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Results for “Injections, Intraventricular”

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PubMed1990

Destruction of the hamster serotonergic system by 5,7-DHT: effects on circadian rhythm phase, entrainment and response to triazolam.

The role of the serotonergic system in the regulation of hamster circadian rhythms was analyzed using intraventricular injection of the selective neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). Sixty days after 5,7-DHT administration, immunoreactive serotonin in the forebrain, particularly the suprachiasmatic nuclei and intergeniculate leaflets, was severely depleted in 16 animals, moderately depleted in four and only slightly affected in four. 5,7-DHT produced an immediate and sustained advance of the onset of running wheel activity relative to the 24 h light-dark (LD) cycle. Activity onset occurred 0.7 +/- 0.07 h before lights out among 5,7-DHT-treated animals compared with 0.18 +/- 0.04 h after lights out for vehicle-infused controls. This new, advanced phase angle of entrainment was maintained throughout the 60-day period of the study while the animals remained in a LD cycle, including after an 8-h phase advance of the light cycle. 5,7-DHT treatment also delayed the offset of wheelrunning in 16 of 24 animals and reduced the likelihood of a smooth pattern of reentrainment to the shifted LD cycle. The drug treatment did not affect circadian period in constant darkness, the rate of reentrainment to an 8-h phase advance or the amount of wheelrunning activity per day. In addition, 5,7-DHT treatment had no effect on the ability of triazolam, a short-acting benzodiazepine, to accelerate the rate of reentrainment to an 8-h phase advance. These observations show that ascending projections of midbrain raphe serotonin neurons participate in the regulation of the circadian activity phase but are not required for triazolam-induced acceleration of reentrainment to a phase-advanced LD cycle.

5,7-Dihydroxytryptamine↗

PubMed1991

The amnesic substance 2-deoxy-D-galactose suppresses the maintenance of hippocampal LTP.

Male Wistar rats were intraventricularly injected with 2-deoxy-D-galactose (do-gal), a substance interfering with the fucosylation of glycomacromolecules and impairing memory consolidation in various learning tasks. Do-gal was found to have no influence on the monosynaptically evoked field potential (MEFP) recorded in the dentate gyrus upon stimulation of the perforant pathway. However, hippocampal long-term potentiation (LTP) induced in do-gal-pretreated animals by fractionated tetanization of the perforant pathway declined to control levels 2 h after tetanization, whereas it remained constant for 24 h in saline-treated rats. Similar effects were observed in the CA1 region of hippocampal slices. The results indicate a participation of fucosylated macromolecules in the maintenance of LTP. The possible significance of processes involved in LTP for memory formation is discussed.

Amnesia↗

PubMed1991

NMDA antagonists attenuate hypertension induced by carotid clamping in the rostral ventrolateral medulla of rats.

The purpose of these experiments were to study the interactions of N-methyl-D-aspartate (NMDA) with baroreceptor reflexes induced by transient carotid clamping. Adult male Sprague-Dawley rats were anesthetized with urethane. Bilateral common carotid artery occlusion resulted in a reversible and reproducible hypertension in the vagotomized animals. This hypertensive reaction was blocked by intraventricular injection of NMDA antagonists, such as 2-amino-7-phosphono-heptaneoate (AP-7) and phencyclidine (PCP). We also found that blood pressure-sensitive neurons of the rostral ventrolateral medulla (RVLM) could be classified into two groups, on the basis of their responses to norepinephrine given intravenously. Using pressure microejection and single unit recording, we observed that clamping of the common carotids resulted in excitation of type I neurons. This evoked excitation, similar to that induced by NMDA, was blocked by locally applied AP-7. However, the carotid occlusion-induced responses of type II neurons were not blocked by AP-7. In conclusion, the present data suggest that NMDA receptors are involved in hypertensive responses during carotid occlusion, perhaps involving a site in the rostral ventrolateral medulla.

2-Amino-5-phosphonovalerate↗

PubMed1991

Beta-funaltrexamine (beta-FNA) decreases deprivation and opioid-induced feeding.

