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At least 649 records · Page 36Linked to original sources
PubMed1984

[Effect of cerebral intraventricular administration of 5,6-dihydroxytryptamine and 5,7-dihydroxytryptamine on the cyclic secretion of corticosterone in the rat].

The effect of two potent neurotoxic agents for 5HT neurons, 5,6-DHT and 5,7-DHT, intraventricularly injected, has been studied on the values and rhythm of plasmatic corticosterone secretion in the male Wistar rat model, along an entire day: 4 a.m., 8 a.m., noon, 5 p.m. and midnight. The dose administered for each drug was 100 micrograms/animal in a single injection. The levels of corticosterone were determined 15 and 30 days post-injection. The effects observed for both drugs were similar at similar times: highly significant decreases in all the studied points which fall under the same line of secretion and evince an absolute inhibition of the cyclic rhythm. There are no significant differences among the values obtained with different drugs at various times. The contents of NA and 5HT significantly decrease for both drugs especially those of the 5HT on the 15th day. 30 days after the injection there is a small recovery of 5HT, but differences with control values are still significant. On the other hand the recovery of NA was almost total (near 100%). The results are discussed within the highly controversial frame of the influence of central 5HT neurons on the various types of secretion of the hypothalamic-pituitary-adrenal axis. The data obtained with this "chronic model" are confronted with those from other authors who have used drugs with transitory effect on the 5HT brain metabolism.

5,6-Dihydroxytryptamine↗
PubMed1984

Changes in the incorporation of [3H]leucine into proteins of rat hippocampus subregions during the acquisition of a brightness discrimination are lateralized.

The incorporation of intraventricularly injected L-[4,5-3H]leucine into proteins of rat hippocampus subregions ("CA 1", "CA 3" and "Ca 4/area dentata") was studied during the acquisition of a footshock-motivated brightness discrimination. In passive controls, protein synthesis rates in CA 3 was significantly increased over those of CA 1 and CA 4/area dentata. Moreover, in left CA 3 L-leucine incorporation rates were significantly elevated when compared to those of the controlateral side. These differences between hippocampus subregions and left and right CA 3 were found to be not dependent on the technique of L-leucine application, but left-right differences did not exist under in vitro conditions. During training, protein synthesis rate in right CA 3 was increased by about + 30% (p less than 0.05) over that of active or passive controls. The trend in CA 1 was not significant. Protein labelling in left hippocampal subregions and, in addition, right CA 4/area dentata exhibited no differences between trained and non-trained animals. Pretreatment of rats with uridine-5'-phosphate improving long-term memory formation resulted in an augmentation of L-leucine incorporation into proteins of CA 1 and CA 3 of trained animals when compared to controls, whilst in other hippocampal subregions no differences in incorporation rates were found between trained and nontrained rats. The present data provided evidence for a hemispheric asymmetry of training-induced changes in protein synthesis in CA 1 and CA 3 of rat hippocampus.

Animals↗
PubMed1981

Studies on the behavioral and hypotensive effects of intraventricular prostacyclin (PGI2) in rats.

Intraventricular injection of prostacyclin (PGI2) slightly depressed the general behavior and produced a weak hypothermia in rats. It shortened the response to a thermal nociceptive stimulus and intensified catalepsy caused by chloropromazine and haloperidol. PGI2 did not change concentration of noradrenaline, 4-hydroxytryptamine, 5-hydroxyindoleacetic acid and dopamine in different brain areas. It markedly lowered blood pressure and increased respiration. The duration of central hypotensive effect of PGI2 was shortened after 6-hydroxydopamine on 5,6-dihydroxytryptamine pretreatment. The possible involvement of a central mechanism in the hypotensive action of PGI2 requires further clarification.

Animals↗
PubMed1981

[Technique for intraventricular application of antibiotics in bacterial meningitis of the newborn (author's transl)].

