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PubMed1981

Intraventricularly injected growth hormone stimulates somatostatin release into rat hypophysial portal blood.

The effects of GH on the release of somatostatin from the hypothalamus were assessed by measuring the concentrations of immunoreactive somatostatin (IRS) in hypophysial portal blood of urethane-anesthetized male rats. A significant and dose-related increase of IRS in hypophysial portal blood was observed during 20-80 min after a single injection of rat GH (5 and 25 micrograms) into the third ventricle. An intraventricular injection of ovine LH or vehicle alone did not affect IRS values in hypophysial portal blood. When rat GH was repeatedly injected into the cerebral ventricle at 75-min intervals, IRS in hypophysial portal blood rose following each injection in a similar pattern with a latency of 30-45 min. These findings suggest that the release of somatostatin from the hypothalamus is regulated, at least in part, by GH. Furthermore, in view of the inhibitory effect of somatostatin on GH secretion, stimulation by GH of somatostatin release into hypophysial portal blood may be involved in the mechanism by which GH regulates its own secretion.

Animals↗
PubMed1993

[Effect of intraventricular injection of substance P on pulmonary and carotid arterial pressure in rabbits].

In the present investigation changes of pulmonary and carotid arterial pressure in response to injection of substance P(SP) into the 4th ventricle of rabbits were studied. The results were as follows: (1) Intraventricular (ivt.) injection of SP could induce either an increase or a decrease in pulmonary arterial pressure as well as carotid arterial pressor response and bradycardia. (2) Bilateral cervical vagotomy could initiate a definite pulmonary pressor response and a marked decrease in the bradycardiac response to injection of SP in those rabbits originally showing a depressor response of pulmonary artery to SP. (3) Pretreatment by i.c.v. and i.v. phentolamine or alpha 1 blocker, prazosin, could block both the SP-induced pulmonary and carotid pressor responses. (4) alpha 2 blocker, yohimbine, or naloxone could enhance the pressor responses in the both arteries. (5) Propranolol had no effect on the pressor responses in both arteries. (6) The cardiovascular responses to SP could be blocked by the SP blocker (D-Pro2.D-Trp7.9)-SP. It is assumed that increase of SP in the brain may induce an increase in both the pulmonary and carotid arterial pressures and bradycardia by activating the SP receptors. The central mechanism responsible for the SP- induced pressor response involves the participation of adrenergic alpha 1 receptor activities, while the central adrenergic alpha 2 receptor system as well as the endorphin system exerts an inhibitory modulation on the central SP-induced pressor pathway. It appears that SP, catecholamine and opiate substance are all involved in the regulation of blood pressure by brain stem.

Animals↗
PubMed1979

Effects of intraventricular injection of 6-hydroxydopamine in the developing kitten. 1. On the sleepwaking cycles.

Intraventricular 6-OHDA was injected in kittens at different stages of development, and the subsequent sleep polygram was analyzed, in order to determine the role of the catecholaminergic system in the ontogenesis of sleep regulations during the first and the second postnatal months. 6-OHDA, used with or without previous chlorimipramine treatment, led within a 10-day period to drastic reductions of the endogenous monoamines in the forebrain of all age groups. Although the neurotoxicity of 6-OHDA was almost constant among the different age groups, the effects on sleep depended on the age of the animals at the time of the injection. In the 5-week-old injected kittens, 6-OHDA affected PS according to an adult-like pattern. In the 3-week-old kittens, 6-OHDA alone (leading to both catecholamines and serotonin decreases) induced the same PS deficit as in the adult cat. In the 1- and 2-week-old kittens, neither 6-OHDA alone, nor 6-OHDA with previous chlorimipramine treatment, distrubed the sleep regulations. These data are compared to similar experiments performed in the adult cat. They are discussed in terms of sleep control ontogenesis. It is concluded that the catecholaminergic system plays no important role in the mechanisms of sleep regulation in the early postnatal period in the kitten, whereas its regulatory influence on PS is confirmed in the juvenile animal. The functional maturation of the catecholaminergic system in terms of sleep regulation is achieved between the third and the fifth week of postnatal life.

Age Factors↗
PubMed1985

Behavioural and neurochemical effects of chronic intraventricular injections of nerve growth factor in adult rats with fimbria lesions.

