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At least 91 records · Page 5Linked to original sources
PubMed1999

Regulation of gonadal and somatotropic axis by chronic intraventricular infusion of insulin-like growth factor 1 antibody at the initiation of puberty in male rats.

There has been increasing experimental evidence to suggest that insulin-like growth factor 1 (IGF-I) may be one of the essential regulators in the reproductive system of the rat. IGF-I is synthesized in the hypothalamus and IGF-I immunoreactivity increases during puberty. Consequently we hypothesized that centrally located IGF-I might contribute to the initiation of puberty. Centrally located IGF-I was immunoneutralized to assess this hypothesis. Male Wistar rats, 28 days old, were infused intracerebroventricularly with specific purified IgGs from rabbit IGF-I antiserum (IGF-I-Ab). The intracerebroventricular administration of IGF-I-Ab resulted in a reduction in testicular weight and consequently in delayed pubertal development. There was also a reduction in serum testosterone, pituitary immunoreactive (IR) luteinizing hormone (LH) and serum IR follicle-stimulating hormone (FSH). The accumulation of betaLH mRNA was not modified, whereas betaFSH mRNA was increased. An increment in the serum growth hormone (GH) levels was also observed. There were no significant alterations in hypothalamic IR growth hormone releasing factor content, although IR somatostatin (SRIH) content was increased by IGF-I-Ab. The body weight gain remained unaltered. As a whole, our study suggests that centrally located IGF-I influences pubertal development, production and release of gonadotropins and supports the finding that endogenous centrally located IGF-I plays a role at the initiation of puberty in the male rat. It also gives support to the physiological role of centrally located IGF-I in the release of GH mediated by hypothalamic SRIH at the initiation of puberty.

Animals↗
PubMed1991

Intraventricular infusion of epidermal growth factor restores dopaminergic pathway in hemiparkinsonian rats.

We assessed the effect of a 35-day delayed intracerebroventricular (ICV) infusion of epidermal growth factor (EGF) on the survival and function of the substantia nigra (SN) dopaminergic neurons after a unilateral mechanical transection of rat nigrostriatal pathway. EGF infusion for 28 days resulted in a twofold increase in the number of surviving tyrosine-hydroxylase (TH)-positive SN neurons and a significant increase in ipsilateral striatal TH-positive fiber staining compared to controls at 200 days following the injury. In addition, there was a persistent enhancement of behavioral recovery, as indicated by a reduction in amphetamine-induced rotations. We conclude that EGF exerts a neurotrophic effect on the dopaminergic neurons in this experimental model of parkinsonism.

Animals↗
PubMed1994

Shunt removal or replacement based on intraventricular infusion tests.

In 14 children with indwelling ventriculoatrial or ventriculoperitoneal shunts, the need for continued shunt treatment was judged to be uncertain based on clinical symptoms and signs and CT scans. Ventricular outflow resistance (R0) was determined by implantation of a ventricular catheter and steady state infusion of artificial cerebrospinal fluid (CSF) according to the formula R0 = (Pp - P0)/Infusion rate, where P0 is the opening pressure in the lateral ventricle and Pp the plateau pressure recorded at that particular infusion rate. R0 was determined during general anesthesia and steady state ventilation was ensured by mechanical ventilator. Ventricular fluid pressure (VFP) and arterial blood pressure (ABP) were recorded by standard fluid pressure transducers. The cerebral perfusion pressure (CPP = ABP - VFP) was kept above 30 mmHg by reducing the infusion rate in cases of unacceptable increase in VFP. R0 was determined with the shunt clamped. During steady state infusion at the plateau pressure the shunt was unclamped to test shunt patency. Four children had normal R0 values with the shunt clamped. Their shunts were removed. They have done well clinically, and control CT scans have not demonstrated increased ventricular size. Three children demonstrated pathologic R0 values (above 12 mmHg/ml per min) that normalized after shunt unclamping; i.e. each had a well-functioning shunt. Seven children demonstrated increased R0 values even after shunt unclamping. Their shunts were replaced, and clinical improvement has been observed in 6 of them. Ventricular infusion tests appear useful to evaluate shunt dependence and function in difficult cases.

Adolescent↗
PubMed1989

An improved device for continuous intraventricular infusions prevents the introduction of pump-derived toxins and increases the effectiveness of NGF treatments.

