[Biochemical mechanism of the epileptogenic action of folic acid injected intraventricular route and its control by pindolol].
Explore the source record for details and available documents.
Animals↗
SEARCH · PubMed Health
Results for “Injections, Intraventricular”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Cytokine responses to intraventricular injection of interleukin 2 into patients with leptomeningeal carcinomatosis: rapid induction of tumor necrosis factor alpha, interleukin 1 beta, interleukin 6, gamma-interferon, and soluble interleukin 2 receptor (Mr 55,000 protein).
Interleukin 2 (IL-2) is a potent immunostimulant that causes the release of secondary cytokines and the production of lymphokine-activated killer cells. We investigated the cellular and cytokine responses to injection of recombinant human IL-2 into the human cerebrospinal fluid of 11 patients with metastatic tumors involving the spinal or cerebral leptomeninges. After initial intraventricular IL-2 administration (1.25 x 10(5) to 2 x 10(6) Cetus units/injection), cerebrospinal fluid samples were collected at intervals from 0 to 24 h. Enzyme-linked immunosorbent assay results indicated that IL-2 levels gradually decreased during the first 24 h, with an average t1/2 between 4 and 8 h. Induction of tumor necrosis factor alpha, interleukin 1 beta, interleukin 6, gamma-interferon, and interleukin 2 receptor (p55) was also assessed by enzyme-linked immunosorbent assay. Tumor necrosis factor alpha and interleukin 6 levels peaked at 2 to 4 h and 4 to 6 h, with concentrations between 71 to 1,714 pg/ml and 942 to 10,500 pg/ml, respectively. Interleukin 1 beta, gamma-interferon, and soluble IL-2 receptor peaked later, during 6 to 12 h; the levels achieved were 234 pg/ml, 25 NIH units/ml, and 207 units/ml, respectively. All cytokine concentrations returned to near baseline between 12 and 24 h; however, the soluble IL-2 receptor levels remained elevated. Additional observations included a rapid influx of neutrophilic leukocytes, followed by a prolonged presence of lymphocytes. These data indicate a broad and complex potential of the immune response in the central nervous system, as well as further define the cytokine cascade in response to IL-2 alone.
Adenocarcinoma↗
Behavioral effects of intraventricular injections of low doses of ethanol, acetaldehyde, and acetate in rats: studies with low and high rate operant schedules.
Although ethanol is typically classed as a sedative-hypnotic, low doses of ethanol have been shown to stimulate locomotor activity in mice. However, in rats the typical response to peripheral administration of ethanol is a dose-dependent suppression of motor activity and operant responding. The present study was undertaken to determine the effects of intraventricular (ICV) infusions of ethanol, acetaldehyde, and acetate on operant performance in rats. ICV injections of ethanol, acetaldehyde, or acetate were given to rats previously trained on either a differential-reinforcement-of-low-rates-of-responding (DRL) 30-s schedule, which generates low rates of responding, or a fixed ratio 5 (FR5) schedule, which generates relatively high rates. Ethanol, acetaldehyde, and acetate all produced a rate-increasing effect in rats on the DRL 30-s schedule at moderate doses (2.8 and 1.4 micromol, respectively). Acetate also produced a rate-decreasing effect on the DRL 30-s schedule at a larger dose (8.8 micromol). Performance on the FR5 schedule was unaltered by ethanol and acetaldehyde, even at doses as high as 17.6 micromol. However, acetate produced a rate-decreasing effect on the FR5 schedule at doses of 4.4, 5.6, and 8.8 micromol. Central administration of low doses of ethanol and its metabolites can increase operant responding on some schedules in rats. Acetate is the substance that is most potent for producing rate-suppressing effects. These results indicate that the major metabolites of ethanol are pharmacologically active when injected into the brain, and suggest that acetate may mediate some of the rate-suppressing effects of ethanol, such as sedation, ataxia or motor slowing.
Acetaldehyde↗
The turnover rate of acetylcholine in brain nuclei of rats injected intraventricularly and intraseptally with alpha and beta-endorphin.
Explore the source record for details and available documents.
