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PubMed1990

Centrally injected neuropeptide Y (13-36) produces vasopressor effects and antagonizes the vasodepressor action of neuropeptide Y (1-36) in the awake male rat.

Intraventricular injections of the Y2 neuropeptide Y (NPY) receptor agonist porcine NPY (13-36) (pNPY (13-36); 25-3000 pmol) produced a dose-dependent increase (up to 14%; ED50 value of 0.3 nmol for overall effects and 0.97 nmol for the peak effects) in mean arterial blood pressure in the awake, unrestrained male rat without affecting heart rate. Furthermore, a subthreshold dose of pNPY (13-36) (25 pmol) counteracted the vasodepressor action of the parent compound pNPY (1-36) (75 pmol), which also acts at NPY receptors of the Y1 type. These results suggest that NPY receptors of the Y1 and Y2 type have opposing actions in central cardiovascular regulation.

Animals↗
PubMed1980

Cerebrospinal fluid antibiotic levels during treatment of shunt infections.

Twenty patients with documented cerebrospinal fluid shunt infections were treated with daily intraventricular injections of methicillin, cephalothin, or gentamicin without removal of the shunt or external ventricular drainage. Periodic determinations of intraventricular antibiotic concentration revealed significant levels in relation to the established minimum inhibitory concentration in all cases.

Adolescent↗
PubMed1988

Carbamazepine inhibits electroconvulsive shock-induced inositol trisphosphate (IP3) accumulation in rat cerebral cortex and hippocampus.

Carbamazepine is used to treat manic-depressive disorder, and is also an anticonvulsant. Rats were injected with this drug 90 min prior to this experiment, when mild inhibition of convulsions took place. Intraventricular injections of 14 muCi [3H]myoinositol were made 20-24 hrs prior to the experiment. Ninety min after intraperitoneal injection of carbamazepine or vehicle, rats were given electroconvulsive shock or sham procedure and sacrificed 30 sec later. Incorporation of radiolabel into inositol lipids and inositol phosphates was analyzed in cerebral cortex and hippocampus. Carbamazepine's effects on the brain inositol lipid cycle, studied here for the first time, showed 1) enhanced labeling in the polyphosphoinositides (carbamazepine-ECS groups showed increases of about 40% in PIP2); 2) decreased [H]IP1 levels; and 3) inhibition of ECS-induced [3H]-IP3 accumulation.

Animals↗
PubMedDate not supplied

Brain malformations caused by retroviral vector-mediated gene transfer of hippocampal cholinergic neurostimulating peptide precursor protein into the CNS via embryonic mice ventricles.

Hippocampal cholinergic neurostimulating peptide precursor protein (HCNP-pp) is a unique multifunctional protein, being not only the precursor of HCNP, which promotes the phenotype development of septo-hippocampal cholinergic neurons, but also the binding protein of phosphatidylethanolamine, ATP, Raf-1 kinase (known as "Raf-1 kinase inhibitory factor" in peripheral organs), and serine protease. We obtained a high-titer retroviral vector harboring HCNP-pp cDNA by the use of a modified packaging cell line and centrifugation, and by injecting it into embryonic mouse ventricles, we investigated the function of its gene product within the central nervous system (CNS). We found that efficient transduction into hippocampal pyramidal neurons can be achieved by injecting the vector into embryonic brain ventricles on embryonic day 14 (E14). Three days after receiving the intraventricular injection of the high-titer HCNP-pp retrovirus vector on E14, the tissues around the ventricles showed an overexpression of HCNP-pp. This was accompanied by a reduced amount of activated MEK and Erk (as analyzed by histochemical and Western blot methods), suggesting that HCNP-pp also regulates the MAP-kinase cascade within the CNS. Surprisingly, mouse brains that received the HCNP-pp retroviral vector showed massive malformation of the hippocampus and cerebellum when examined 30 days after birth. This shows that strictly regulated HCNP-pp gene expression is necessary for the normal development of the mouse brain, and that the moderate overexpression achieved by retroviral vector-mediated gene transfer is sufficient to cause severe abnormality of entire brain structures.

Animals↗
PubMed1994

Intravenous losartan inhibits the increase in plasma luteinizing hormone and water intake produced by intraventricular angiotensin II.