Rats received bilateral lesions of the fimbria. These lesions impaired their ability to learn a radial maze. Rats given repeated intraventricular injections of nerve growth factor (NGF, 10 micrograms twice weekly during 4 weeks after the lesion) learned the maze problem more rapidly than rats with the same injury but treated with a control protein (cytochrome c). When retested after a period of 6 weeks without NGF treatment, the performance of NGF-treated and cytochrome c-treated rats with fimbria lesions did not differ. Whereas our previous study showed an increase in choline acetyltransferase (ChAT) activity in the septum and the hippocampus 4 days after the last NGF injection, the present study found that after the retest period (i.e. 10 weeks after the last NGF injection) ChAT activity was increased in the septum but not in the hippocampus. The relationship between the NGF-induced changes in ChAT activity and behaviour is discussed.

Animals↗
PubMed1991

Immunohistochemical detection of a monoclonal antibody directed against the NGF receptor in basal forebrain neurons following intraventricular injection.

It has been shown by autoradiography that, following intraventricular administration, a monoclonal antibody directed against the rat nerve growth factor (NGF) receptor is specifically accumulated bilaterally by numerous cholinergic neurons of the basal forebrain. This is consistent with the evidence that cholinergic basal forebrain neurons have NGF receptors and respond to NGF under a variety of experimental conditions. The present study demonstrates that the immunohistochemical detection of unmodified monoclonal antibody in cholinergic forebrain neurons following transport from CSF is feasible, although injection of larger amounts of the antibody is required to obtain an image equivalent to the one obtained with the autoradiographic method. The location of the immunohistochemical product clearly indicates that the antibody has been internalized, probably in an endosomal compartment.

Animals↗
PubMed2003

Open field locomotor effects in rats after intraventricular injections of ethanol and the ethanol metabolites acetaldehyde and acetate.

The typical response to acute peripheral administration of low to high doses of ethanol in rats is a dose-dependent depression of motor activity. Nevertheless, recent studies indicate that intraventricular (ICV) injections of ethanol can produce signs of behavioral activation. In addition, considerable evidence indicates that brain metabolism of ethanol is involved in modulating some of the behavioral effects of this drug, which suggests that ethanol may have active metabolites with central actions. The present study was undertaken to investigate the effects of ICV ethanol, and its two major metabolites acetaldehyde and acetate, on open field locomotor activity in rats. Male Sprague-Dawley rats received different doses of ethanol, acetaldehyde or acetate ICV and immediately were placed in an open field chamber in which locomotion was measured. Rats injected with ICV ethanol or acetaldehyde showed an inverted U-shaped dose-response curve, with moderate doses increasing motor activity. In contrast, acetate produced a dose-dependent decrease in motor activity. These results demonstrate that central administration of low doses of ethanol can increase locomotor activity in rats, and suggest that acetaldehyde may be an active metabolite of ethanol that also can facilitate locomotor activity. Moreover, it is possible that some of the motor suppression or sedation produced by ethanol is due to the central actions of acetate.

Acetaldehyde↗
PubMed1986

Time course of the metabolite patterns of intraventricularly injected [3H]noradrenaline in rat brain regions.

In the hypothalamus, septum, pons with medulla, and hippocampus regions of rat brain, the level of radioactivity of [3H]noradrenaline and of five of its metabolites were determined up to 6 h after intraventricular injection of the tritiated amine. The following main results were found: In anterior hypothalamus and septum, the [3H]noradrenaline level declined in two phases. Similar turnover curves were obtained for the primary deaminated metabolites, with almost the same final half-lives as for [3H]noradrenaline. The level of the initial methylation product, normetanephrine, also showed a biphasic decline, which did not correspond to that of [3H]noradrenaline but rather was faster throughout the experiment. The final metabolites (i.e., the glycol sulfates) reached maximal levels in hypothalamus and septum earlier than in other regions. Thereafter, their levels declined with almost similar rates in all areas tested, but always faster than the [3H]noradrenaline level. The following conclusions were drawn: In areas rich in catecholaminergic nerve terminals, there seems to be a site, in addition to the vesicular storage pool, that accumulates exogenous noradrenaline and then releases it with relatively short half-lives. The contents of primary deaminated metabolites followed the turnover of [3H]noradrenaline at both sites. Exogenous [3H]noradrenaline seems to be methylated at two extraneuronal sites, which are distinguished by the rates of subsequent deamination. The size of the pool of slowly deaminated [3H]normetanephrine that is formed immediately after [3H]noradrenaline injection determined the apparent turnover of this product throughout the experiment and, thus, like the final metabolites, reflects for several hours the initial degradation of the unstored [3H]noradrenaline, rather than the metabolism of the stored amine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Search for the structures initiating seizures triggered by intraventricular injection of the mu opioid agonist dermorphin in rats.