Acetylcholine↗
Intraventricular injection of melatonin inhibits naloxone-induced, but not NMDA- or LHRH-induced LH release in ovariectomized estrogen-primed rats.
The present study was aimed to examine the possible functional relationship between melatonin and hypothalamic transmitters, endogenous opioids and excitatory amino acids in controlling gonadotropin secretion in ovariectomized estrogen-primed rats. An intravenous injection of naloxone (mu opioid receptor antagonist), N-methyl-D-aspartate (NMDA; NMDA receptor agonist) or luteinizing hormone-releasing hormone (LHRH) significantly elevated serum luteinizing hormone (LH) concentrations within 10 min. An intraventricular treatment with melatonin, which did not affect the basal LH concentration by itself, significantly suppressed the effect of naloxone. However, the same melatonin treatment did not inhibit the NMDA-induced or LHRH-induced LH secretion. These results support the hypothesis that melatonin has a suprapituitary site of action to inhibit LHRH release, and suggest that the site of its action may be located downstream to that of naloxone action and upstream to that of NMDA in the hypothalamic LHRH neuronal pathway.
Animals↗
The effects of intraventricular injection of beta-endorphin on initial estrogen action to induce lordosis behavior.
Ovariectomized female rats subcutaneously (SC) injected or intracerebrally implanted with estradiol benzoate (EB), and given progesterone SC were used as experimental animals to assess the effects of the beta-endorphin (beta-EP) neuronal system on lordosis behavior. In intraventricular (IV) injection of beta-EP at the onset of sc EB priming, the lordosis behavior was significantly (p < 0.001) facilitated. In contrast, the lordosis behavior was significantly (p < 0.001) inhibited by IV injection of naloxone, an opioid receptor antagonist. beta-EP facilitation of lordosis was observed exclusively within the initial stage of estrogen action. The behavior was significantly (p < 0.001) facilitated by IV injection of beta-EP given with an intracerebral implantation of crystalline EB into the septal-preoptic regions. However, the lordosis behavior was significantly (p < 0.001) inhibited by beta-EP when EB was implanted into the ventromedial hypothalamus. Animals receiving EB implants into the mesencephalic reticular formation were not affected by beta-EP. The present study suggests that the beta-EP neuronal system stimulates sexual receptivity through an action on the central nervous system in relation to the site of estrogen-initial activation to induce the lordosis reflex. The sites of beta-EP action may be the estrogen receptive septal-preoptic and hypothalamic regions; the former for facilitatory effect and the latter for inhibitory effect.
Animals↗
Penetration, diffusion, and uptake of recombinant human alpha-L-iduronidase after intraventricular injection into the rat brain.
Central nervous system disease can have devastating consequences in the severe or Hurler form of mucopolysaccharisosis I (MPS I). Intravenously administered recombinant human alpha-L-iduronidase (rhIDU) is not expected to reach and treat the brain disease due to the blood-brain barrier. To determine whether administration of rhIDU into the cerebrospinal fluid could successfully treat the brain, we studied intraventricular administration of rhIDU in rats. RhIDU was stereotactically administered directly to the lateral ventricle of the intact rat brain and the brain tissues assessed by enzyme assays, immunofluorescence and confocal microscopy 30 min, 24 h, or 7 days later. Quantitation of activity revealed that rhIDU was widely distributed throughout the brain following injection into the lateral ventricle, with activities increased by a factor of 3.3 higher than control in most samples 30 min-24 h after injection and highest levels on the side of injection. The enzyme crossed the ependymal lining of the ventricle and entered neurons into lysosomal-like vesicles. The enzyme was able to diffuse through brain tissue as demonstrated by a decreasing signal gradient from 0.2 to 4.8 mm from the ventricle surface. The largest amount of rhIDU, as detected by immunostaining, was observed 24 h after injection and decreased approximately 50% during the first 7 days. Although the immunostaining decreased with time, specific vesicular staining was still detectable 28 days after injection. The data suggest that rhIDU given into the ventricle can diffuse, penetrate at least several millimeters of brain tissue and be taken up into neurons and glial cells.