In the presence of sex hormones, intraventricular injection of angiotensin II in female rats increases luteinizing hormone (LH) secretion, and this response is blocked by intraventricular losartan. There is evidence that in doses of 3 mg/kg or more systemically administered losartan blocks brain as well as peripheral AT1 angiotensin II receptors. Therefore, we tested the effect of intravenous losartan, 1 and 10 mg/kg, on the LH response to intraventricular angiotensin II in ovariectomized rats treated with estrogen and progesterone. The larger dose of losartan abolished the LH response. It also produced a marked reduction in the drinking response to intraventricular angiotensin II. The data provide additional evidence that in larger doses, peripherally administered losartan can penetrate the brain, and support the hypothesis that in female rats, the brain renin-angiotensin system plays an excitatory role in the regulation of LH secretion.

Angiotensin II↗
PubMed1980

Inhibition of secretion of luteinizing hormone induced by electrochemical stimulation of the anterior cingulate cortex mediated by a beta-adrenergic mechanism.

Release of LH occurred in ovariectomized, oestrogen-primed rats when the medial preoptic area (mPOA) was electrically stimulated with monophasic square pulses of 1 ms duration (50 Hz, 150 microA, 15 s on and 15 s off for 30 min). Electrochemical stimulation of the anterior cingulate area applied immediately after the first 15 min period of stimulation in the mPOA completely prevented the rise in LH normally observed during the following 15 min. This effect was suppressed either by selective blockade of noradrenaline synthesis with diethyldithiocarbamate, or following systemic or intraventricular injection of the beta-adrenergic blocker, propranolol, whereas it did not change after systemic atropine, pimozide or phenoxybenzamine. Isoprenaline, a beta-adrenergic agonist, injected into the third ventricle of rats stimulated in the mPOA mimicked the effect of the cortical stimulation, this effect was also blocked by propranolol. Intraventricular administration of propranolol or of isoprenaline had no effect on the release of LH induced by the injection of gonadotrophin releasing hormone, showing that their action is not directly on the pituitary gland. Intraventricular injection of noradrenaline, which failed to affect the release of LH induced by stimulation in the mPOA, inhibited this release when animals were pretreated with phenoxybenzamine. On the other hand, the LH-releasing potency of noradrenaline was greatly increased if the beta-receptors were blocked. From these results it may be concluded (1) that inhibition of the secretion of LH evoked by electrochemical stimulation of the anterior cingulate cortex is mediated by an adrenergic mechanism involving a beta-receptor and (2) that noradrenaline exerts an inhibitory effect on the secretion of LH through a beta-receptor in addition to the known facilitatory action through an alpha-receptor.

Animals↗
PubMed1993

Histamine-induced, central nervous system-mediated hyperglycemia is suppressed by atropine in the brain.

We investigated the relationship between histamine and muscarinic cholinergic neurons in central nervous system (CNS)-mediated glucose regulation in anesthetized fed rats. The injection of pyrilamine (5 x 10(-7) mol) into the third cerebral ventricle suppressed the hyperglycemia induced by intraventricular injection of histamine (5 x 10(-7) mol). Ranitidine (5 x 10(-7) mol), however, did not suppress this hyperglycemia. The injection of atropine (5 x 10(-9)-5 x 10(-7) mol) into the third cerebral ventricle suppressed the histamine-induced hyperglycemia in a dose-dependent manner. These findings suggest that histamine induction of CNS-mediated hyperglycemia involves neuronal transmission not only via H1 receptors but also, at least in part, by muscarinic cholinergic neurons.

Animals↗
PubMed2005

Effect of amylin on prolactin release.

