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Results for “Injections, Intraventricular”

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At least 199 records · Page 11Linked to original sources

PubMed1991

Effect of intraventricular injection of an anti-Purkinje cell antibody (anti-Yo) in a guinea pig model.

Female guinea pigs had intraventricular injections of either IgG from a patient with paraneoplastic cerebellar degeneration (PCD) and anti-Purkinje cell antibodies (anti-Yo IgG) or control IgG. In animals that received a single injection of control or anti-Yo IgG and were killed at different time intervals, IgG immunoreactivity was present in the cytoplasm of Purkinje cells at 2 h and persisted at 24 h. In guinea pigs injected for 15 days with control or anti-Yo IgG and sacrificed 24 h after the last injection, IgG was detected into the Purkinje cells in both groups, whereas animals killed 7 and 30 days after the last injection had no staining for IgG in the Purkinje cells. Clinical or pathologic evidence of cerebellar involvement was not seen in any of the animals. This study suggests that anti-Yo antibody alone may not be the cause of the Purkinje cell loss in PCD.

Animals↗

PubMed2005

Intraventricular injections of tachykinin NK3 receptor agonist reduce the gain of the baroreflex in unrestrained rats.

The tachykinin neuropeptides acting at NK3 receptors affect mean arterial pressure (MAP) through both neuroendocrine and neural mechanisms. NK3 receptors are found in brainstem nuclei that mediate the baroreflex, but the effects of NK3 receptor stimulation on baroreflex function are unknown. The present study tests the effects of intraventricular injections of senktide, a selective NK3 receptor agonist, on the sensitivity of the baroreflex in three stains of rats: Charles River Laboratory, Long-Evans, and Brattleboro rats, which lack the ability to synthesize vasopressin. Rats with lateral ventricle cannulas were administered injections of isotonic saline, 100 ng, or 200 ng senktide, and 5 min later arterial baroreceptor-heart rate (HR) function was examined by constructing full-range blood pressure-HR curves using alternating doses (5-20 microg kg min) of phenylephrine and nitroprusside to raise and decrease blood pressure approximately 50 mm Hg over a period of 1 min, respectively. Intraventricular injections of 200 ng senktide had no significant effect on baseline MAP, but significantly decreased the gain of the baroreflex in all three rat strains whereas the 100 ng dose had no effect on the baroreflex. These results show that NK3 receptor stimulation modulates the baroreflex that is independent of any action of vasopressin.

Animals↗

PubMed1987

Relationship between hypertensive response and brain kinin level in the rat injected intraventricularly with glandular kallikrein.

Hypertensive action was observed in conscious rats injected intraventricularly with glandular kallikrein (EC 3.4.21.35) in a dose-dependent manner (4-16 KU), which was associated with the enhancement of brain kinin level. Concurrently administered aprotinin, a kallikrein inhibitor, led to an inhibition of these effects of kallikrein. These results suggest that the central hypertensive action of kallikrein is mediated via the kinin liberated from a kininogen in the brain.

Animals↗

PubMed1999

Differential effects of intraventricular injections of tachykinin NK1 and NK3 receptor agonists on normal and sham drinking of NaCl by sodium-deficient rats.

The effects of lateral ventricular injections of succinyl-[Asp6, N-Me-Phe8]-substance P (SENK; 25, 100, 200 ng), a tachykinin NK3 receptor agonist, and [Sar9, Met(O2)11]-substance P (Sar Met; 100, 200 ng), an NK1 receptor agonist, on normal (gastric fistula closed) and sham drinking (gastric fistula open) of hypertonic NaCl by sodium-deficient rats were compared. Intraventricular injections of Sar Met had no effect on NaCl intake in either condition. Injections of 100 ng and 200 ng SENK caused an equal suppression of NaCl intake in the 2 fistula conditions. The latency to drink was not affected, but the initial lick rate was significantly lower and decayed more rapidly after 100 ng SENK than after saline or 25 ng SENK. The results show that (a) the tachykinin subtypes are not equally involved in the control of need-induced salt intake; (b) negative feedback from the stomach and distal gastrointestinal tract is not required for intraventricular injections of SENK to suppress sodium appetite; (c) the activation of NK3 receptors decreases the oral excitatory influence of hypertonic NaCl in sodium-deficient rats.

