks (operant conditioning in the Skinner box or a spatial memory task using a 4-hole board). In both behavioral tasks intraventricular injection of 1 microgram of physostigmine 20 min before the acquisition session reverses the disruptive effect of pretraining hippocampal stimulation. Our results seem to indicate that the memory deficits produced by pretraining electrical stimulation of the hippocampus result from both a decrease in ChAT activity and a corresponding reduction of acetylcholine availability in the hippocampal formation.

Acetylcholine↗

PubMed1996

Active and passive avoidance learning in rats neonatally treated with intraventricular 6-hydroxydopamine.

To clarify the behavioral characteristics of rats neonatally treated with 6-hydroxydopamine (6-OHDA), their performance on 4 aversive learning tasks, 3 active (shuttle, one-way, and rearing) avoidance tasks and one passive (step-through) avoidance task, was examined. On days 2 and 4 after birth, each rat of F344/Du strain received bilateral intraventricular injections of 6-OHDA (35 micrograms x 2) or vehicle solution following desmethylimipramine (20 mg/kg, s.c.) pretreatment. From day 90, each rat was trained in one of the 4 avoidance tasks. 6-OHDA-treated rats showed significantly less avoidance responses in the shuttle and the one-way avoidance tasks, but their performance on the rearing and the step-through passive avoidance tasks was not significantly different from that of control rats. The differential impairment of avoidance suggests that 6-OHDA treatment does not cause a general learning deficit, but facilitates rearing and/or jumping responses in aversive situations, which results in inappropriate escape responses.

Animals↗

PubMed1996

Brain sites mediating the discriminative stimulus effects of nicotine in rats.

Pharmacological studies suggest that the discriminative stimulus (DS) produced by nicotine is mediated centrally. The aim of the present study was to identify neuroanatomical substrates that mediate the DS properties of nicotine. Specifically, the nucleus accumbens, a brain region known to mediate the DS effects of amphetamine and cocaine, was investigated using a two-lever operant drug discrimination paradigm. Male hooded rats were trained to discriminate nicotine (0.2 mg/kg s.c.) from saline with a tandem schedule of food reinforcement. Once stimulus control was attained, a randomised sequence of nicotine microinjections (2-8 micrograms) was tested for generalisation during brief extinction tests. It was confirmed that the stimulus produced by the systemic administration of nicotine generalized to nicotine administered bilaterally into the dorsal hippocampus, with significant decreases in overall response rates. Microinjections of nicotine (1-8 micrograms) into the nucleus accumbens failed to produce any dose-related increases in responding on the nicotine-appropriate lever although these microinjections also produced significant decreases in response rates. Smaller doses (1-4 micrograms) of nicotine administered into the fourth ventricle produced characteristic prostration responses but these microinjections failed to produce generalization in tests carried out 20 min later, when the disabling effects of prostration had dissipated. These results suggest that the DS effects of nicotine may be mediated, at least in part, through the dorsal hippocampus. Results from intra-accumbens and intraventricular injections suggest that these regions may not be important in mediating the DS effects of nicotine.

Animals↗

PubMed1994

Interleukin-1 beta increases basic fibroblast growth factor mRNA expression in adult rat brain and organotypic hippocampal cultures.

In situ hybridization was used to study the effect of IL-1 beta on acidic fibroblast growth factor (aFGF) and basic fibroblast growth factor (bFGF) mRNA expression in rat brain. Intraventricular injection of recombinant human IL-1 beta did not affect hybridization to aFGF mRNA but did induce significant and widespread increases in hybridization to bFGF mRNA. IL-1 beta induced increases in bFGF mRNA were bilaterally distributed and appeared to correspond with the distribution of non-neuronal cells. Thus, hybridization was increased in regions of both gray and white matter (e.g., corpus callosum), the ependymal lining of the third ventricle, and the pia matter. In hippocampus of IL-1 beta injected rats, hybridization was markedly increased in the molecular layers but not significantly increased in the neuronal cell layers. Elevations in bFGF mRNA were transient, peaking at 8 h postinjection in most areas. To determine if IL-1 beta effects were independent of activation of the hypothalamo-pituitary-adrenal axis, and to compare the cellular localization of increases in bFGF mRNA expression induced by IL-1 beta and bFGF, the regulation of bFGF expression was also studied in organotypic hippocampal slice cultures. Treatment of cultures with either IL-1 beta or bFGF stimulated the same general distribution of increases in bFGF mRNA as seen after IL-1 beta treatment in vivo with an additional effect on immature neurons within the hilar side of stratum granulosum; hybridization of bFGF mRNA was not increased in association with the more mature neurons of stratum pyramidale or stratum granulosum. Colocalization of bFGF cRNA hybridization with immunostaining for glial fibrillary acidic protein demonstrated that increases in bFGF mRNA induced both by IL-1 beta in vivo and in vitro and by bFGF in vitro were largely associated with astroglial cells. These findings suggest that IL-1 beta induction of bFGF contributes to the coactivation of these substances following various forms of insult to the CNS and initiates a cascade of trophic interactions that regulates processes of glial proliferation, neurotrophic factor expression, and neuroprotection.