OBJECTIVE: Amylin is a 37-amino acid peptide that is secreted from the pancreatic beta cells. This peptide is cosecreted with insulin from the pancreas by glucose. Amylin plays a role in glucose homeostasis and in the regulation of lipid metabolism. Amylin receptors were identified in central nervous system of rats. There is no available data on the effects of amylin on the pituitary hormones secretion. The aim of this study was to evaluate the effect of amylin on prolactin release in vivo and in vitro experiments in male adult Wistar Kyoto rats. METHODS: Amylin in a dose of 1 microg/5 microl was injected intraventricularly (i.c.v) during 5 min. using automatic pump. The control group received 5 microl cerebrospinal fluid. Amylin was injected intravenously (i.v) in a dose of 10 microg in 300 microl 0.9% NaCl. The control group received 300 microl 0.9% NaCl. In vitro experiment was performed in the pituitary cells culture conditions. Amylin was added to pituitary cell culture in a dose of 1, 10, 100 nM. Prolactin concentrations were determined using RIA methods. RESULTS: Central or peripheral administration of amylin caused a significant decrease of serum PRL concentrations as compared with control after 120 min. After 240 minute incubation of the pituitary cells culture with amylin in doses of 10 nM and 100 nM a significant inhibition of the release of PRL was found. However we found that the effect of amylin on the release of PRL depended on dose and time of incubation. A significant increase of PRL level was observed in cultured media in the presence of 1 nM of amylin after 60 min. CONCLUSION: Our results indicate that amylin administrated centrally and peripherally as well in the cell culture inhibits PRL release.

Amyloid↗
PubMed1976

Effects of intraventricular glutamic acid on the acquisition, performance, and extinction of an operant response, and on general activity.

This study was designed to investigate the effects of intracerebral injections of glutamic acid on acquisition and extinction of a bar-press response, performance of that response, and behavior activity. Nineteen food-deprived rats bearing chronic ventricular cannulae were tested in operant conditioning chambers or in an open field. Just prior to each testing session each animal was injected intraventricularly with 10 mul of either normal or acidified saline solution (control groups), or 10 mul of 100 mMol glutamic acid solution. Acquisition of the bar-pressing response by the glutamic acid group was significantly retarded as compared to the control groups, and the responding of the glutamic acid group was suppressed during the beginning of the first few sessions of testing on a fixed-interval schedule and during extinction. Other behavioral measures, such as operant level, performance of the response on a continuous schedule, performance on fixed-interval and extinction schedules except during the start of the first few sessions, and behavioral activity, were either unaffected or only slightly affected. It is concluded that interference with the normal neurophysiological activity of glutamic acid in the central nervous system interferes with learning and suppresses behavioral output in certain situations.

Animals↗
PubMed1975

H3-p-chloroamphetamine: cerebral levels and distribution.

Whole-brain levels of radioactivity were assessed at 0,2,6,12, or 24 hours, 1 1/2,2,7,10, and 14 days after intraventricular injection of H3 -p-CA. Urinary excretion and peripheral distribution were also followed for one week. The rate of elimination of total radioactivity from brain is biphasic with a T 1/2 of 1.2 hours and 2.5 days after intraventricular and 4.2 hours and 1.9 days after intraperitoneal injection of p-CA. The distribution into cerebellum, neocortex, brainstem, and telencephalon was studied at 1 hour, 2,3,5, and 7 days after injection. At both three and seven days, the radioactivity is still present in all the areas of the brain. The contribution of H3-p-CA to total radioactivity in the toluene extractable fraction was measured. By twelve hours, four chromatographically distinct peaks of radioactivity can be isolated from the toluene extract. The radiolabel in the subcellular fractions was also determined. There is a significant shift of radiolabel from the supernatant to organelle-bound phases between three and seven days.

Amphetamines↗
PubMed1976

Central hyperglycemic effect of carbachol in rats.

Intraventricular injection of carbachol produces hyperglycemia in rats at doses which are ineffective when given subcutaneously. This effect is suppressed by intraventricular administration of small amounts of atropine, further supporting the suggestion that the effect of carbachol is due to its action on central cholinergic receptors. Carbachol-induced hyperglycemia is not abolished by adrenalectomy and hypophysectomy, or pretreatment with reserpine.

Adrenal Glands↗
PubMed1993

Activation of GABAA receptor in the brain suppresses neostigmine or histamine-induced central nervous system-mediated hyperglycemia.