A new technique for intraventricular application of antibiotics by means of an indwelling catheter is described for the treatment of bacterial meningitis in the newborn. In cases of neonatal gram-negative meningitis with proven ventriculitis resistant to systemic therapy alone, a ventricular tap is performed. Through the needle an indwelling catheter is inserted into the right lateral ventricle. After removal of the needle the remaining catheter is used for obtaining ventricular fluid for diagnostic purposes as well as for direct intraventricular injection of antibiotics. This catheter can easily be inserted while the child is in the incubator in a neonatal intensive care unit, avoiding neurosurgery. Our present treatment procedure for neonatal meningitis is described.

Ampicillin↗
PubMed1980

Effect of kynurenine and quinolinic acid on the action of convulsants in mice.

Intraventricular injection of DL-kynurenine and L-kynurenine sulfate (40 microgram) into conscious mice potentiated convulsions and lethality produced by strychnine (1 mg/kg) and not by thiosemicarbazide nor pentylenetetrazol. Another metabolite of tryptophan with convulsive effect, quinolinic acid, was ineffective. Intraperitoneal injection of DL-kynurenine sulfate and quinolinic acid (25-100 mg/kg) was associated with prolongation of the latency of strychnine and thiosemicarbazide (only the former drug) seizures. Nicotinic, picolinic, and anthranilic acids (100 and 250 mg/kg) did not modify the action of convulsants. Data and suggestions about probable involvement of brain glycine and gamma-aminobutyric acid receptors in the convulsive action of kynurenines is discussed.

Animals↗
PubMedDate not supplied

[The electroencephalographic effects of GABA when using perfluorocarbon emulsions in rats].

Awake and freely moving rats were used to study the electroencephalographic effects of GABA administered into the lateral ventricle of the brain during preliminary central and peripheral use of emulsions of organoperfluorine compounds (OPFC). The central (intraventricular) injections of OPFC emulsion and the surfactant proxanol used in it were demonstrated to inhibit the effects of GABA. The peripheral (intravenous) injection of the emulsion caused no changes in the electroencephalographic effects of GABA.

Animals↗
PubMed1994

[The central mechanism of feeding-associated circadian corticosterone rhythm in rats: analyses of paraventricular noradrenaline by in vivo microdialysis].

A prefeeding peak of plasma corticosterone level in rats under a periodic feeding schedule is controlled by a food-entrainable circadian rhythm, an oscillatory mechanism of which is located outside of the suprachiasmatic nucleus. A stimulatory role of the catecholaminergic neurons innervating the paraventricular nucleus (PVN), where the corticotropin releasing hormone (CRH) producing neurons are located, have been suggested in the expression of the hormone peak. A periodic feeding schedule with free-access to meal from 10 to 12 (14) hour was imposed on male Wistar rats for 2-3 weeks under the light-dark cycle. Prefeeding peaks of plasma corticosterone and wheel running activity that appear during a 3 day food deprivation after the periodic feeding schedule were suppressed by the intraventricular injection of 6-OHDA, a catecholamine deprivator. The release of endogenous noradrenaline in the vicinity of PVN was measured by means of in vivo microdialysis. A 24 hour variation of noradrenaline release was observed in rats under ad libitum feeding with a peak in the dark period. On the other hand, under periodic feeding noradrenaline release was significantly increased prior to daily meal, and decreased after meal intake. And the noradrenaline release was also enhanced during the time of previous meal feeding when food was deprived for 3 days after the periodic feeding schedule. The finding indicates that the central noradrenergic neurons innervating the PVN mediates the food-entrainable circadian oscillation to the hypothalamus-pituitary-adrenocortical axis as well as the locomotor activity.

Animals↗
PubMedDate not supplied

[The effect of new ACTH fragments on the behaviors of self-stimulation, avoidance and grooming in rabbits].

We studied the influence of new cyclic analogues of ACTH fragments EHFRWGKPVG-NH2 and KHFRVG-NH2 on self-stimulation (SS) and active avoidance (AA) behaviour. Intraventricular injection of EHFRWGKPVG-NH2 in low doses (0.5-2.5 mcg) was shown to increase, that in higher doses (4-5 mcg) to decrease SS frequency. Injection of KHFRWG-NH2 in doses of 0.1-5 mcg resulted in 25-30% decrease of SS frequency during the first 15 min, its subsequent return to the background level and repeated decrease. In 24-48 h SS was 5-8% higher than the background level and practically was unchanged in the course of 2 h of experiment. When testing AA behaviour EHFRWGKPVG-NH2 in doses of 0.5-2 mcg induced twice shorter "anxiety time" and longer latency of AA. Both fragments (0.1-5 mcg) evoked excessive grooming. These effects persisted for 24-72 h. The role of the cyclic analogues of ACTH fragments in the mechanisms of positive and negative reinforcement is discussed.