Free-moving rats received intraventricular (i.c.v.) or intravenous (i.v.) injections of the mu opioid agonist dermorphin (DRM). The EEG activity of the cortex and of several structures near the injected lateral ventricle was recorded. The intravenous injections of DRM did not induce epileptiform activity. The intracerebroventricular injections of DRM triggered several types of electrical seizures and interictal spikes. With the aim of determining which structure gave rise to the epileptiform discharges, we compared the time relationships of epileptiform phenomena occurring in different structures. Epileptiform discharges, at once generalized, appeared first in the CA3 area of the ventral hippocampus, with involvement of the CA1 area of ventral hippocampus, the entorhinal cortex and the amygdala following immediately. We conclude that, after intracerebroventricular injection of a mu opiate agonist, epileptiform activity originates in the CA3 area of the ventral hippocampus.

Analgesics, Opioid↗
PubMed1969

Hypothermia following intraventricular injection of hemicholinium-3 in rats.

1. In unanaesthetized rats, a dose of 50 mug of hemicholinium-3 injected into the cerebral ventricles produced a prolonged hypothermia which was unaffected by the simultaneous administration of choline. This suggests that it was not due to inhibition of acetylcholine synthesis.2. An intraperitoneal injection of 50 mug of hemicholinium-3 also produced hypothermia which, however, was blocked by choline which suggests that it is due to inhibition of acetylcholine synthesis.3. Hyoscine and hexamethonium did not block the hypothermia produced by intraventricular hemicholinium-3, but some antagonism was obtained with phentolamine, imipramine and amphetamine.4. When hemicholinium-3 was administered intraventricularly to rats pretreated with desmethylimipramine, a lethal hyperthermia developed.5. It is concluded that no central cholinergic mechanism is involved in the hypothermia of the rat resulting from an intraventricular injection of hemicholinium-3.

Acetylcholine↗
PubMed1981

Effect of intraventricular injection of neurotensin and other various bioactive peptides on plasma immunoreactive somatostatin levels in rat hypophysial portal blood.

The role of various bioactive peptides in the control of secretion of hypothalamic somatostatin into the hypophysial portal blood was examined in anesthetized rats. Hypophysial portal blood was withdrawn at a rate of 5.0 microliter/min into a chilled tube through a cannula placed over the stump of the pituitary stalk and segmented every 20 min by air bubbles. Immunoreactive somatostatin (IRS) in the plasma was extracted with acetic acid and acetone and quantified by RIA. Basal levels (mean +/- SE) of plasma IRS in the hypophysial portal blood were 646 +/- 36 and 317 +/- 44 pg/ml in urethane- and pentobarbital-anesthetized rats, respectively. Under urethane anesthesia, injection of synthetic neurotensin into the lateral ventricle at various doses in the range of 0.016--2 microgram/rat caused a significant and dose-related increase of plasma IRS levels in the hypophysial portal blood, and this effect of neurotensin was significantly (P less than 0.05) suppressed by pretreatment with diphenhydramine (1 mg/100 g BW, iv), a histamine receptor blocker. Enhancement of IRS release by neurotensin was also observed in pentobarbital-anesthetized rats. Intraventricular injection of substance P (10 microgram/rat), beta-endorphin (1 and 5 microgram/rat), or [Met5]enkephalin had no effect on the level of somatostatin in the hypophysial portal blood of urethane-anesthetized rats. These results suggest a release of hypothalamic somatostatin into the hypophysial portal blood in response to intraventricular administration of neurotensin, probably by a histaminergic mechanism.

Animals↗
PubMed2000

Intraventricular injection of tachykinin NK3 receptor agonists suppresses the ingestion of NaCl-associated tastes.