We investigated the effect of GABA receptor agonists on the central nervous system (CNS)-mediated hyperglycemia induced by neostigmine or histamine in anesthetized fed rats. The injection of muscimol, GABAA receptor agonist (1, 2.5 nmol) into the third cerebral ventricle suppressed the hyperglycemia induced by intraventricular injection of neostigmine (1 x 10(-8) mol) or histamine (5 x 10(-7) mol). Baclofen, GABAB receptor agonist (1, 2.5 nmol), however, did not suppress these hyperglycemia. Neither muscimol nor baclofen (2.5 nmol) affected plasma glucose levels. These findings suggest that activation of GABAA receptor in the CNS suppresses the hyperglycemia induced by the stimulation of cholinoceptive neuron or histaminergic neuron, but activation of GABAB receptor does not affect them.

Animals↗
PubMed1992

Evidence that nitric oxide modulates drinking behaviour.

The involvement of the L-arginine-nitric oxide (NO) pathway in brain, in the regulation of drinking behaviour, has been evaluated by injecting L-arginine and N omega-nitro-L-arginine methyl ester (L-NAME) into the lateral cerebral ventricle (i.c.v.). L-Arginine (5 and 10 micrograms/rat), but not D-arginine, was antidipsogenic when administered to 24 hr water-deprived rats but did not change the intake of water in normally hydrated rats. However, L-NAME (5 and 10 micrograms/rat) did antagonize the effect of L-arginine in water-deprived animals but, by itself, did not increase thirst. L-Arginine (100 ng), when injected into the preoptic area significantly reduced water deprivation-induced drinking. The same dose was unaffective when given intraventricularly. Finally, L-arginine (5 and 10 micrograms/rat, i.c.v.) inhibited drinking induced by intraventricular injection of angiotensin II (250 ng/rat). The effect was dose-dependent. The results indicate that: (1) NO acts as an inhibitory mechanism when thirst is stimulated by water deprivation or by angiotensin II; (2) the preoptic area might be one of the central sites of antidipsogenic action of NO and (3) nitric oxide synthase might be inhibited during water deprivation.

Angiotensin II↗
PubMed1985

Noradrenaline and functional plasticity in kitten visual cortex: a re-examination.

A quantitative re-examination was made of the influence of noradrenergic depletion on the epigenesis of kitten visual cortex. Two methods were used to deplete noradrenaline at the cortical level: stereotaxically controlled injection of 6-hydroxydopamine (6-OHDA) in the coeruleus complex, from which the noradrenergic input to visual cortex arises; intraventricular injection of 6-OHDA. The latter chemical lesion also depleted dopamine levels in the brain. Lesion of the noradrenergic or catecholaminergic systems was performed neonatally or at an age of 3-4 weeks in kittens submitted to five different rearing procedures: normal rearing, dark rearing, monocular rearing, monocular exposure following dark rearing and monocular deprivation following normal rearing. Forty-two kittens between 3 and 12 weeks of age were used for this biochemical and electrophysiological study. Noradrenaline and dopamine levels were measured by a radioenzymatic method in the primary visual cortex of twenty-six kittens. A total of 1263 cells were recorded in area 17 of twenty-six kittens. Combined biochemical and electrophysiological data were obtained in ten 6-OHDA-lesioned kittens. Whatever the mode of chemical lesion used, cortical noradrenergic depletion failed to block either maturation or vision-dependent processes which are known to affect orientation selectivity and/or ocular dominance during the critical period. However, in some cases, the amplitude of the epigenetic functional modifications was slightly reduced in 6-OHDA-treated kittens. The cortical effects of monocular deprivation starting from the age of 5 weeks were studied quantitatively both in lesioned and intact kittens. Disappearance of noradrenaline in area 17 did not prevent the loss of binocularity in cortical cells. However, even when monocular occlusion had been maintained for 2 or 3 weeks in 6-OHDA-treated kittens, ocular dominance shifts were limited to a stage equivalent to that observed in the intact kitten after 5-8 days of monocular occlusion. The amplitude of this partial protective effect was found to be unrelated either to the delay following the chemical lesion, or to the level of noradrenaline remaining in lesioned kitten cortex. Although a putative gating role of noradrenaline cannot be excluded in the development of the intact animal, this report shows that its presence is not required for functional plasticity to occur in kitten area 17.

Animals↗
PubMed1983

Histamine-induced prolactin release: pharmacological characterization of receptors in male rats.