Adrenocorticotropic Hormone↗
PubMed1993

[Protective effect of nerve growth factor on cholinergic neurons corpus striatum of new born rat subjected to hypoxia-ischemia].

Cerebral hypoxia-ischemia was produced in 7 day old rats by right common carotid artery occlusion combined with systemic hypoxia. In the hypoxic-ischemic group animals, striatal ACh contents on both sides were reduced to a significant extent in commensurate to AChE histochemical image analysis. All these changes could be restored to normal control by a protection dose (50 micrograms) of NGF intraventricularly injected.

Acetylcholine↗
PubMedDate not supplied

[A comparative analysis of the effects of the systemic and intraventricular administration of serotonin antibodies on the behavioral reactions and nociceptive sensitivity in animals].

The antibodies to serotonin modulate behavioural reactions of animals depending on the mode of administration (intracerebroventricular or intraperitoneal) and the testing time. Intraventricular injection induces inhibition of behavioural activity within 1--2 hours. Systemic injection produces a biphasic effect on the serotoninergic system, i. e., the activation in the early period and the steady inhibition later. Effects of the intraperitoneally injected serotonin antibodies on the CNS are probably mediated either by serotonin binding in blood or by involvement of neurotrophic factors of the immune system. Both ways of administration of the serotonin antibodies result in late hyperalgesia.

Animals↗
PubMed1983

Interaction between renin-angiotensin system and cholinergic system in brain.

Intracerebroventricular (i.c.v.) injection of hemicholinium-3 (HC-3; 20 micrograms), which depletes acetylcholine stores in brain, reduced the increase in mean arterial pressure (MAP) and the drinking, but not the decrease in heart rate (HR), induced by intraventricular injection of angiotensin II (ANG II, 50 and 100 ng) in conscious rats. Intraventricular injection of atropine (up to 1 microgram) decreased only the pressor effect, while larger doses (up to 10 micrograms) decreased the bradycardia, too. Mecamylamine (100 micrograms i.c.v.) reduced the pressor response induced by angiotensin, without influencing the decrease in heart rate. A dose of 50 micrograms of mecamylamine had no effect. Neither atropine (10 micrograms i.c.v.) nor mecamylamine (50 micrograms i.c.v.) affected thirst induced by angiotensin. Intravenous (i.v.) atropine, but not atropine methylbromide, strongly reduced the drinking effect. The increase in arterial pressure and the decrease in heart rate induced by intraventricular injection of physostigmine, as well as the drinking behaviour after carbachol (250 ng, i.c.v.) or the increase in arterial pressure following intravenous injection of physostigmine (in methylatropine-pretreated rats), were not influenced by either saralasin (up to 10 micrograms/kg, i.c.v.) or captopril (up to 50 micrograms, i.c.v.). These results suggest that: (1) the increase in mean arterial pressure and drinking behaviour, induced by intraventricular injection of angiotensin II, are partially mediated via acetylcholine in brain, acting through muscarinic receptors; (2) decrease in heart rate induced by angiotensin II is not baroreceptor reflex-mediated; (3) the brain renin-angiotensin system does not participate in the cardiovascular and behavioural effect induced by cholinergic stimulation in the brain.

Angiotensin II↗
PubMed1975

An evaluation of the use of intraventricularly administered [3H]5-hydroxytryptamine as a marker for endogenous brain 5-hydroxytryptamine.