Animals↗

PubMed1985

Effects of intravenous and intraventricular injection of antisera directed against corticotropin-releasing factor on the secretion of anterior pituitary hormones.

To determine the physiological significance of corticotropin-releasing factor (CRF) in the control of pituitary hormone secretion, highly specific antibodies directed against the peptide were injected either intravenously or intraventricularly (third ventricle) and the effect on plasma levels of pituitary hormones was determined before and after application of ether stress for 1 min. The intravenous injection of CRF antiserum (0.5 ml) did not significantly alter basal corticotropin (ACTH) levels in freely moving ovariectomized rats but largely blocked the increase in plasma ACTH resulting from ether stress. These antibodies had no effect on the ether-induced decline in plasma growth hormone (GH), and they failed to modify plasma luteinizing hormone levels. In a second experiment, CRF antiserum (3 microliter) or normal rabbit serum was injected into the third ventricle. A blood sample was drawn 24 hr later and immediately thereafter another injection of CRF antiserum or normal rabbit serum was made. There was no modification in the level of any of the hormones 24 hr after the first injections, and they were similar in CRF antiserum and normal rabbit serum-injected animals. After imposition of ether stress, the response of plasma ACTH was nearly completely blocked by the intraventricular CRF antiserum, but the degree of blockade was slightly less than that obtained by intravenous injection. The decline in plasma GH after ether stress was blocked by the intraventricular CRF antiserum. There was no effect of the intraventricular injection of the antiserum on the levels of the other pituitary hormones. The results with intravenous injection of the antisera indicate that CRF plays an extremely important but probably not completely indispensable role in the release of ACTH after ether stress. The results of the intraventricular injection of the antiserum suggest strongly that endogenous CRF may also modify its own release in response to stress, augmenting it by a positive ultrashort loop feedback, and that the antisera against the peptide blocked this action; however, an action at the pituitary of these intraventricularly injected antibodies cannot be completely ruled out. The blockade of the stress-induced suppression of GH release by the CRF antibodies suggests that CRF released intrahypothalamically during ether stress brings about an alteration in the hypothalamic control of GH secretion such that the stress-induced inhibition of GH release is blocked.

Adrenocorticotropic Hormone↗

PubMed1982

Calcitonin-induced anorexia in rats: a structure-activity study by intraventricular injections.

The anorectic potency of salmon, porcine and human calcitonins (sCT, pCT and hCT, respectively) and two sCT-fragments were compared in rats. Intraventricular injections of sCT (0.062 and 0.031 nmole/animal) significantly reduced the normal feeding and body weight. The effect appeared to be dose-dependent, reversible and lasted longer than 6 hr. No anorexia ensued, however, on injections of mammalian hormones though tested in relatively high doses (pCT: up to 3.7 nmole, hCT: 3.7 nmole). The C-terminal fragments of sCT, sCT (10-32) and sCT (22-32) were also found to be devoid of anorectic activity; but when administered with sCT, the longer fragment (1.2 nmole) significantly decreased the effect of sCT and even the shorter one (18 nmole) tended to act as an antagonist. This property was not recorded with pCT and hCT in the doses examined. On the one hand, these results indicate a novel specificity of the anorectic receptor in rat brain; and on the other hand, they seem to strongly argue against the hypothesis that in mammals thyroidal calcitonin secreted postprandially might participate in the regulation of subsequent feeding, unless the presence of the sCT-like molecule can be detected in mammals. All the more because detection of such a molecule must await development of a specific assay, the antagonistic property of the sCT fragment found herein would have use for clarifying the physiological significance of the anorectic receptor which is possibly in the hypothalamus.

Animals↗

PubMed1987

Behavioural and ECoG spectrum power effects after intraventricular injection of drugs altering dopaminergic transmission in rats.