Animals↗

PubMedDate not supplied

Neuropeptide Y: a potent inducer of consummatory behavior in rats.

Neuropeptide Y (NPY) is a 36 amino acid peptide with potent cardiovascular effects. In the present study, intraventricular injection of NPY was shown to markedly stimulate feeding and drinking during the illuminated period of the light/dark cycle, a time when rats ingest small amounts of food. It also enhanced nocturnal food and water intake following a 24 hour period of food deprivation and during nocturnal feeding. The NPY induction of food intake was suppressed by the opiate antagonist, naloxone, and by the dopamine antagonist, haloperidol. Phentolamine, an alpha adrenergic antagonist, failed to suppress NPY-induced feeding. Based on the maximum quantity of food which was ingested following central administration of NPY, this peptide appears to represent one of the most potent stimulators of feeding yet to be described.

Animals↗

PubMedDate not supplied

Prostaglandin D2 stimulates vasoactive intestinal polypeptide release into rat hypophysial portal blood.

The effect of prostaglandin D2 (PGD2) on vasoactive intestinal polypeptide (VIP) release from the hypothalamus was examined by determining plasma VIP levels in rat hypophysial portal blood. Intraventricular injection of PGD2 (5 micrograms/rat) caused a 3-fold increase in the concentration of plasma VIP in hypophysial portal blood in anesthetized rats. A PGD2 metabolite, 13,14-dihydro-15-keto PGD2, did not affect VIP levels in portal blood. The flow rate of hypophysial portal blood was not changed after the injection of PGD2. The intraventricular injection of PGD2, but not PGD2 metabolite, resulted in an increase in peripheral plasma prolactin (PRL) levels in the rat. These findings suggest that PGD2 plays a stimulatory role in regulating VIP release from the hypothalamus into hypophysial portal blood and causes PRL secretion from the pituitary in rats.

Animals↗

PubMedDate not supplied

The effects of gastric inhibitory polypeptide (GIP) on the release of anterior pituitary hormones.

Several members of the secretin family of hormones have been demonstrated to alter anterior pituitary hormone secretion. Here we report the action of gastric inhibitory polypeptide (GIP) on gonadotropin and somatotropin release. Intraventricular injection of 1 microgram (0.2 nmole) GIP (2.5 microliters) produced a significant decrease in plasma FSH at 30 (p less than 0.02) and 60 min after its injection (p less than 0.01). The FSH-lowering effect of a higher dose of 5 micrograms (1 nmole) of GIP was already developed at 15 min (p less than 0.01) and was prolonged until the end of the experiment (60 min, p less than 0.05). No change in plasma LH was detected at any time during the experimental period. If 5 micrograms of estradiol-benzoate were given SC 48 hr prior to experiment, the initial values of FSH and LH were markedly decreased. In these animals GIP failed to influence plasma FSH and LH. When dispersed anterior pituitary cells from OVX rats were cultured overnight and incubated in vitro with GIP, the peptide was found to induce both FSH and LH release. Highly significant release occurred with the lowest dose tested of 10(-7) M and there was a dose-response effect for both hormones. The slope of the dose-response curve was similar for both FSH and LH release. GIP was less potent than LHRH which produced a greater stimulation of both FSH and LH release at a dose of 10(-9) M than did 10(-7) M GIP. The two peptides had an additive effect on the release of both FSH and LH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