The present experiments evaluated whether a salty taste was required for injections of a neurokinin-3 (NK3) receptor agonist (senktide) to suppress intake or whether senktide would reduce the intake of tastes that are predictive of NaCl. During training, different groups of rats were given access to 1% almond + water, 1% almond + 0.3 M NaCl, or 1% almond + 0.1 M sucrose. On the test day, rats were administered intraventricular injections of either saline or 200 ng senktide and then given access to 1% almond + water. Senktide had no effect on the intake of the water-associated or sucrose-associated almond. In contrast, senktide significantly reduced the intake of NaCl-associated almond. Senktide had no effect on almond intake by water-deprived rats. These results show that activation of NK3 receptors reduces the intake of NaCl and of a neutral taste that is predictive of sodium but not of calories.

Animals↗
PubMed2000

Distribution of Fos-like immunoreactivity within the rat brain following intraventricular injection of the selective NK(3) receptor agonist senktide.

Neurokinin B (NKB) is one member of an evolutionarily conserved family of neuropeptides, the tachykinins. Preferential binding of NKB to endogenous NK(3) receptors affects a variety of biological and physiological processes, including endocrine secretions, sensory transmission, and fluid and electrolyte homeostasis. In light of its widespread biological actions, immunohistochemical detection of the c-Fos protein product was used to study the distribution of neuronal activation in the rat brain caused by intraventricular (icv) injections of the selective NK(3) receptor agonist (succinyl-[Asp(6), N-Me-Phe(8)] substance P [6-11]), senktide. Quantitative analysis revealed that treatment with isotonic saline or 200 ng senktide resulted in the differential expression of Fos-like immunoreactivity (FLI) throughout the brain. Senktide induced the highest number of FLI neurons in the lateral septum, bed nucleus of the stria terminalis, amygdala, paraventricular nucleus of the hypothalamus, median preoptic nucleus, organum vasculosum of the lamina terminalis, supraoptic nucleus, periaqueductal gray, and medial nucleus of the solitary tract compared to isotonic saline controls. Additional regions that contained elevated FLI following icv injection of senktide, relative to saline injection, included the cerebral cortex, lateral hypothalamic nucleus, suprachiasmatic nucleus, ventral tegmental area, substantia nigra, inferior colliculus, locus coeruleus, zona incerta, and arcuate nucleus. Our data indicate that activation of NK(3) receptors induces the expression of FLI within circumscribed regions of the rat brain. This pattern of neuronal activation overlaps with nuclei known to regulate homeostatic processes, such as endocrine secretion, cardiovascular function, salt intake, and nociception.

Animals↗
PubMed2006

Correction of cardiac abnormalities in fabry mice by direct intraventricular injection of a recombinant lentiviral vector that engineers expression of alpha-galactosidase A.

BACKGROUND: Recombinant lentiviral vectors (LVs) offer the possibility of stable, long-term expression of transgenes even in non-dividing cells. In the present study this vector system was applied to a clinically relevant cardiovascular problem. METHODS AND RESULTS: Fabry disease results from deficient activity of alpha-galactosidase A (alpha-gal A) and cardiac abnormalities are a common and an important cause of death in patients with the disease. A therapeutic LV that delivers the alpha-gal A cDNA has been synthesized. In vitro studies established efficient transduction of the H9c2 rat cardiomyocytes and showed overexpression of enGFP (control) and alpha-gal A. In in vivo studies, the enGFP cDNA was transferred into C57BL/6 mouse hearts by direct intraventricular injection. Next, in a mouse model of Fabry disease, the recombinant therapeutic construct was delivered analogously. In cardiac tissue, alpha-gal A activity rose to 23% of normal levels at day 7 after LV injection, which is encouraging because levels of correction approximating 5% of normal may be curative for this disorder. There was also a corresponding reduction in globotriaosylceramide accumulation. Other organs assayed showed no detectable changes in alpha-gal A activity levels in injected animals. CONCLUSION: A localized benefit of directly injecting a therapeutic LV into the heart has been shown, confirming the utility of this delivery system for research and therapy for a variety of cardiovascular disorders.

Animals↗
PubMed1996

Acute immobilization stress and intraventricular injection of CRF suppress naloxone-induced LH release in ovariectomized estrogen-primed rats.

