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PubMed1978

Estradiol potentiation of hypothalamic uptake of LH-RH from the CSF.

Ovariectomized (Ovx) rats were treated (s.c.) with estradiol benzoate (E2B) for 7 days, and then 10, 25 or 100 ng LH-RH were microinjected into the 3rd ventricle. Intraventricular LH-RH elevated plasma LH at 10 and 30 min in a dose-response manner. In experiment 2, Ovx rats were treated with E2B or oil for 7 days and then intraventricularly injected with 25 ng LH-RH. Two days later, 100 ng LH-RH were systemically administered. E2B treatment resulted in a greater release of LH in response to the intraventricular administration of LH-RH but not to the systemic injection. A direct measure of median eminence (ME) uptake of LH-RH was used in experiment 3. Ovx-E2B or oil-treated rats were decapitated 10 min after intraventricular injection of 125I-LH-RH, 125I or 3H-glycine. The ME region of the hypothalamus, cortex, anterior pituitary (AP) and plasma were solubilized and their radioactivity determined. E2B increased the radioactivity in the ME following injection of 125I-LH-RH but not in other tissues. Tissue uptake of 125I and 3H-glycine were similar in E2B or oil-treated rats. These data indicate E2B facilitates the incorporation of LH-RH into the ME from the cerebrospinal fluid (CSF).

Animals↗
PubMed1994

The effect of selective opioid antagonists on butorphanol-induced feeding.

Butorphanol tartrate (BT) potently stimulates food intake in satiated rats. The opioid receptor profile of BT is complex and is dependent upon the assay and animal species studied. In the present study we utilized three selective opioid antagonists; namely beta-funaltrexamine (beta-FNA), naltrindole (NTI) and norbinaltorphimine (nor-BNI), to probe the opioid receptor profile of BT as an orexigenic agent. Intracerebroventricular administration of nor-BNI (kappa) antagonized the feeding effects of BT (8 mg/kg, s.c.) at doses of 1, 10 and 100 nmol at the 1-2 h time point and decreased feeding at all time points for the 10 nmol dose. After 1 h, the 100 nmol dose of nor-BNI decreased BT-induced feeding by about 72%. In contrast, intraventricular injection of only the highest dose of the selective mu opioid antagonist, beta-FNA (50 nmol), decreased BT-induced feeding. Intraventricular administration of the delta opioid agonist, NTI, failed to alter BT-induced feeding at doses as high as 50 nmol. These data suggest that BT is dependent upon the kappa and perhaps the mu opioid receptors to increase food intake in satiated rats.

Animals↗
PubMed1981

CSF perfusion to treat intraventricular penicillin toxicity.

A shunt infection and meningitis developed in a patient receiving methotrexate intravenously for CNS leukemia. Convulsions and respiratory failure followed the intraventricular administration of 300,000 units of penicillin G potassium. Perfusion with 900 mL of Ringer's lactate removed an amount of penicillin equal to that injected intraventricularly plus some from systemic treatment.

Adult↗
PubMed1986

The effect of L-erythro-dihydroxyphenylserine injected into the lateral ventricle and the hypothalamus on the locomotor activity.

The effect of dihydroxyphenylserine (DOPS) on locomotor activity was studied using the Animex activity meter. One microgram of L-erythro-DOPS, a precursor of d-noradrenaline, was injected into the lateral ventricle once a day for one week or into the anterior hypothalamic area (AHA) once. After the intraventricular injection, the total locomotor activity (from 8:00 p.m. to 8:00 a.m.) of the rats injected with DOPS was significantly less than that of the rats injected with an artificial cerebrospinal fluid (5-ion). Analysis of the locomotor activity in consecutive 2-hr periods showed that the activity of the DOPS group during the time intervals of 10 p.m.-12 a.m., 12 a.m.-2 a.m. and 2 a.m.-4 a.m. was significantly less than that of the control group. After injection of DOPS or 5-ion into AHA, the total activity of the DOPS group was significantly less than that of the control. Analysis of the activity of the DOPS group for each 2-hr period between 10 p.m.-4 a.m. was also significantly less than that of the control. On the basis of these findings, the effect of DOPS in the brain noradrenergic system are discussed.