Following the intraventricular injection of a small amount of [3H]5-hydroxytryptamine ([3H]5-HT), the amount of radioactivity in telencephalic structures on the injected side was 6--7 times larger than that in corresponding areas on the opposite side. Moreover, a multiphasic disappearance of [3H]5-HT from whole brain or midbrain was found after the intraventricular injection of the labeled amine. However, after the intraventricular injection of [3H]tryptophan, the levels of [3H]5-HT in midbrain declined in a monophasic manner. A significant portion of the labeled amine derived from intraventricularly administered [3H]5-HT was resistant to the depleting effect of Ro4-1284 or to that elicited by destruction of the midbrain raphe nuclei, both of which caused an almost complete loss of endogenous 5-HT and labeled 5-HT formed from tryptophan. It thus appears that the intraventricular injection of [3H]5-HT leads to the formation of artifactual pools which are not present if the amine is synthesized in vivo. Studies with 6-hydroxydopamine suggested, however, that uptake of [3H]5-HT into adrenergic neurons did not occur to any great extent.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed2005

Central injection of hypertonic saline activates angiotensin II-sensitive neurons in the anterior hypothalamic area of rats.

We have previously reported that microinjection of angiotensin II into the anterior hypothalamic area (AHA) produces pressor responses and that angiotensin II-sensitive neurons in the AHA are tonically activated by endogenous angiotensins in rats. Central injection of hypertonic saline causes pressor responses via release of angiotensins in brain. In this study, we examined whether angiotensin II-sensitive neurons in the AHA are responsive to intracerebroventricular injection of hypertonic saline and whether endogenous angiotensins in the AHA are involved in the central hypertonic saline-induced pressor response. Male Wistar rats were anesthetized and artificially ventilated. Extracellular potentials were recorded from single neurons in the AHA. Intraventricular injection of hypertonic saline increased the neural activity of angiotensin II-sensitive neurons, whereas pressure application of hypertonic saline onto angiotensin II-sensitive neurons themselves did not affect their neural activities. The intraventricular hypertonic saline-induced increase of unit activity of AHA neurons was inhibited by pressure application of the angiotensin AT1 receptor antagonist losartan onto the same neurons. The hypertonic saline-induced increase of unit firing was also blocked by intraventricular injection of the amiloride-sensitive sodium channel blocker benzamil. In conscious rats, intraventricular injection of hypertonic saline produced pressor responses, and the hypertonic saline-induced pressor response was inhibited by bilateral microinjection of losartan into the AHA. Repeated intraventricular injection of hypertonic saline caused an increase in the release of angiotensins in the AHA of anesthetized rats. These findings indicate that intracerebroventricular injection of hypertonic saline increases neural activity of angiotensin II-sensitive neurons trans-synaptically via endogenous angiotensins in the AHA. In addition, these findings also indicate that the intracerebroventricular injection of hypertonic saline produces a pressor response at least partly via release of angiotensins in the AHA.

Action Potentials↗
PubMed1988

Biotin transport and metabolism in the central nervous system.

The mechanisms by which biotin enters and leaves brain, choroid plexus and cerebrospinal fluid (CSF) were investigated by injecting [3H]biotin either intravenously or intraventricularly into adult rabbits. [3H] biotin, either alone or together with unlabeled biotin was infused at a constant rate into conscious rabbits. At 180 minutes, [3H]biotin had entered CSF, choroid plexus, and brain. In brain, CSF, and plasma, greater than 90% of the nonvolatile 3H was associated with [3H]biotin. The addition of 400 mumol/kg unlabeled biotin to the infusion syringe decreased the penetration of [3H]biotin into brain and CSF by approximately 70 percent. Two hours after an intraventricular injection, [3H]biotin was cleared from the CSF more rapidly than mannitol and minimal metabolism of the [3H]biotin had occurred in brain. However, 18 hours after an intraventricular injection, approximately 35% of the [3H]biotin remaining in brain had been covalently incorporated into proteins, presumably into carboxylase apoenzymes. These results show that biotin enters CSF and brain by saturable transport systems that do not depend on metabolism of the biotin. However, [3H]biotin is very slowly incorporated covalently into proteins in brain in vivo.

Animals↗
PubMed1986

Pantothenic acid transport and metabolism in the central nervous system.