Animals↗
Effects of intraventricularly injected isoosmolar glycerol on brain water and electrolytes in the rat.
The infusion of isoosmolar glycerol (0.35 mol/dm-3) into the ventricles of laboratory rats for 120 minutes led to an increase in the serum osmolality by 11 mosm/kg and to hypernatremia. The brain water content of the cerebral hemispheres decreased by 0.9% (P less than 0.05). A corresponding intraventricular infusion of saline or d-glucose did not cause significant changes in these parameters. These findings support the view that glycerol, even in a dose incapable of creating a major osmotic gradient between plasma and brain, could have a beneficial effect in the control of intracranial volume-pressure perturbations. It is hypothesized that, besides acting as an osmotic dehydrating agent in certain concentrations, glycerol influences the central neuroendocrine system responsible for brain ion and volume homeostasis. By its presumed reduction of central and peripheral vasopressin release through lowering the cerebrospinal fluid sodium concentration, it may help in decreasing the brain water content.
Animals↗
Locomotor stimulant effects of intraventricular injections of low doses of ethanol in rats: acute and repeated administration.
RATIONALE: Low doses of ethanol stimulate locomotion in mice, but in rats the typical response to peripheral ethanol administration is a dose-dependent suppression of locomotion. Moreover, chronic ethanol administration fails to produce signs of locomotor sensitization in rats. OBJECTIVE: The present study was undertaken to determine whether intraventricular (i.c.v.) infusions of low doses of ethanol (as determined by comparisons with systemic doses, and by analyses of brain extract ethanol levels) could increase locomotor activity in rats after acute or repeated administration. METHODS: Male rats received acute doses of ethanol i.p. (0.0, 0.25, 0.5, 1.0, or 2.0 g/kg) or i.c.v. (0.0, 0.7, 1.4, or 2.8 micromol) and were tested for motor activity. In a third experiment, repeated i.c.v. vehicle or ethanol (2.8 micromol) was administered for 15 sessions over a 30-day period, and motor activity was recorded. This phase was followed by a single challenge session, in which a low dose of ethanol (0.7 micromol) was injected i.c.v. to both groups of rats. RESULTS: Rats injected with i.p. ethanol showed no increase in activity at low doses, with higher doses suppressing activity. In contrast, i.c.v. injections of low doses of ethanol increased motor activity. After repeated administration, ethanol-treated rats were more sensitive than control-treated rats to the locomotor stimulant effect of ethanol. CONCLUSIONS: These results demonstrate that central administration of low doses of ethanol can increase locomotor activity in rats and suggest that i.c.v. ethanol can produce some signs of motor sensitization, a characteristic that has been related to the potential addictive properties of many drugs.
Animals↗
A new experimental model of epilepsy based on the intraventricular injection of endothelin.
Injection of endothelin-1 (ET-1, 9 pmol) into a lateral cerebral ventricle (LCV) of rats produces barrel-rolling and other convulsive signs that resemble those of generalized seizures in some types of epilepsy. Using the quantitative autoradiographic [14C]deoxyglucose technique, we documented that the neuroanatomical metabolic correlates of the ET-1-induced convulsions in rats are high rates of glucose utilization by structures near the site of LCV injection and throughout a diverse circuit of anatomically related brain regions. We speculate that this circuitry connects the caudate nucleus (putative site of initial stimulation in the forebrain) to the paramedian lobule and vermis of the caudal cerebellar cortex in the hindbrain. We evaluated the behavioral, physiological, and hypermetabolic responses to central ET-1 in the presence of three agents with anticonvulsant properties, providing clues about the cellular mechanisms of this convulsive and hypermetabolic state. Intraventricular MK-801 [a noncompetitive antagonist of glutamic acid N-methyl-D-aspartate (NMDA) receptors], nimodipine (an antagonist of dihydropyridine-sensitive, voltage-gated calcium L-channels), or methylene blue (an inhibitor of guanylate cyclase, the enzyme on which nitric oxide acts) each produced significant attenuation of the behavioral and cerebral metabolic activation. The results introduce several quantitative parameters for an experimental model of employing intraventricular ET-1 in rats to study mechanisms of peptidergic convulsive disorders and the efficacies of promising anticonvulsant compounds in the treatment of epilepsy.
