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Results for “Injections, Intraventricular”

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PubMed1984

Intraventricular arginine vasopressin maintains ethanol tolerance.

Tolerance to the hypnotic effect of ethanol in mice is prolonged by once daily intraventricular injections of arginine vasopressin. This action is similar to that reported previously when vasopressin was administered subcutaneously. The results indicate that maintenance of ethanol tolerance by vasopressin is a centrally mediated action of the peptide, and is not due to possible aversive properties of peripherally administered vasopressin.

Analysis of Variance↗

PubMed1984

Influence of clonidine on the ACTH-induced behavioral syndrome.

In male rats, clonidine in a dose range of 1-3000 micrograms/kg i.p. antagonized the stretching-yawning syndrome induced by the intraventricular injection of ACTH-(1-24) (3 micrograms/rat) dose-dependently. On the other hand, the effect of clonidine on ACTH-induced penile erections was potentiation at low doses (5 and 10 micrograms/kg) and inhibition at the highest doses (1000 and 3000 micrograms/kg), the intermediate doses (50 and 100 micrograms/kg) being without effect. There was no relationship between these behavioral effects and the effect on arterial blood pressure.

Adrenocorticotropic Hormone↗

PubMed1984

Depletions of central norepinephrine by intraventricular xylamine in rats.

A series of neurochemical studies evaluated the selectivity of the depletions of norepinephrine produced by intraventricular injections of xylamine. Brain monoamines were assayed by liquid chromatography with electrochemical detection. With ether anesthesia, bilateral injections of 50 or 100 micrograms xylamine reduced hippocampal levels of norepinephrine and serotonin without affecting striatal dopamine or serotonin. The depletion of hippocampal norepinephrine was significant as soon as 24 h. Animals treated with the combination of 20 mg/kg fluoxetine and 100 micrograms xylamine had selective depletions of central norepinephrine with no significant changes in serotonin.

Animals↗

PubMed1987

Effects of pertussis toxin on the alpha 2-adrenoceptor-inhibitory GTP-binding protein-adenylate cyclase system in rat brain: pharmacological and neurochemical studies.

Behavioral excitement and the increase in locomotion were observed in male adult rats four days after an intraventricular injection of 5 micrograms pertussis toxin (IAP). Clonidine (100 micrograms/kg s.c.)-induced locomotor hypoactivity was not observed in animals pretreated with 1 and 5 micrograms IAP. IAP caused a significant (P less than 0.05) decrease in the KD value of [3H]clonidine binding and enhanced GTP (1 microM)-induced decrease in the binding to cortical membranes from rat brain. In addition, the inhibition of adenylate cyclase induced by alpha 2-receptor stimulation (100 microM adrenaline plus 100 microM propranolol) was completely suppressed in the cerebral cortical membranes by IAP pretreatment. It is suggested that the system consisting of alpha 2-receptor, the inhibitory GTP-binding protein (Ni) and adenylate cyclase inhibits some animal behaviors and cyclic AMP formation. Moreover, IAP seems to inactivate Ni, subsequently producing behavioral excitement and it inhibits clonidine-induced sedation.

Adenylate Cyclase Toxin↗

PubMed1991

Central effects of muscarinic agonists and antagonists on hippocampal theta rhythm and blood pressure in the anaesthetised rat.

The in vivo central effects of a range of full and partial muscarinic receptor agonists have been investigated on hippocampal theta rhythm and blood pressure. In the isoflurane-anaesthetised rat, pretreated with N-methylscopolamine, i.v. administration of arecoline, oxotremorine, arecaidine propargyl ester, aceclidine and pilocarpine produced dose-dependent increases in the frequency of hippocampal theta rhythm and blood pressure, with an order of potency of arecoline = oxotremorine = arecaidine propargyl ester greater than aceclidine greater than or equal to pilocarpine. To increase theta wave frequency, pilocarpine showed a low maximum response and possessed antagonist activity against arecoline, indicating that pilocarpine was acting as a partial agonist. AF102B failed to alter blood pressure or theta rhythm. Intraventricular injections of scopolamine and the M1 receptor-selective antagonist, pirenzepine, produced dose-dependent antagonism of the enhanced theta wave frequency and hypertensive response produced by arecoline. The differences in antagonist potency for the two responses was less than 6-fold, which indicated that both the increase in hippocampal theta wave activity and increase in blood pressure may have been mediated through muscarinic receptors of the M1 subtype. Further studies using a wider range of antagonists will be required to confirm this conclusion.