We studied the effect of the mu antagonist, beta-funaltrexamine (beta-FNA) on deprivation and opioid-induced feeding. Intracerebroventricular pre-treatment of 20 h deprived rats with 0.1, 1, 10 and 20 nmol of beta-FNA decreased feeding by 24%, 50%, 50% and 38% during the first hour. Central administration of beta-FNA (0.1, 1 and 10 nmol) also decreased feeding induced by the mu opioid agonist, DAMGO by 57%, 60% and 71%. Feeding induced by the delta agonist, DSLET, was decreased by pre-treatment with beta-FNA; but only during the 1-2 h time points, a time when relatively little food was ingested. Intraventricular injection of beta-FNA failed to alter feeding stimulated by the kappa opioid agonist, U-50,488H. These data further substantiate a role for the opioid receptor in deprivation and opioid-induced feeding.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1991

2-Hydroxysaclofen, a potent GABAB receptor antagonist, stimulates luteinizing hormone secretion in female rats.

An intraventricular injection of a potent GABAB receptor antagonist, 2-hydroxysaclofen, elicited luteinizing hormone (LH) secretion in a dose-dependent manner under the negative feedback condition in ovariectomized estrogen-primed rats. Significant reduction of the effect of 2-hydroxysaclofen by baclofen, a selective GABAB agonist, suggested that the antagonist stimulated LH secretion through interaction with the GABAB receptor. These results provide evidence that the endogenous GABA acting at the GABAB receptor plays a physiological role in controlling basal LH secretion.

Animals↗

PubMed1991

The mode of GABAB receptor-mediated inhibition of the preovulatory luteinizing hormone surge in female rats.

In estrogen-primed ovariectomized rats, intraventricular injections of baclofen, a selective GABAB receptor agonist, either delayed, eliminated or disrupted the steroid-induced LH surge, depending on the time and the dose of the agonist injected. The delay in the onset of the LH surge was not due to a phase delay in the circadian clock, since the retarded LH surge, when observed, had a short duration, terminating in the evening simultaneously with the termination of the normal LH surge in control animals. Rather, rapid disruption of the ongoing LH surge after baclofen injection during the surge suggested a direct involvement of the GABAB receptor-mediated inhibitory component in the LH surge mechanism.

Activity Cycles↗

PubMed1992

Protection against dendrotoxin-induced clonic seizures in mice by anticonvulsant drugs.

Various anticonvulsant drugs were evaluated for their ability to protect against clonic seizures induced in mice by intraventricular injection of the K+ channel blocking peptide dendrotoxin (DTX). Phenytoin, the phenytoin-like anticonvulsant carbamazepine and the broad spectrum drug valproate were effective in this model, whereas the GABA-enhancers diazepam and tiagabine, the NMDA antagonists (+/-)-CPP and (+)-MK-801, the AMPA antagonist NBQX, the antiabsence drug ethosuximide and the Ca2+ channel antagonist nimodipine were inactive. In contrast to the lack of activity of other NMDA antagonists, phencyclidine and ADCI [(+/-)-aminocarbonyl-10,11-dihydro-5H-dibenzo [a,d]cyclohepten-5,10-imine] were potent antagonists of DTX-induced seizures.

Animals↗

PubMed1994

Bromocriptine protects mice against 6-hydroxydopamine and scavenges hydroxyl free radicals in vitro.

Pretreatment with bromocriptine (5 mg/kg, i.p., 7 days) completely protected against the decrease in mouse striatal dopamine and its metabolites induced by intraventricular injection of 6-hydroxydopamine after intraperitoneal administration of desipramine, but similar pretreatment with L-DOPA/carbidopa (75/7.5 mg/kg, i.p., 7 days) showed only partial protective effect. Furthermore, in an in vitro system that generated.OH from FeSO4-H2O2, bromocriptine dose-dependently reduced the number of .OH radicals. These findings indicate that bromocriptine has a neuroprotective effect against neurotoxins such as 6-hydroxydopamine, probably due, in part, to its hydroxyl radical scavenging activity and inhibiting effect on dopamine turnover rate. This suggests that early introduction of bromocriptine in the therapy of Parkinson's disease may be superior to treatment with L-DOPA alone.