Animals↗
[Distribution of 1-14C palmitic acid in brain tissue after intraventricular injection in the conscious cat].
The distribution of (1-14C) palmitic acid in the brain tissue following the injection into the cerebral ventricles of conscious cats was investigated. The radioactive material was found in the brain tissue surrounding the cerebral ventricles and in the cerebral cortex, but in varying amounts : the smallest amounts were found in the cerebral cortex, while the highest in the thalamus and in the hippocampus. Radioactive material was also found in the peripheral venous blood. The amount of the radioactive material in the grey matter lining the cerebral ventricles as well as in the cerebral cortex was time-dependant. The labelled material in the structures surrounding the cerebral ventricles and in the cerebral cortex increased within first four hours after its intraventricular administration. Thereafter, throughout subsequent 48 hours either it slowly disappeared in the caudate nucleus and in the thalamus, or it was retained in the hypothalamus and in the floor of the IV ventricle.
Animals↗
Renin antisense injected intraventricularly decreases blood pressure in spontaneously hypertensive rats.
Brain renin-angiotensin system plays an important role in blood pressure regulation and is suggested to play a role in the development and maintenance of hypertension. To test the hypothesis that brain renin may play a significant role in hypertension in spontaneously hypertensive rats (SHR), phosphorothioated antisense oligodeoxynucleotides targeted to renin mRNA were administered intracerebroventricularly in SHR. Administration of an antisense but not its sense oligodeoxynucleotide produced a prolonged duration of decrease in blood pressure. Intra-arterial administration of the antisense oligodeoxynucleotide at the same dose that decreased blood pressure when administered intraventricularly did not affect blood pressure. Furthermore, renin mRNA but not angiotensin AT1 receptor mRNA levels were decreased in the hypothalamus of the antisense oligodeoxynucleotide-treated rats. These results suggest that brain renin may play a significant role in hypertension in SHR.
Animals↗
5-hydroxytryptamine injected intraventricularly fails to influence the brain water content.
Measurement of the content of brain water and electrolytes after the intraventricular administration of 5-hydroxytryptamine in rats, with and without exposure to osmotic stress, failed to show water accumulation in the brain parenchyma. It is suggested that elevation of serotonin in the cerebrospinal fluid--resembling pathological situations such as subarachnoid hemorrhage--does not play a primary role in brain edema formation.
Animals↗
Antinociceptive activity of salmon calcitonin injected intraventricularly in mice: modulation of morphine antinociception.
Salmon calcitonin (sCT) was tested i.v.t. for its ability to produce antinociception in mice as quantitated by the tail-flick, hot-plate and p-phenylquinone (PPQ) writhing tests. sCT from two sources, Bachem (Torrance, CA) and Armour Pharmaceutical Co. (Chicago, IL), was shown to have naloxone reversible antinociceptive activity in the tail-flick and hot-plate tests. However, the sCT analgesic activity in the PPQ test was only partially naloxone reversible. sCT produced a naloxone reversible potentiation of doses of morphine that had low analgesic activity, but sCT failed to potentiate higher doses of morphine in the tail-flick test. sCT has a similar biphasic effect on morphine in the PPQ test in that low doses of morphine were selectively potentiated. However, the potentiation in the PPQ test was not naloxone reversible. sCT was shown not to be cross-tolerant to morphine in the PPQ test. Thus, sCT appears to produce its antinociceptive effects via interaction with both opiate and nonopiate mechanisms.
Analgesics↗
Influence of noradrenaline, 5-hydroxytryptamine and acetylcholine injected intraventricularly on the rat's behaviour.
Explore the source record for details and available documents.
Acetylcholine↗
The effect of intraventricular injections of noradrenaline, 5-hydroxytryptamine, acetylcholine and tranylcypromine on the ox (Bos taurus) at different environmental temperatures.