The recent demonstrations of the ability of nerve growth factor (NGF) to protect and promote the welfare of certain cholinergic neurons in the adult CNS have increased the need for safe, accurate, and reliable procedures for intracerebral administration of protein and other experimental agents. Osmotic minipumps have been used to infuse NGF into the lateral ventricle of adult rats, but a sustained and harmless performance of such infusions has not been fully evaluated. The study reported here has led to (i) the recognition that cytotoxic substances, released from some minipumps into the infusion fluid, may be responsible for various degrees of periventricular tissue damage, and (ii) the redesigning of an infusion device which, among other modifications, uses the osmotic pump to propel infusion fluid into the ventricle but prevents pump-derived materials from entering the infusate itself. Besides several other advantages, the modified infusion device has permitted the demonstration that NGF can fully protect experimentally axotomized medial septum cholinergic neurons and can do so with less variability than previously observed and without creating tissue damage.

Animals↗
PubMed1991

Chronic administration of beta-carboline-3-carboxylic acid methylamide by continuous intraventricular infusion increases GABAergic function.

The repeated, intraperitoneal administration of the benzodiazepine receptor inverse agonist, FG 7142 (beta-carboline-3-carboxylic acid methylamide), leads to pharmacological kindling and an associated decrease in GABA-stimulated influx of 36Cl- into cortical membrane preparations. The chronic administration of benzodiazepine agonists results in the development of tolerance and also results in a decrease in GABA-stimulated uptake of 36Cl-. The present study was designed to evaluate further the paradoxical reports that both chronic treatment with benzodiazepine receptor agonists and inverse agonists results in a decreased ability of GABA to stimulate uptake of 36Cl- into cortical membrane preparations. The effects of continuous administration of FG 7142 on GABA-stimulated uptake of 36Cl-, the threshold for bicuculline-induced seizures and the proconvulsant actions of acute administration FG 7142 were evaluated. The continuous administration of FG 7142 resulted in an increased capacity of GABA to stimulate the uptake of 36Cl- into cortical membrane preparations and a significant increase in the seizure threshold for bicuculline following the acute administration of FG 7142. These data, therefore, indicate that changes in GABAergic function following chronic administration of GF 7142 are dependent on the regimen of administration of drug. The results also suggest that the GABA receptor homeostatically responds to continuous occupation by inverse agonists by an upregulation of its functional response to GABA.

Animals↗
PubMed1996

Subchronic intraventricular infusion of quinolinic acid produces working memory impairment--a model of progressive excitotoxicity.

It has been proposed by Yamada et al. [Neurosci. Lett. 118: 128-131 (1990); J. Pharmacobiodyn. 14: 351-355 (1991)] that subchronic i.c.v. infusion of the NMDA receptor agonist quinolinic acid may serve as a model for some aspects of neurodegenerative dementia. In the present study, quinolinic acid (9 mM) was infused i.c.v. by ALZET osmotic minipumps for 2 weeks. This treatment produced a short-term working memory deficit in the T-maze (alternation) but no change in reversal learning in the same test. The working memory deficit in the T-maze was progressive i.e. seen after 14, but not 3 days of infusion and persisted for at least for 3 weeks after the termination of the infusion. Histological examination revealed a modest decrease in the number of cells in the nucleus basalis magnocellularis but not in the striatum, entorhinal cortex, or hippocampus. However, in most of the structures studied, morphological changes such as swollen somata and irregular shape were observed indicative of alterations in neuronal function. Autoradiography in the hippocampus revealed a decrease in [3H]hemicholinium and [3H]quinuclidinyl benzilate (QNB) binding to choline uptake sites and muscarinic receptors respectively. Surprisingly no change was observed in [3H]MK-801 binding to NMDA receptor channels in the hippocampus and cortex. The subchronic infusion of quinolinic acid may serve as a model of progressive deterioration of cognitive functions.

Alzheimer Disease↗
PubMed1991

Food intake and serum insulin responses to intraventricular infusions of insulin and IGF-I.