Animals↗

PubMed1994

Early response of brain resident microglia to kainic acid-induced hippocampal lesions.

We investigated the early response of microglia with complement and other proteins in well controlled rat central nervous system lesions. A selective neuronal degeneration in the hippocampal CA3 region was induced without direct tissue damage by an intraventricular injection of a small amount of kainic acid. As early as 1 h post injection, complement proteins C1q, C4, and C3 and immunoglobulin(Ig)G were found in the lesioned area. After 2 h, non-specific leakage of other plasma proteins occurred. By 3 h, reactive microglia gathered around the injured pyramidal neurons. Areas surrounding the lesions were depleted, on the other hand, indicating that these reactive microglia had originally resided in and migrated from such vacant areas. Upregulation of ICAM-1 expression by vascular endothelial cells commenced after 6 h. LFA-1-positive leucocytes were, then, accumulated in the vasculature, which was followed by an infiltration of leucocytes into the lesioned brain parenchyma. These results indicate that, following an acute neuronal injury, the response of the humoral factors such as complement proteins and IgG precedes the microglial reaction. Activation of vascular endothelial cells and subsequent infiltration of blood leucocytes occurs much later than the activation and migration of brain resident microglia. The origin of complement proteins and IgG in the lesioned brain parenchyma remains to be determined, although the production of complement proteins by microglia is suggested.

Animals↗

PubMed1995

Role of the cholinergic system in the regulation of neurotrophin synthesis.

Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) are members of the family of neurotrophins that are highly expressed in the adult hippocampus, and to a lesser extent, in the cerebral cortex and olfactory bulb. Since neuronal expression of neutrophins is controlled by some neurotransmitters and there is a topographical correlation between neurotrophin expression and cholinergic terminal distribution from the cholinergic basal forebrain (CBF) neurons in these areas, the question arises as to whether the cholinergic system can also regulate neurotrophin gene expression in the CNS. When CBF neurons were selectively and completely destroyed by intraventricular injection of 192 IgG-saporin, resulting in a cholinergic deafferentation of the hippocampus, cortex, and olfactory bulb, there were no significant changes in NGF, BDNF and/or NT-3 mRNA levels in these areas from 1 week to 5 months after the lesion. These results suggest that afferents from CBF neurons may not play a significant role in maintaining basal levels of neurotrophin gene expression in the adult rat brain under physiological conditions. However, potential cholinergic regulation of brain neurontrophin expression may occur under other circumstances.

Animals↗

PubMed1980

Effects of hemicholinium-3 and choline on hippocampal electrical activity during immobility vs. movement.

Earlier studies have shown that the hippocampal rhythmical slow activity (RSA or theta) which may occur during behavioral immobility (IRSA) is abolished by systemically administered atropine (is atropine-sensitive), although the RSA which accompanies movements, such as walking, running or swimming (MRSA) is atropine-resistant. This study was designed to manipulate brain cholinergic activity in ways other than through the use of postsynaptic receptor antagonists, and to determine the effects of such manipulations on IRSA and MRSA. The IRSA elicited by electrical stimulation of the reticular formation in urethanized rats was severely attenuated by intraventricular injections of hemicholinium-3 (HC-3), a drug which depletes brain acetylcholine. A subsequent systemic injection of choline chloride restored IRSA elicited by electrical stimulation. In contrast, HC-3 had no deleterious effects on the MRSA recorded from freely moving rats. Therefore, atropine-sensitive IRSA is also HC-3 sensitive, and atropine-resistant MRSA is also HC-3 resistant. These results support the hypothesis that there are two pharmacologically distinct neurochemical systems which may produce hippocampal RSA. It is suggested that acetylcholine is necessary for the production of IRSA, but is not necessary for the production of MRSA.

Animals↗

PubMed1977

Decreased anticonvulsant activity of carbamazepine in 6-hydroxydopamine-treated rats.