1. Noradrenaline, 5-hydroxytryptamine (5-HT), acetylcholine and tranylcypromine were injected or infused into the lateral ventricle of the ox. The effects of these drugs on heart and respiration rates, heat production, rectal, skin and hypothalamic temperatures and skin evaporative loss were measured when the animal was exposed to environmental temperatures ranging from -1 degrees C to +30 degrees C.2. Acetylcholine (0.001-2 mg) had no detectable effect on temperature regulation at 20 degrees C.3. In small doses (0.005-0.05 mg) 5-HT had no detectable effect. Larger doses (2-5 mg) given in a cold environment (-1 degrees C) also had no effect but the same doses given in warm environments (15-30 degrees C) caused increases in skin temperatures, skin evaporative loss and respiratory rate, and decreases in rectal and hypothalamic temperatures.4. Infusion of tranylcypromine (0.107 ml./min of a 1 in 50 solution) in a warm environment (20 degrees C) also caused a decrease in rectal temperature after a delay of 1-1(1/2) hr during which no effects were apparent.5. Noradrenaline (2 mg) had no effect on temperature regulation when injected into animals in a warm environment (30 degrees C). When injected (1 mg) into animals in a cold environment (-1 degrees C) shivering stopped and heat production and rectal and hypothalamic temperatures were decreased.6. It is concluded that intraventricular 5-HT and noradrenaline both cause a decrease in body temperature, and it is unlikely that central temperature regulation in the ox is mediated only by these two substances.
Acetylcholine↗
[Successful treatment of Echovirus 27 meningoencephalitis in agammaglobulinaemia with intraventricular injection of gammaglobulin. A case report].
BACKGROUND: Meningoencephalitis due to enteroviruses is particularly serious when occurring in patients with agammaglobulinaemia. This disease is associated with a high mortality and a significant risk for neurological sequelae in such circumstances. We report here a new case treated with intraventricular immunoglobulin, whose evolution was favourable. CASE REPORT: A three-year-old boy with agammaglobulinaemia, while he was treated with gammaglobulin with an IgG residual concentration of 10 g/l, presented neurological symptoms related to Echovirus 27 meningo encephalitis. Under treatment with intraventricular gammaglobulin by means of an Ommaya reservoir, the patient recovered. CONCLUSION: Favourable evolution is rare in meningo encephalitis in agammaglobulinaemic patients. Prognosis depends on an early diagnosis and on the extent of dissemination of the infection. Intraventricular gammaglobulin administration may contribute to a favourable outcome.
Child, Preschool↗
The disposition of intraventricularly injected 14C-5,6-DHT-melanin in, and possible routes of elimination from the rat CNS. An autoradiographic study.
14C-5,6-DHT-Melanin was injected into the left lateral ventricle of adult rats and its fate followed by light and EM autoradiography and by TEM of structures identified as labeled in preceding light micrographs. Shortly after injection, melanin particles were seen ingested by supraependymal and epiplexus cells, by cells residing in the pia-arachnoid, i.e. free subarachnoidal cells and perivascular cells, and by subependymally located microglia-like cells with intraventricular processes. Up to day four, an increase in the number of labelled phagocytes in the CSF was noted which transformed into typical reactive macrophages. After this time, many intraventricular melanin-laden phagocytes formed rounded clusters; cells of such clusters were subsequently found to invade the brain parenchyma by penetrating the ependymal lining and to accumulate in the perivascular space of brain vessels. 14C-Melanin-storing macrophages were found in the marginal sinus of the deep jugular lymph nodes suggesting emigration of CNS-derived phagocytes via lymphatics or pre-lymphatics that contact the subarachnoidal space compartment. This does not exclude the possibility that some of the macrophages leave the brain via the systemic circulation by penetrating the vascular endothelium; these may be disposed of in peripheral organs other than the lymph nodes. The ability of supraependymal, epiplexus, free subarachnoidal and perivascular cells in the pia and of subependymal microglia cells to accumulate synthetic melanin by phagocytosis suggests that these cells are local variants of the same type of resting potential phagocytes of the mammalian brain. The present study shows that 14C-5,6-DHT-melanin is an ideal phagocytic stimulant and marker for phagocytosis.
5,6-Dihydroxytryptamine↗