In rats with cannulae permanently implanted into the third cerebral ventricle, the effects of different pharmacological manipulations affecting dopaminergic mechanisms, were studied on behaviour and electrocorticographic (ECoG) activity, continuously quantified in its spectrum power. The intraventricular injection (0.1-1 nmol) of (-)3PPP[3-(3-hydroxyphenyl) N-n-propylpiperidine], a specific agonist at dopamine (DA) autoreceptors, produced dose-dependent behavioural sedation or sleep and an increase in ECoG spectrum power, with a predominant increase in the lower frequency bands. Short episodes of stereotyped movements, wet-dog syndrome, penile grooming and erection were also observed. Similar behavioural and ECoG effects were elicited by the intraventricular injection of R-(+)-8-chloro-2,3,4,5-tetrohydro-3-methyl-5-phenyl-1H-3-benzazepi ne-7-ol (SCH 23390), a selective antagonist at D1 postsynaptic receptors, although these were preceded by a short period of behavioural and sexual stimulation. In addition, the intraventricular administration of some neuroleptics, chloropromazine and haloperidol, produced behavioural and ECoG slow wave sleep. No significant changes were observed with a neuroleptic drug, 1-sulpiride, which is reputed to act selectively as an antagonist at dopamine D2 receptors. In conclusion, the present experiments add new evidence in favour of the idea that dopaminergic mechanisms are involved in mammalian species in the control of arousal and that both post-synaptic D1 and D2 receptors may take part in such a control.

Animals↗

PubMed1987

Transport of p-aminohippuric acid (3H-PAH), inulin and dextran out of the cranial cavity: a methodological study using intraventricular injection and sample combustion.

Material injected into the cerebral ventricles can leave the cerebrospinal fluid (CSF) but remain in the cranial cavity. To analyze the disappearance of 3H- and of 14C-labelled material from the cranial cavity, such material was injected into the lateral ventricles together with a bulk flow marker, labelled with the other radionuclide. In the present pilot study 3H-PAH and 14C-inulin were used. Five microliter of a mixture was injected into each lateral cerebral ventricles in rats, which were killed at various intervals. The whole skull was analyzed without opening the CSF space after homogenization in the deep-frozen state. The samples were combusted and analyzed by liquid scintillation counting. Probenecid, injected intraperitoneally, inhibited the removal of 3H-PAH from the skull cavity, as anticipated. Immediately after the intraventricular injection, however, 3H-PAH was transiently retained, probably by uptake into actively transporting tissue. After injection of probenecid, this delay in removal was reduced. The difference in disappearance rate between 3H-PAH and 14C-inulin was estimated by comparing the 3H/14C ratio in the skulls with that in the injected solution, which appeared to be a better method than comparing the recovery of each compound.

Aminohippuric Acids↗

PubMed1990

Central glucoregulation in the pigeon Columba livia. Effects of intraventricular injections of carbachol and catecholamines on blood glucose concentration.

The effect of chemical stimulation of the central nervous system on glucoregulation was studied in pigeons (Columba livia). Adrenaline (30 nmol), noradrenaline (30 or 80 nmol) and carbachol (27 nmol) were injected in 1 microliter NaCl directly into the lateral ventricle and changes in blood glucose concentration were measured. The intraventricular injection of adrenaline resulted in rapid hyperglycemia, whereas the injection of either carbachol or noradrenaline into the lateral ventricle did not cause any significant changes in blood glucose concentration. These results suggest that adrenaline-containing neurons may be involved in central mechanisms controlling blood glucose concentration in the pigeon.

Animals↗

PubMed1992

Accumulation of amyloid precursor protein in neurons after intraventricular injection of colchicine.

To study a possible relationship between inhibition of axonal flow and amyloidogenesis, the authors examined amyloid precursor protein (APP) immunoreactivity in rat brain treated with colchicine. After intraventricular injection of colchicine, the proximal axons of exposed neurons became swollen and showed a large increase in APP immunoreactivity, whereas the cytoplasm and dendritic processes showed lesser increases. These changes were seen in ipsilateral neurons of the hippocampus, lateral septal nucleus, amygdala, and entorhinal, parietal and temporal cortices, as well as bilaterally in the periventricular hypothalamic nucleus. The increase of APP immunoreactivity appeared as early as 3 hours after the injection. It peaked at around 24 hours, and began to clear after about 4 days. A few strongly APP-positive dystrophic neurons remained. In serial sections at these later time periods, some strongly argentophilic neurons and Alz-50 positive neurons, each with abnormal neurities, could be demonstrated. The result suggests that APP may undergo fast axoplasmic flow in rat brain and that argentophilic changes of Alz-50 immunoproduction may follow APP accumulation caused by inhibition of axoplasmic flow.

Amyloid beta-Protein Precursor↗

PubMed1981

Excitatory effects of intraventricular injections of oxytocin on the milk ejection reflex in the rat.