Anesthesia↗

PubMed1993

delta-Opioid receptor-mediated regulation of central dopaminergic neurons in the rat.

Effects of intraventricular injections of the delta-opioid receptor agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) and antagonist 17-cyclopropylmethyl-6,7-dehydro-4,5-epoxy-3,14-dihydroxy-6,7,2',3'-indo l morphinan (naltrindole) hydrochloride were determined on the activities of mesolimbic, nigrostriatal, tuberoinfundibular and periventricular-hypophysial dopaminergic neurons in brains of male rats. Dopaminergic neuronal activity was estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and accumulation of 3,4-dihydroxyphenylalanine (DOPA) after administration of the decarboxylase inhibitor 3-hydroxybenzylhydrazine in regions of the brain (nucleus accumbens, striatum, median eminence) and the intermediate lobe of the pituitary which contain terminals of these neurons. DPDPE produced a dose- and time-related increase in concentrations of DOPAC and accumulation of DOPA in nucleus accumbens and median eminence, but had no effect in striatum or intermediate lobe of the pituitary. Naltrindole hydrochloride had no effect per se, but blocked the ability of DPDPE to increase DOPAC concentrations in nucleus accumbens and median eminence. These results reveal that activation of delta-opioid receptors selectively increases the activities of mesolimbic and tuberoinfundibular but not of nigrostriatal or periventricular-hypophysial dopaminergic neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Agonists for metabotropic glutamate receptors in the rat delay recovery from halothane anesthesia.

Intraventricular injection of (2S,1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV), a potent agonist for metabotropic glutamate receptors, to rats retarded dose-dependently the recovery from halothane anesthesia at a dose range from 30 to 300 pmol/rat. At a dose of 300 pmol/rat, recovery was prolonged up to about 630% of the control. (2S,1'S,2'S)-2-(carboxycyclopropyl)glycine (L-CCG-I) and (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid ((1S,3R)-ACPD) also delayed recovery, but doses much higher than those of DCG-IV were required (about 300 and 1000 times, respectively). These results suggest that some agonists for a certain kind of metabotropic glutamate receptors have a central depressant action in the rat.

Adenylyl Cyclase Inhibitors↗

PubMed1983

Effects of intraventricular curarimimetics on hippocampal electrical activity.

The effects on the hippocampal electroencephalogram (EEG) of intraventricular injections of the nicotinic ligand alpha-Naja naja toxin, and of d-tubocurarine, were studied in rats immobilized with gallamine or anesthetized with urethane. The EEG recordings were taped and processed off-line to calculate power spectra, autocorrelation functions, and averages. In addition, the times at which spike-and-wave complexes appeared were identified and autocorrelation histograms and cross correlations (with the EEG) were made. Naja toxin and d-tubocurarine provoked a 3.5- to 5-Hz theta rhythm in both hippocampi. Higher doses elicited rhythmic epileptic spike and wave complexes which appeared at a preferred phase of theta rhythm. Atropine and medial septal lesions blocked the rhythm and disrupted the rhythmicity of epileptiform activity. We conclude that different neural subsystems sustain the theta rhythm and epileptiform spikes, and discuss the possible mechanisms involved.

Animals↗

PubMed1987

Selective uptake by Purkinje neurons of antibodies to S-100 protein.

Forty-eight hours after intraventricular injection, affinity-purified antibodies to S-100 protein localized in Purkinje cells whereas affinity-purified antibodies to goat immunoglobulin or to bovine serum albumin did not. This selective up-take may account for the susceptibility of some neurons to immunologic insult, and may provide further evidence to support hypotheses which invoke autoimmune mechanisms in the pathogenesis of central nervous system disorders.

Animals↗

PubMed1990

Long-term administration of mouse nerve growth factor to adult rats with partial lesions of the cholinergic septohippocampal pathway.

Nerve growth factor (NGF), a neurotrophic factor acting on cholinergic neurons of the basal forebrain, has been proposed as a treatment for Alzheimer's disease. Experimental support for its pharmacological use is derived from short-term studies showing that intraventricular administration of NGF during 2-4 weeks protects cholinergic cell bodies from lesion-induced degeneration, stimulates synthesis of choline acetyltransferase, and improves various behavioral impairments. To investigate the consequences of long-term NGF administration, we tested whether cholinergic cell bodies are protected from lesion-induced degeneration and whether cholinergic axons are stimulated to regrow into the denervated hippocampus following fimbrial transections. We found that intraventricular injections of NGF twice a week for 5 months to adult rats resulted in extended protection of cholinergic cell bodies from lesion-induced degeneration and did not produce obvious detrimental effects on the animals. NGF treatment mildly stimulated growth of cholinergic neurites within the 2-mm area directly adjacent to the fimbrial lesion but it failed to induce significant homotypic growth of cholinergic neurites into the deafferented hippocampus.