Animals↗
PubMed2004

Intraventricular thrombolysis speeds blood clot resolution: results of a pilot, prospective, randomized, double-blind, controlled trial.

OBJECTIVE: Animal models and clinical studies suggest that intraventricular thrombolysis improves clot resolution and clinical outcomes among patients with intraventricular hemorrhage. However, this intervention may increase the rates of rebleeding and infection. To assess the safety and efficacy of intraventricular thrombolysis, we conducted a pilot, randomized, double-blind, controlled, multicenter study. METHODS: Patients with intraventricular hemorrhage requiring ventriculostomy were randomized to receive intraventricular injections of normal saline solution or urokinase (25000 international units) at 12-hour intervals. Injections continued until ventricular drainage was discontinued according to prespecified clinical criteria. Head computed tomographic scans were obtained daily, for quantitative determinations of intraventricular hemorrhage volumes. The rate of clot resolution was estimated for each group. RESULTS: Twelve subjects were enrolled (urokinase, seven patients; placebo, five patients). Commercial withdrawal of urokinase precluded additional enrollment. The urokinase and placebo groups were similar with respect to age (49.6 versus 55.2 yr, P = 0.43) and presenting Glasgow Coma Scale scores (7.14 versus 8.00, P = 0.72). Randomization to the urokinase treatment arm (P = 0.02) and female sex (P = 0.008) favorably affected the clot resolution rate. The sex-adjusted clot half-life for the urokinase-treated group was reduced 44.6%, compared with the value for the placebo group (4.69 versus 8.48 d). CONCLUSION: Intraventricular thrombolysis with urokinase speeds the resolution of intraventricular blood clots, compared with treatment with ventricular drainage alone.

Adult↗
PubMed1989

Electroencephalographic and behavioral assessment of intracerebroventricular somatostatin and a substance P analogue.

Chronically implanted rats were injected either with somatostatin (SST) lumbar intrathecally (i.t.) (100 micrograms, n = 5), into the fourth ventricle (3 micrograms, n = 5; 10 micrograms, n = 6; 30 micrograms, n = 5) or into the lateral ventricle (10 micrograms, n = 6; 30 micrograms, n = 6), or received an injection of the substance P (SP) analogue, [D-Pro2, D-Trp7,9]SP into the fourth ventricle (0.3 micrograms, n = 2; 1 micrograms, n = 4; 3 micrograms, n = 4; 10 micrograms, n = 1) or lateral ventricle (3 micrograms, n = 3). A dose-dependent EEG depressant effect was observed following fourth and lateral ventricular injections of SST and of the SP analogue. Acute death due to respiratory depression was observed following i.t. and fourth ventricular injection of SST, and fourth ventricular injection of the SP analogue. Prominent motor behavior (barrel rotation, circling, cranial stereotypies) was observed, without signs of EEG seizure activity, following intraventricular injection of both drugs. Present findings indicate neurotoxic effects of SST and SP analogue at the cerebral level.

Animals↗
PubMed2000

Cellular uptake and spread of the cell-permeable peptide penetratin in adult rat brain.

Investigation of normal and pathological diseases of the central nervous system (CNS) has been hampered by the inability to effectively manipulate protein function in vivo. In order to address this important topic, we have evaluated the ability of penetratin, a novel cell-permeable peptide consisting of a 16-amino acid sequence derived from a Drosophila homeodomain protein, to act as a carrier system to introduce a cargo into brain cells. Fluorescently tagged penetratin was injected directly into rat brain, either into the striatum or the lateral ventricles, and rats were perfusion-fixed 24 h later in order to assess the brain response to the peptide. Immunohistochemistry following intrastriatal injection showed that injection of 10 microg penetratin caused neurotoxic cell death and triggered recruitment of inflammatory cells in a dose-dependent fashion. Doses of 1 microg or less resulted in reduced toxicity and recruitment of inflammatory cells, but interestingly, there was some spread of the penetratin. Injections of an inactive peptide sequence, derived from the same homeodomain, caused little toxicity but could still, however, trigger an inflammatory response. Intraventricular injections showed extensive inflammatory cell recruitment but minimal spread of either peptide. These results suggest that a dose of 1 microg of penetratin peptide is suitable for directing agents to small, discrete areas of the brain and as such is an interesting new system for analysing CNS function.