Previous studies reported that intracerebroventricular (ICV) infusion of insulin decreased food intake in rats and baboons. Insulin can bind to insulin-like growth factor I (IGF-I) receptors and mimic the response of IGF-I. Our objective was to determine the effects of ICV infused-insulin or IGF-I on food intake in sheep. In the present study, a 6-day ICV infusion of insulin (123 ng/kg of body weight/day) but not of IGF-I (123 ng/kg of body weight/day) decreased food intake by 40% (p less than 0.003) and body weight (p less than 0.015) compared with control sheep. In addition, sheep that received ICV insulin or IGF-I had only half the concentration of insulin in serum as compared with controls. Our results support the hypothesis that ICV insulin does not decrease food intake through IGF-I receptors. Nevertheless, apparently both insulin and IGF-I in the brain can influence the concentration of insulin in blood.

Animals↗
PubMed1997

Memory disturbance and hippocampal degeneration induced by continuous intraventricular infusion of a protease inhibitor, leupeptin.

Effects of a protease inhibitor, leupeptin, on the memory function and the morphological changes in the hippocampus were examined in rats. The leupeptin was infused by an implanted-osmotic minipump into the lateral ventricle of the rats for 14 days. The acquisition and the maintenance of memory were evaluated by a step-down passive avoidance task. The control rats, infused with an artificial cerebral spinal fluid, showed good retention for the passive avoidance training for 21 days after training. The leupeptin-treated rats showed good retention for 7 days following training; however, pronounced impaired retention was observed on day 10 and thereafter. These rats were accompanied by a degeneration of the dentate gyrus in the histological examinations on Days 14 and 21. The granule cells in the dentate gyrus of the hippocampus appeared much more eosinophilic pyknotic. Numerous eosinophilic spherical structures of the cell processes were seen in the neuropil beneath the granule cell layer. Electron microscopic examination disclosed a marked accumulation of lipofuscin-like granules in the perikaryon of the cells and in the dendrites and the axons. These findings suggest that the memory impairment is closely related to the degeneration of the dentate gyrus in the hippocampus in the leupeptin-treated rats.

Animals↗
PubMed1997

Intraventricular infusion of arginine vasotocin induces singing in a female songbird.

Arginine vasotocin (AVT) has been implicated in the activation of courtship and aggressive behaviors in many vertebrate taxa. Here, we tested its effect on singing and other vocal behavior in a songbird. Female white-crowned sparrows (Z. l. gambelii) were implanted with chronic cannulae aimed at the third ventricle. Infusions of AVT dramatically increased the number of songs and other vocalizations during a 40 min period following infusion. Half of the subjects sang full song following AVT treatment. No bird sang after treatment with saline; any type of vocalization after saline treatment was rare. Female white-crowned sparrows are known to sing in both spring and winter in the wild; this behavior is thought to be aggressive, functioning in dominance interactions and territoriality. Central infusion of AVT induced singing and other vocalizations in estrogen-primed, photostimulated subjects as well as in non-reproductive subjects housed on short photoperiods. Thus, the effects of AVT on vocal behavior may not require breeding levels of gonadal steroids and are probably not seasonal. We hypothesize that both in the breeding and non-breeding seasons, AVT increases motivation to sing.

Animals↗
PubMed1991

Intraventricular infusion of the selective sigma-agonist 1,3-di-ortho-tolylguanidine (DTG) mitigates ischaemic brain damage in the hippocampus.

Experimental evidence suggests that neuronal pharmacologic sites termed sigma (sigma) may be related, but not identical to PCP sites in the ion channel linked to NMDA excitatory receptors. These receptors may play a role in schizophreniform psychoses, and clinical trials of putative sigma-ligands have begun. Because of this, and because of the relationship of sigma-ligands to NMDA receptors, we studied the effect of the most selective presently available sigma-ligand on ischaemic neuronal death throughout the rat brain after transient forebrain ischaemia. Ventricular delivery of DTG at 0.5 mumol/h via an osmotic minipump was chosen to allow continuous access of the drug to brain tissue, control animals receiving artificial CSF. After one week survival, selective neuronal necrosis was reduced in the hippocampus, but not in the neocortex or striatum, contrasting with our previous findings in this model with pure NMDA antagonists. The results indicate that ischaemic neuronal necrosis in the hippocampus may be mitigated by sigma-agonists, possibly via an interaction with NMDA receptors.

Animals↗