Acetylcholinesterase↗

PubMed1995

Destruction of the cholinergic basal forebrain using immunotoxin to rat NGF receptor: modeling the cholinergic degeneration of Alzheimer's disease.

Degeneration of cholinergic neurons in the basal forebrain (CBF) is a prominent neuropathological feature of Alzheimer's disease and is thought responsible for some cognitive deficits seen in patients. An animal model of pure CBF degeneration would be valuable for analysis of the function of these neurons and testing therapeutic strategies. CBF neurons express receptors for nerve growth factor. In order to selectively destroy these neurons, we developed an immunotoxin using monoclonal antibody (192 IgG) to rat NGF receptor (p75NGFr) armed with the ribosome inactivating protein, saporin. In vitro 192-saporin was highly toxic to neurons expressing p75NGFr. Intraventricular injections of 192-saporin destroyed the CBF and impaired passive avoidance learning. These results indicate that 192-saporin treated rats can be used to model a key feature of Alzheimer's disease and that anti-neuronal immunotoxins are a powerful approach to selective neural lesioning.

Alzheimer Disease↗

PubMed1988

Release of a dynorphin A (1-8) degrading enzyme from the spinal cord by intraventricular morphine in the rat.

Intraventricular injection of morphine sulfate, 40 micrograms, released an enzyme from the spinal cord into the perfusate which degraded dynorphin A (1-8) and, to a lesser extent, dynorphin A (1-13) in urethane anesthetized rats. The enzyme did not degrade dynorphin A (1-17), Met-enkephalin, Leu-enkephalin, substance P and neurotensin. This dynorphin A (1-8) degrading enzyme was inhibited by aprotinin, thiorphan, and, to a lesser extent, by bacitracin but was not inhibited by bestatin. A kinetic study of the interaction between dynorphin A (1-8) and aprotinin with the enzyme indicated that it is competitive in nature. The pharmacological significance of the findings is still unknown.

Animals↗

PubMed1988

Effect of taurine on growth hormone and prolactin secretion in rats: possible interaction with opioid peptidergic system.

The effect of taurine on growth hormone (GH) and prolactin (PRL) secretion was investigated in the urethane-alpha-chloralose anesthetized rats, considering the interaction with endogenous opioid peptidergic system. Intraventricular injection of taurine (0.25 and 1.0 mumol) stimulated GH and PRL secretion in a dose-dependent manner. However, 4.0 mumol taurine failed to show these effect. The intravenous infusion of naloxone (4 mg/kg b.w.) completely inhibited both the GH and PRL secretion induced by taurine (1.0 mumol). The combined treatment of taurine (1.0 mumol) and FK33-824 (Met-enkephalin derivative, 100 micrograms/kg b.w., i.v.) significantly increased GH and PRL responses induced by taurine or FK33-824 alone. These results indicate that taurine is an effective stimulator of GH and PRL secretion in rats, and that the mechanism of this action involves the opioid peptidergic system in the hypothalamus.

Anesthesia↗

PubMed1991

Effects of kainate on glucose metabolising enzymes in the brain.

Hexokinase and glucose-6-phosphate dehydrogenase activities were studied in brain regions after intraventricular injection of kainic acid. Hexokinase activity was decreased by 10-15% in various regions while glucose-6-phosphate dehydrogenase activity remained unaltered. Soluble hexokinase activity, which remained the smaller fraction of total hexokinase activity, showed slightly more dramatic decreases of 15-35% compared to normal activities in brain regions. This decrease of hexokinase activity in the cytosolic compartment could partly account for the kainate-induced decreases seen in glucose metabolism.

Animals↗

PubMed1994

Activation of central GABAA receptors suppresses the alteration of plasma catecholamine levels induced by neostigmine or histamine in rats.