Age Factors↗
PubMed1978

Centrally mediated hypotension and bradycardia induced by an aminotetralin derivative: TL-68.

An aminotetralin derivate, N,N-dipropyl-2-amino-1,2,3,4-tetrahydronaphthalene (TL-68) induced a prolonged decrease in blood pressure and heart rate when administered i.v. in anesthetized cats. The compound inhibited the blood pressure and heart rate responses induced by central stump stimulation of the sciatic nerve indicating inhibition of sympathetic transmission. TL-68 caused a weak inhibition of the positive chronotropic response induced by stimulation of the cardioaccelerator nerve. When comparatively low doses of TL-68 were injected into the left vertebral artery, a considerable dose-dependent decrease in blood pressure and heart rate developed. The same doses had only small or negligible effects on blood pressure and heart rate when given intravenously. When TL-68 was injected into a lateral cerebral ventricle of unanesthetized rats, a significant hypotension and bradycardia was observed which could be prevented by prior intraventricular injection of phentolamine. The results suggest that this compound exerts its effect through a central mechanism of action, perhaps by stimulation of alpha-adrenoreceptors.

Animals↗
PubMed1980

CSF bicarbonate regulation in metabolic acidosis: role of HCO3- formation in CNS.

In metabolic acidosis, cerebrospinal fluid bicarbonate content (CSF [HCO3-]) falls in parallel with reductions in CSF CO2 tension (PCO2), and the fall is minimal with isocapnia. Regulation of CSF HCO3- was therefore investigated during 6 h of isocapnic metabolic acidosis in dogs. One group received intraventricular injections of acetazolamide to inhibit the centrally located carbonic anhydrase, essential in central nervous system (CNS) HCO3- formation, while the control group received intraventricular saline. Plasma [HCO3-] was reduced by 10 meq/l with iv infusion of 0.2 N HCl. CSF [HCO3-] fell in the control group from 22.8 to 17.7 meq/l at 6 h, whereas in the acetazolamide group it fell from 22.9 to 13.0 meq/l. Brain ammonia content was 1,286 +/- 153 microgram/100 g in the controls and 666.2 +/- 103 microgram/100 g in the acetazolamide-treated group at 6 h. Therefore, some reduction in CSF [HCO3-] occurred during 6 h of isocapnic metabolic acidosis along the chemical concentration gradient between CSF and blood, but further falls, in CSF [HCO3-] were minimized by de novo, carbonic anhydrase-dependent HCO3- formation within the CNS. Some of H+ formed were buffered by the increase in brain ammonia. These central mechanisms contribute to local CNS H+ homeostasis in metabolic acidosis.

Acetazolamide↗
PubMed2000

Orphanin FQ/nociceptin inhibits morphine withdrawal.

The influence of orphanin FQ/nociceptin (OFQ/N) on the morphine-withdrawal symptom was investigated. Withdrawal syndrome was induced in the morphine-dependent rats by an intraperitoneal (i.p.) injection of 2 mg/kg naloxone hydrochloride--an opioid receptors antagonist. Wet-dog shakes were used as a measure of the abstinence syndrome. Intraventricular injections of OFQ/N (5-20 microg/animal) caused significant inhibition of the withdrawal signs at doses between 15-20 microg, in the morphine-dependent rats. OFQ/N alone did not change behavior of the morphine-dependent animals. The obtained results indicate that OFQ/N can inhibit the morphine withdrawal symptoms induced by naloxone.

Animals↗
PubMed1980

Enhanced behavioural, electrocortical and hyperthermic effects of serotonin-like agents after impairment of serotonin transmission in fowl brain.