An intraventricular injection of 6-hydroxydopamine, which produced a marked decrease of catecholamines in the forebrain, significantly lowered the electroconvulsive threshold in rats. The anticonvulsant effect of carbamazepine was also significantly reduced in the animals treated with 6-hydroxydopamine. The results are consistent with the hypothesis that brain catecholamines may play an important role in seizure susceptibility as well as in the anticonvulsant activity of carbamazepine in rats.

Animals↗

PubMed1978

Distinct dopaminergic systems in ACTH-induced grooming.

Excessive grooming behavior induced in rats by intraventricular injection of ACTH1-24 was inhibited by selective pharmacological manipulation of two functionally distinct types of dopaminergic terminals (DAe and DAi) in the neostriatum or the nucleus accumbens. It is concluded that when ACTH1-24 produces the behavioral response it modulates the activity of both the DAe and the DAi systems.

Adrenocorticotropic Hormone↗

PubMed1979

Influence of histamine on the serotonergic system of rat brain.

Both histamine and 4-methylhistamine, after intraventricular injection into normal rats, reduced the levels of serotonin and increased those of 5-hydroxyindoleacetic acid in hypothalamus; after injection into tranylcypromine-treated rats, head twitches were induced which were blocked by antiserotonin agents. 2-Pyridylethylamine, an agonist of histamine H1 receptors, neither influenced serotonin level in hypothalamus nor evoked behavioural changes. It is concluded that injected histamine may release serotonin from the hypothalamus and that this produces the behavioural changes.

Animals↗

PubMed1979

Action of posterior pituitary neuropeptides on the nigrostriatal dopaminergic system.

The effect of vasopressin, oxytocin and the C-terminal tripeptide of oxytocin, prolyl-leucyl-glycinamide (PLG), were tested on rotational behavior, following unilateral 6-OHDA-enduced lesion of the dopaminergic cell bodies in the substantia nigra. Intraventricular injection of lysine8-vasopressin, oxytocin or PLG caused ipsilateral (towards the lesioned side) rotation, as did peripheral administration of amphetamine. Direct local microinjection of the peptides into the substantia nigra on the intact side was without effect. The data suggest that posterior pituitary neuropeptides (vasopressin and oxytocin) caused presynaptic activation of the nigrostriatal dopaminergic terminals.

Amphetamine↗

PubMed1980

The hypotensive effect of centrally administered tyrosine.

Intraventricular injection of 15 microgram L-tyrosine results in a significant reduction in blood pressure in the spontaneously hypertensive rat. An increase in the turnover of norepinephrine as indexed by MOPEG-SO4 is observed concurrently. The data are consistent with the previously suggested depressor role of certain central noradrenergic neurons.

Animals↗

PubMed1980

Modulation of ACTH-induced grooming by [Des-Tyr1]-gamma-endorphin and haloperidol.

Intraventricular administration of ACTH1-24 into the rat induced excessive grooming behavior. This response could be blocked by local administration of of neuroleptics into either the nucleus accumbens or the neostriatum. Local administration of [Des-Tyr1]-gamma-endorphine (LPH62-77) but not alpha-endorphin (LPH61-76) in either the nucleus accumbens or the neostriatum mimicked the effect of the neuroleptics. A second intraventricular injection of ACTH1-24 4 h after the first did not cause excessive grooming suggesting the development of acute tolerance. Both haloperidol and DT-gamma-E reduced the development of acute tolerance to ACTH-induced grooming. It is suggested the DT-gamma-E modulates the dopaminergic activity underlying the display of ACTH-induced excessive grooming.

Adrenocorticotropic Hormone↗

PubMed1982

Differential effects of D-Ala2 analogues of enkephalins on substance P-induced analgesia in rodents.

The systemic administration of subanalgesic doses of [D-Ala2, D-Leu5]enkephalin significantly potentiated the analgesia elicited in rats or mice by intraventricular injection of substance P. On the contrary, systemic administration of low doses of [D-Ala2,Met5]enkephalinamide antagonized the substance P-induced analgesia. The results support the notion of different physiological functions for the enkephalins and suggest an integrated role for enkephalins and substance P in the control of pain at supraspinal levels.

Animals↗