We investigated the effects of intraventricular injection of muscimol, the GABAA receptor agonist, on the alteration of plasma epinephrine (E) and norepinephrine (NE) levels induced by neostigmine or histamine in anesthetized rats. Injection of neostigmine (10 nmol) into the third cerebral ventricle increased plasma levels of E more than NE, while histamine (500 nmol) increased plasma levels of NE more than E. Concomitant injection of muscimol (2.5 nmol) with neostigmine or histamine significantly suppressed the alteration of E and NE levels induced by neostigmine or histamine. These findings suggest that activation of central cholinergic neuron stimulates the adrenal medullary response more than the sympathetic nervous system, while activation of central histaminergic neuron stimulates the sympathetic nervous system more than the adrenal medullary response in anesthetized rats. Activation of GABAA receptors in the CNS suppresses these effects.

Animals↗

PubMed1984

Evidence for an involvement of GABA receptors in the mediation of the proconvulsant action of ethyl-beta-carboline-3-carboxylate.

The kinetic characteristics of binding of [3H]-GABA and the pattern of isoniazid-induced convulsions were studied in rats treated with repeated intraventricular injections of ethyl-beta-carboline-3-carboxylate (beta-CCE) (10 micrograms/rat, twice daily for 8 days). Thirty-six hours after the last injection, the total number of binding sites for [3H]-GABA was decreased (25%) in the cerebral cortex and hippocampus. On the other hand, there was no significant difference in the dissociation constant (KD) between beta-CCE and solvent-treated rats. The decrease in binding sites for [3H]-GABA was paralleled by a strong potentiation of the convulsant pattern elicited by isoniazid. The results suggest that the proconvulsant effect elicited by beta-CCE is mediated by the decrease in the total number of binding sites for GABA, secondary to the interaction between beta-CCE and the benzodiazepine receptor coupled to the GABA receptor.

Animals↗

PubMed1987

Central serotonergic influences on renal electrolyte and water excretion.

These studies examined the effects of altered activity or levels of serotonin (5-HT) in the central nervous system (CNS) on renal water and excretion of electrolytes and on arterial blood pressure. Rats were implanted with intracerebroventricular cannulae and then continuously hydrated with a hypotonic solution in order to induce a diuresis. In two separate experimental series, samples of urine were collected before and after intraventricular (i.v.t.) administrations of drug, and the effects on the excretion of sodium were determined. In the first experimental series, 5-HT in the CNS was manipulated by intraventricular administration of p-chloroamphetamine (PCA), an agent known to increase synaptic concentrations of 5-HT. Significant increases in urinary excretion of sodium (UNa V) and the Na/K ratio were observed after the administration of p-chloroamphetamine (200-600 micrograms i.v.t.). p-Chloroamphetamine in large doses also increased blood pressure and antidiuresis. The natriuresis, but not the pressor or antidiuretic responses, were attenuated by pretreatment with either p-chlorophenylalanine, an inhibitor of tryptophan hydroxylase, or fluoxetine, a drug which inhibits the release of 5-HT following the administration of p-chloroamphetamine. Thus, the natriuretic response appeared to be due to a p-chloroamphetamine produced increase of synaptic 5-HT. A further test of the role of 5-HT in the central control of sodium excretion was made in a second experimental series where hydrated rats received intraventricular injections of 5-HT. After direct application of 5-HT to the CNS, significant increases in UNa V and in the Na/K ratio were observed, concomitant with depressor effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Absence of sparing of spatial navigation, skilled forelimb and tongue use and limb posture in the rat after neonatal dopamine depletion.

Depletion of caudate-putamen dopamine (DA) was produced by intraventricular injection of 6-hydroxydopamine (6-OHDA) in three day old rats. When adult, the rats were given cognitive and motor tasks sensitive to adult dopamine depletion, including: tests of cue and place spatial navigation in a swimming pool, a test of skilled forelimb use, requiring reaching for small pellets of food, a test of tongue protrusion, requiring tongue extension to lick mash from a spatula, a test of limb posture, sensorimotor tests of orienting to tactile stimulation and catalepsy. Despite apparent normal physical appearance and locomotor behavior, the rats were impaired on all tasks except orienting to tactile stimulation and catalepsy. There was a significant positive correlation between the degree of impairment on the behavioral tasks and the extent of caudate-putamen dopamine depletion. The results show that sparing of function following neonatal dopamine depletion is selective and incomplete. The results are discussed with respect to the questions of sparing of function following neonatal lesions, the heterogeneous nature of the neonatal depletions and the contributions of dopamine to complex spatial and motor behavior in the rat.

Animals↗