The effects of oxytocin, administered into the 3rd cerebral ventricle, on the milk ejection reflex, were studied in urethane-anaesthetized lactating rats. Intramammary pressure, electrical activity of oxytocinergic neurones and EEG were recorded simultaneously. Intraventricular injection of oxytocin (6, 60 and 600 microU) significantly increased both milk ejection frequency and the number of spikes in the oxytocinergic neurones characteristic bursts. The amount of hormone released for each milk ejection was higher after intraventricular oxytocin injection than before. The strongly excitatory effect of intraventricular oxytocin injection on the milk ejection reflex was not reproduced with arginine-vasopressin.

Animals↗

PubMed1974

Some shortcomings of direct intraventricular injection in mice.

The use of X-ray photography following injection of iophendylate to verify that intraventricular injections in mice have been satisfactorily accomplished is misleading since it fails to detect leakage into the periphery. Radioactive labelling reveals that a substantial proportion of the injected material is rapidly carried to the periphery in the bloodstream.

Animals↗

PubMed1981

Release and synthesis rates of catecholamines in hypothalamic, limbic and midbrain structures following intraventricular injection of beta-endorphin in male rats.

Serum hormone levels and turnover rates of dopamine (DA), norepinephrine (NE) and epinephrine (E) in tissue of pontine midbrain, limbic caudate, and hypothalamic structures were measured following intraventricular injection of 20 microgram beta-endorphin. Turnover of DA was increased in the locus coeruleus and in structures innervated by the nigrostriatal and mesolimbic DA systems while it decreased in the posterior hypothalamus. The NE turnover was reduced in the locus coeruleus and posterior mediobasal hypothalamus. In all tissues examined, beta-endorphin treatment had no significant effect on E turnover. Serum levels of prolactin and corticosterone increased following beta-endorphin treatment whereas LH, FSH and TSH levels decreased. The observed effects of beta-endorphin on preoptic and hypothalamic DA and NE turnover rates may explain these hormonal changes. The reduced NE turnover in the locus coeruleus may be induced by increased DA turnover. The observation, that NE turnover in structures innervated by locus coeruleus neurons may go in different direction suggest that NE turnover is regulated independently from the activity of locus coeruleus neurons, hence that the regulation must occur at the terminals by a direct or indirect interaction with endorphinergic neurons.

Animals↗

PubMed1976

Uptake of 5-hydroxytryptamine in different parts of the brain of the rabbit after intraventricular injection.

1 The uptake of 5-hydroxytryptamine (5-HT) was investigated in different areas of the rabbit brain (anterior hypothalamus, the raphe, the region of the substantia nigra, several cortical areas and the medulla oblongata) after intraventricular injection in pargyline pretreated animals by the formaldehyde-induced histochemical fluorescence method. 2 The distribution of fluorescence showed that the uptake of 5-HT, after circulation in the cerebrospinal fluid, caused a general increase in intensity of green yellow to yellow background fluorescence. There was an increased fluorescence in the nerve terminals, but no uptake occurred either in the cell bodies of neurones or in the glial cells.

Animals↗

PubMed1985

Effect of intraventricular injection of 5,6-dihydroxytryptamine on spermatogenesis and plasma testosterone levels in the rat.

Quantitative evaluation of spermatogenesis at stage VII of the cycle of the seminiferous epithelium and radioimmunoassay of plasma testosterone were performed in adult Wistar rats after intraventricular injection of 5,6-dihydroxytryptamine (5,6-DHT). The rats were killed 2, 10 and 21 days after injection. Brain 5-hydroxytryptamine (5-HT) and plasma testosterone levels were found to be significantly lower in all rats treated with 5,6-DHT. A significant reduction in step 7 spermatid count was also observed after 10 and 21 days. Supplementation with human chorionic gonadotrophin for 21 days in rats injected with 5,6-DHT partially prevented the step 7 spermatid degeneration and increased testosterone levels without producing any effect on brain concentrations of 5-HT. These results suggest that changes in testicular steroidogenesis and spermatogenesis are secondary to pituitary gonadotrophin release which, in turn, is under the influence of brain 5-HT neurones.