Studies were undertaken to investigate the nature of receptors involved in the prolactin-releasing action of histamine in male rats. The increase of plasma prolactin levels induced by third-ventricle injection of histamine was blocked by intraventricular injection of ranitidine, an H2-antagonist, but not by systemic administration of mepyramine, an H1-antagonist. The H2-histamine agonists 4-methylhistamine and Dimaprit, given intraventricularly in unrestrained and ether-anesthetized rats, enhanced prolactin release. The effect of 4-methylhistamine was dose-dependent, whereas Dimaprit had opposite effects depending on the dose. In low doses, Dimaprit decreased whereas in higher doses it increased plasma prolactin levels. The stimulatory effects of both agonists, similar to those produced by histamine itself, were blocked by metiamide (H2-antagonist), but not by intraventricular mepyramine. High doses of mepyramine only partially decreased the effects of 4-methylhistamine. Ranitidine was able to prevent the prolactin response to 4-methylhistamine. The selective H1-histamine agonist 2,2-pyridylethylamine had no action on prolactin release. 2-Methylhistamine, which exhibits predominantly H1-mediated actions, increased the release of prolactin. Its effect, however, was blocked by low doses of metiamide and was obtained at higher concentrations than 4-methylhistamine. Mepyramine prevented 2-methylhistamine action only at high doses. It is concluded that the increased release of prolactin evoked by histamine in male rats is mainly due to its action on H2-receptors. In addition, the results altogether indicate that H1-receptors have not a significant participation.

Anesthesia↗
PubMed1982

Effects of the convulsant methionine sulfoximine on striatal dopamine metabolism.

Experiments were conducted to investigate the effects of the convulsant L-methionine-DL-sulfoximine (MSO) on striatal dopamine (DA) metabolism. Intraventricular injections of MSO produced a transient increase in striatal DA release followed by inhibition of DA release for up to 3 days, which paralleled the inhibition by MSO of the enzyme glutamine synthetase (GS). DA synthesis was decreased for up to 24 h after injection of MSO, but returned to normal within 3 days after MSO administration. Intrastriatal injections of MSO produced a pronounced decrease in striatal DA release and inhibition of striatal GS activity 24 h postinjection but, unlike intraventricular MSO, did not produce behavioral convulsions. Glutamate-DA interactions may be responsible for the observed effects.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Stimulant and convulsive effects of kynurenines injected into brain ventricles in mice.

Each of six kynurenines tested (DL-kynurenine, quinolinic, 3-hydroxy-anthranilic, xanthurenic, picolinic, and nicotinic acids) injected into brain ventricles in mice in doses of 25--60 mcg produced motor excitement and/or clonic convulsions. Anthranilic acid did not produce these effects. The strongest metabolite was quinolinic acid, which was active in a dose of 1 mcg. It was also the only compound which produced motor excitement and convulsions after intraperitoneal injection (in doses of 400--600 mg/kg, i.e. 10,000--15,000 mcg per mouse). The hypothermic effect of intraventricularly-injected kynurenines was roughly similar to that of intraperitoneally-injected material at 100--1000 times higher doses. These data suggest poor penetration of kynurenines formed in the liver into the brain, and the possible involvement of these metabolites of tryptophan (particularly if they are formed inside the brain) in the mechanism of seizures.

Animals↗
PubMed1979

Intraventricular 2-deoxyglucose, glucose, insulin, and free fatty acid mobilization.

The possibility of eliciting changes in the activity of lipomobilizing centers in the rat central nervous system was investigated by injecting glucose or substances that affect glucose metabolism directly into the cerebrospinal fluid of conscious, unrestrained rats. Intracerebroventricular administration of minute amounts of 2-deoxyglucose to fed rats induced a rapid increase in the concentration of plasma free fatty acids (FFA) without affecting plasma insulin levels. Furthermore, small amounts of either glucose or insulin injected intraventricularly reduced the increased plasma FFA levels of normal fasted rats without affecting the glycemia or plasma insulin levels in these animals. In diabetic rats, the increased levels of plasma FFA were not affected by intraventricular administration of glucose, but clearly decreased after intraventricular insulin. The results suggest that the lipomobilizing centers are insulin sensitive and that their activity is modulated by the rate of glucose uptake, rather than by external hexose concentration. The data are also consistent with our previous hypothesis of a direct control of the sympathetic tonus of adipose tissue by these centers.

Adipose Tissue↗