The mechanisms by which pantothenic acid (PA) enters and leaves brain, choroid plexus, and cerebrospinal fluid (CSF) were investigated by injecting [3H]PA either intravenously or intraventricularly into adult rabbits. [3H]PA, either alone or together with unlabeled PA, was infused at a constant rate into conscious rabbits. At 180 min, [3H]PA readily entered CSF, choroid plexus, and brain. In brain, CSF, and plasma, greater than 90% of the 3H was associated with [3H]PA. The addition of 200 mumol/kg PA to the infusion syringe decreased the penetration of [3H]PA into brain and CSF by approximately 70%. Two hours after the intraventricular injection of [3H]PA, [3H]PA was rapidly cleared from the CSF by a probenecid-sensitive mechanism. No metabolism of the [3H]PA occurred in brain. However, 18 h after the intraventricular injection of 37 microCi (34 nmol) of [3H]PA, approximately 40% of the 3H remaining in forebrain was converted to [3H]CoA. These results show that PA enters and leaves CSF and brain by saturable transport systems. However, [3H]PA is very slowly converted to [3H]CoA in brain in vivo.

Animals↗
PubMed1977

Simple and compact cannula system for mice.

A small and simple device is described for applying substances to the brain of freely moving mice. The effectiveness of the technique was evaluated by intraventricular injections of d-amphetamine sulfate. It was observed that intraventricular injections of d-amphetamine (50-200 microgram) produced a dose dependent increase in activity.

Animals↗
PubMed1992

Nerve growth factor (NGF) prevents the shift in ocular dominance distribution of visual cortical neurons in monocularly deprived rats.

The hypothesis that NGF could play a role in the plasticity of the developing mammalian visual cortex was tested in monocularly deprived (MD) rats. In particular, we have asked whether an exogenous supply of NGF could prevent the changes in ocular dominance distribution induced by monocular deprivation. Hooded rats were monocularly deprived for 1 month, starting at postnatal day 14 (P14), immediately before eye opening, by means of eyelid suture. In eight rats, only monocular deprivation was performed; in eight rats, monocular deprivation was combined with intraventricular injections of beta-NGF, and in three rats, with intraventricular injections of cytochrome C. Injections (2 microliters) were given every other day for a period of 1 month. Single neuron activity was recorded in the primary visual cortex of MD rats, MD rats treated with NGF, and MD rats treated with cytochrome C at the end of the deprivation period, and in normal rats of the same age. We found that monocular deprivation caused a striking change in the ocular dominance distribution of untreated MD rats, reducing binocular cells by a factor of two and increasing by a factor of eight the number of cells dominated by the nondeprived eye. In MD NGF-treated rats, the ocular dominance distribution was indistinguishable from the normal. Cytochrome C treatment was completely ineffective in preventing the ocular dominance shift induced by monocular deprivation. To test whether NGF affected cortical physiology or interfered with transmission of visual information, we evaluated in NGF-treated rats the spontaneous discharge and the orientation selectivity. We found these functional properties to be in the normal range. We conclude that NGF is effective in preventing the effects of monocular deprivation in the rat visual cortex and suggest that NGF is a crucial factor in the competitive processes leading to the stabilization of functional geniculocortical connections during the critical period.

Animals↗
PubMedDate not supplied

[Incorporation of labeled sex hormones into the ependyma of the mediobasal hypothalamus of rats after intraperitoneal and intraventricular administration].

Histoautoradiography was used to demonstrate the ability of ependyma element of the 3d brain ventricle to incorporate the label after intraperitoneal and intraventricular injection of labeled sexual hormones. The least label incorporation after intraventricular injection of 3H-estradiol and 3H-testosterone and the maximal label incorporation after intraperitoneal injection of 3H-estradiol was demonstrated by beta 1-tanicytes. The basal processes of these cells terminate in the lateral part of the external zone of the median eminence where gonadoliberin is released to the portal capillaries of the hypophysis. The data obtained warrant an assumption that beta 1-tanicytes are responsible for the transport of sexual hormones primarily from the pericapillary space of the median eminence of the hypothalamus to the cerebrospinal fluid, thereby possibly taking part in the regulation of gonadoliberin release to the portal circulation of the hypophysis.

Animals↗