5,6-Dihydroxytryptamine↗

PubMed1982

Distribution of hippocampal glycoproteins as demonstrated in rats by lectin binding and autoradiography after intraventricular injections of labelled fucose, N-acetyl-glucosamine and mannose.

The present study demonstrates distinct distribution patterns of glycoproteins in rat hippocampus, with respect to synthesis from precursors (autoradiography) and endogenous contents (lectin binding). The autoradiographic analysis performed 1, 2, 8 and 24 h after intraventricular injections of tritium-labelled L-fucose. N-acetyl-D-glucosamine and D-mannose revealed that up to 2 h after application of any of the three precursors, radioactivity occurred in the pyramidal and granular cell layers. Afterwards, however, rapid migration of label proceeded from the cell bodies into the neuropil after application of fucose and acetylglucosamine, while after injection of mannose a considerable amount of radioactivity stayed in the cell body layers, even 24 h after administration of labelled precursor. These findings were consistent with the histochemical visualization of glycoprotein constituents by fluorescent wheat germ lectin (preferentially binding to glucosaminyl residues) and concanavalin A-horseradish peroxidase (preferentially binding to mannosyl residues). These showed a heavy staining predominantly in neuropil and somata, respectively, with concanavalin A-binding giving more distinct patterns than the application of labelled mannose. The usefulness of the three glycoprotein precursors as correlates with functional behavioural changes in discussed.

Acetylglucosamine↗

PubMed1993

Intraventricular injection of agents that enhance cyclic adenosine monophosphate formation leads to inhibition of proestrous luteinizing hormone surge in rats.

The effect of increasing hypothalamic levels of 3',5'-cyclic adenosine monophosphate (cAMP) on the preovulatory surge of luteinizing hormone (LH) and ovulation was studied in cycling rats. Animals hearing chronically implanted guiding cannulae into the third ventricle were injected with agents known to enhance the cellular levels of cAMP. Hourly blood samples from the unanesthetized, unrestrained rats were obtained between 11.00 and 17.00 h through a plastic cannula inserted into the jugular vein. Intraventricular injections of serotonin (7.5 mg/ml; 2 microliters) in the morning of proestrous blocked the preovulatory surge of LH and ovulation. This effect was assigned to an increased neuronal level of cAMP because it was prevented by a serum anti-cAMP. Third-ventricle injections of 2 microliters of forskolin (0.5 mmol/l), guanosine 5'-O-(3-thiotriphosphate)(2 mmol/l) or dibutyryl-cAMP (1 mmol/l) at 11.00 h on the day of proestrus mimicked the inhibitory effect of serotonin on the proestrous release of LH. It is suggested that serotonin inhibits LH surge by acting directly on LH-releasing hormone neurons and/or on neurons that provide inputs to these neurons involving cAMP as a second messenger. Neurons releasing gamma-aminobutyric acid (GABA) may serve as interneurons sensitive to serotonin, as well as to cAMP, inasmuch as the inhibitory effect of forskolin on the release of LH was partially blocked by the GABA antagonists, picrotoxin and bicuculline.

Animals↗

PubMed1976

[Role of the adrenergic system in lateral hypothalamic self stimulation behavior: effects induced by intraventricular injection of epinephrine, norepinephrine, isoproterenol and dopamine].

A bipolar electrode was stereotaxically implanted in or near the medial forebrain bundle at the level of the posterior lateral hypothalamus of male albino Wistar-Imamichi rats. The relationship between the adrenergic system and the lateral hypothalamic self-stimulation (SS) behavior was investigated by intraventricular injection (by the use of the modelled hypodermic needle) of catecholamines. l-Epinephrine(Ep), l-norepinephrine (NE) facilitated the SS behavior dose-dependently. On the other hand, l-isoproterenol and dopamine revealed no detectable effects. Phentolamine inhibited the SS behavior, but propranolol had no marked effects. Facilitation by NE for the SS behavior was not induced when the current was cut off at the time of the injection of NE. These results suggest the following: a) the adrenergic or the noradrenergic system in the brain may play a more important role in the positive reinforcement of the lateral hypothalamic SS behavior than does the dopaminergic system. b) The action of Ep or NE may be facilitated through alpha-receptors rather than through beta-receptors. c) Facilitation by NE for the lateral hypothalamic SS behavior may not be due to the non-specific facilitation of lever pressing, but rather may be related to intracranial stimulation.

Animals↗