In adult fowls and in young chicks (Gallus domesticus) the effects were studied on body temperature, behaviour and electrocortical activity of 5-HT and other direct or indirect serotonin agonists given into the III cerebral ventricle in conditions of prolonged impairment of serotoninergic transmission. In chicks pretreated with 5,6-dihydroxytryptamine the subsequent intraventricular injection of 5-HT produced more intense and longer-lasting hyperthermic response and behavioural and electrocortical sleep. On the other hand fenfluramine given intraventricularly in fowls pretreated with 5,6-DHT did not produce significant body temperature and behavioural changes. After 14 and 21 day treatment with methysergide the subsequent administration of 5-HT, fenfluramine and quipazine produced in fowls an hyperthermic response and behavioural sleep more marked and longer-lasting than in control animals. The present experiments show that in conditions of chronic impairment of 5-HT function there is an enhanced behavioural and body temperature response to 5-HT and drugs acting by releasing endogenous 5-HT or 5-HT agonists.

5,6-Dihydroxytryptamine↗
PubMed1983

Effects of oxytocin, des-glycinamide-oxytocin and anti-oxytocin serum on the alpha-MPT-induced disappearance of catecholamines in the rat brain.

Oxytocin (OXT) attenuates memory processes and endogenous OXT might be regarded as an amnesic neuropeptide. In this study, the mode of action of OXT on brain catecholaminergic neurotransmission has been analyzed. Peripheral injection of OXT facilitated the alpha-MPT-induced disappearance of noradrenaline (NA) in the mesencephalon. Dopamine (DA) disappearance was inhibited in the mesencephalon and facilitated in the striatum. The accelerated striatal DA disappearance was not observed if the peptide was given together with alpha-MPT, but only if OXT was injected after alpha-MPT treatment. Intraventricular injection of OXT or des-glycinamide-oxytocin (DG-OXT) caused a decrease in the DA disappearance in the mesencephalon, whereas central administration of anti-oxytocin serum (anti-OXT) accelerated the DA disappearance in the same region. The data raise the possibility that DA utilization in the mesencephalon may be correlated with the influence of OXT on CNS processes.

Animals↗
PubMed1983

Effects of reserpine, alpha-methyl-p-tyrosine, p-chlorophenylalanine and 5,7-dihydroxytryptamine on the hippocampal kindling effect in rats.

The role of the brain monoamines in the development of hippocampal kindling was studied. Reserpine markedly facilitated the formation of hippocampal kindling. The high amplitude spike waves in the amygdala and reticular formation appeared earlier in the reserpine treated rats than in the saline injected rats. alpha-Methyl-p-tyrosine did not have any effect on the formation of hippocampal kindling. Systemic injection of p-chlorophenylalanine and intraventricular injection of 5,7-dihydroxytryptamine also did not have any effect on the formation of hippocampal kindling. Progressive changes of afterdischarge elicited by hippocampal stimulation in the alpha-methyl-p-tyrosine, p-chlorophenylalanine and 5,7-dihydroxytryptamine treated rats are the same as those in the saline injected rats. These results indicate that the decrease in both catecholamines and serotonin levels caused a marked facilitation of the hippocampal kindling formation, but the separate decrease in either catecholamines or serotonin did not produce a significant effect.

5,7-Dihydroxytryptamine↗
PubMed1990

[Angiotensin mechanism of auriculo-acupuncture dental analgesia].

In unanaesthetized rabbits auriculo-acupuncture electrostimulation with frequency of 15 Hz decreased the amplitude of somatosensory EP second component in response to the tooth pulp electrostimulation which was blocked by intravenous injection of naloxone but not by intraventricular injection of saralasin. The same effect of auriculo-acupuncture electrostimulation with frequency 100 Hz was blocked by saralasin, was increased by angiotensin II, was diminished by methysergide but wasn't changed by naloxone. It's suggested that there is angiotensinergic antinociceptive mechanism of dental pain which is activated by auriculo-acupuncture electrostimulation with frequency 100 Hz.

Acupuncture Analgesia↗
PubMedDate not supplied

[Effect of nonsteroidal anti-inflammatory agents on the myocardial blood supply and oxygen regimen].