The present study was undertaken to evaluate the role and possible interaction of the endogenous opioid peptide (EOP) and corticotropin-releasing factor (CRF) in the acute stress-induced suppression of gonadotropin secretion in ovariectomized estrogen-primed rats. An intravenous (i.v.) injection of naloxone (10 or 20 mg/kg), an EOP antagonist, significantly elevated serum luteinizing hormone (LH) levels within 10 min in non-stressed animals. The naloxone-induced LH release was completely eliminated when tested 30 min after the onset of acute immobilization. In a subsequent study, it was found that suppression of the naloxone-induced LH release occurred as early as 5 min after the stress onset, and was still evident 60 min after the end of a 30-min period of immobilization. The effect of naloxone was restored 3 h after liberation of the animal from the 30-min immobilization. An intraventricular (i.c.v.) injection of CRF (1 or 5 micrograms) also significantly suppressed, in a dose-related manner, the effect of a subsequent i.v. injection of naloxone. However, an i.c.v. injection of alpha-helical CRF(9-41) (25 or 50 micrograms), a CRF antagonist, prior to immobilization, could not interfere with the suppressive effect of stress on naloxone-induced LH release. These results suggest that both acute immobilization stress and CRF can inhibit the LH secretory activity without mediation by EOP neurons. However, the stress-related suppression may involve non-CRF mechanism(s).

Analysis of Variance↗
PubMed1989

Anti-Thy-1 immunotoxin, OX7-saporin, destroys cerebellar Purkinje cells after intraventricular injection in rats.

Thy-1 is an abundant surface glycoprotein of rat neurons. OX7 is a monoclonal antibody with high affinity for Thy-1. This study sought to determine if intraventricularly administered OX7 could serve as a carrier to deliver cytotoxin to neurons, thus destroying those neurons. Saporin (Sap), a ribosome-inactivating protein was disulfide-coupled to OX7 (OX7-Sap). OX7-Sap, OX7, saporin alone, pooled non-immune mouse IgG, and an irrelevant immunotoxin, RFT-1-Sap, were injected into the lateral ventricles of anesthetized adult rats. Animals were observed for 1-8 days. OX7-Sap-injected animals developed coarse head tremor and gait/truncal ataxia in a dose-dependent manner beginning 24 h or more after injection. All control animals remained healthy. After OX7 or OX7-Sap injection, immunoperoxidase staining for mouse IgG was most intense and specific in the molecular and Purkinje cell layers of the cerebellar cortex. Cresyl violet staining demonstrated destruction of the Purkinje cell layer in the OX7-Sap-treated animals but not in controls. These results indicate that intraventricular injections of OX7 can be used to deliver biologically active moieties to the Purkinje cells. This approach may prove useful in analysis of Purkinje cell function and as a model of cerebellar degeneration.

Animals↗
PubMed1984

Cold acclimation increases physiological responsiveness to intraventricular injection of beta-endorphin in pentobarbital anaesthetized rats. II. Metabolic function.

beta-endorphin administered intraventricularly into pentobarbital anaesthetized rats led to a reduction in rectal temperature and a dose dependent biphasic response in metabolic rate with increase at low doses (7-10 nmol/kg) and decrease at high doses (30-300 nmol/kg) in rats acclimated to 22 degrees. These metabolic responses to beta-endorphin were enhanced both in magnitude and in duration in rats acclimated to 5 degrees for 3 weeks, indicating an increased responsiveness to beta-endorphin. Naloxone antagonized the metabolic effects of beta-endorphin in rats acclimated to both 22 degrees and 5 degrees, indicating the metabolic effects of beta-endorphin were via the naloxone sensitive opiate receptors.

Acclimatization↗
PubMed1993

Intraventricular injection of neostigmine increases dopaminergic and noradrenergic nerve activities: hyperglycemic effects and neurotransmitters in the hypothalamus.

The contents of hypothalamic neurotransmitters were examined under inducement of hyperglycemia by intraventricular administration of neostigmine, after pretreatment with microwave irradiation. Extracellular levels of the metabolites of these neurotransmitters were also measured using in vivo microdialysis. Our data suggest that neostigmine affects not only the cholinergic system but also the noradrenergic and dopaminergic systems in the hypothalamus. In order to clarify the relationship between excitement or regulation of physiological events and activities of central specific neurons, we therefore suggest that studies by chemical stimulation are insufficient on their own; it is also necessary to measure fluctuations both in neurotransmitter content and in extracellular levels of their metabolites.

3,4-Dihydroxyphenylacetic Acid↗