Experiments on intact cats were made to study the effect of intravenous injection of voltaren (4 mg/kg) and intraventricular injection of indomethacin (4 mg/kg), ibuprophen (5 mg/kg), and butadion (22 mg/kg) on the coronary circulation and oxygen consumption by the myocardium. Indomethacin and butadion decreased the volumetric velocity of the coronary circulation and to a lesser degree oxygen consumption by the myocardium in all the experiments, whereas voltaren in 8 of 15 experiments. Ibuprophen and voltaren (in part of experiments) led to an increase in the coronary circulation and to greater oxygen utilization by the myocardium.

Animals↗
PubMedDate not supplied

Effects of histamine and H1 and H2-receptor antagonists on wet-dog-shake episodes in rats induced with tranylcypromine and 5-methoxytryptamine.

Intraperitoneally administered tranylcypromine and 5-methoxytryptamine induced in rats the so called wet-dogs-shake behaviour. Histamine injected intraventricularly had no effect on the number or episodes of this behaviour during the first 40 minutes of observation. On the other hand, dimaprit in doses of 5 micrograms/rat injected also intraventricularly increased the number of these episodes. Thenalidine and antazoline--antagonists of the H1-receptor, and cimetidine and ranitidine--antagonists of the H2-receptor, decreased the number of these episodes proportionally to the injected dose. Similar effects were obtained after cimetidine injection into the lateral ventricle. In the light of these observations it may be supposed that these antihistaminic agents exert an inhibitory effect not only on the histaminergic system but decrease indirectly also the activity of the serotoninergic system.

5-Methoxytryptamine↗
PubMed1976

The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain.

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.

Acetazolamide↗
PubMed1988

Regulatory role of galanin in control of hypothalamic-anterior pituitary function.

The role of the neuropeptide galanin in the regulation of anterior pituitary function was studied in vivo in conscious male rats and in vitro with cultured anterior pituitary cells. Galanin (50-200 ng; 15-60 pmol) injected into the third cerebral ventricle of rats produced highly significant, dose-related increases of plasma growth hormone (GH) concentrations, whereas galanin increased prolactin (PRL) and decreased thyroid-stimulating hormone (TSH) levels only at the highest dose (60 pmol) tested. Intravenous galanin failed to alter PRL and TSH levels in these rats. In contrast with the results with intraventricular injection of the peptide, intravenous injection of 30 or 300 pmol of galanin produced small, brief, dose-related increases in plasma GH. The response to the 300-pmol dose was less than that induced by a factor-of-20-lower intraventricular dose, which establishes a central action of galanin. Galanin in concentrations ranging from 1 nM to 1 microM failed to alter significantly GH, PRL, or TSH release from dispersed anterior pituitary cells. It also failed to alter GH secretion in response to 100 nM GH-releasing hormone; however, at this dose galanin did potentiate the effect of 100 nM TSH-releasing hormone on TSH and PRL release. Thus, the effects of third-ventricular injection of the peptide are mediated by the hypothalamus. To determine the physiological significance of galanin in control of pituitary hormone release, highly specific antiserum against galanin was injected intraventricularly. Third-ventricular injection of 3 microliter of galanin antiserum resulted in a dramatic decrease in plasma GH values as compared with those of normal rabbit serum-injected controls within 15 min, which persisted until the end of the experiment (5 hr postinjection). Galanin antiserum did not decrease plasma PRL or TSH levels at any time period after its third-ventricular injection; however, a transient increase of plasma TSH levels occurred after 30 and 60 min in comparison with TSH levels in normal rabbit serum-injected controls. Since there was no effect of the antiserum on plasma PRL and only a transient elevation in TSH, galanin may not be physiologically significant enough during resting conditions to alter PRL and TSH release in the male rat. The results of the experiments with galanin antiserum indicate that endogenous galanin has a tonic action within the hypothalamus to stimulate GH release. The rapidity of onset of the effects of galanin and the antiserum directed against it suggest that it acts to stimulate release of GH-releasing hormone from periventricular structures, which then stimulates the release of GH.

Animals↗