SEARCH · PubMed Health

Results for “Infusions, 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.

At least 37 records · Page 2Linked to original sources

PubMed1992

Intraventricular infusion of N-methyl-D-aspartate. 1. Acute blood-brain barrier consequences.

The purpose of this study was to document the early cerebrovascular consequences of excessive N-methyl-D-aspartate (NMDA) receptor activation. Five microliters of NMDA (100 nmol/microliters) or vehicle was infused over a 15-min period into the lateral ventricle of adult rats. The protein tracer horseradish peroxidase (HRP) was injected intravenously for blood-brain barrier (BBB) studies. The intraventricular infusion of vehicle (n = 5) caused no alterations in arterial blood pressure or microvascular damage away from the intraventricular probe tract. In contrast, NMDA infusion (n = 8) led to a gradual increase in arterial blood pressure (mean 36 mm Hg). Multifocal regions of HRP extravasation were observed bilaterally throughout the neuraxis following NMDA infusion. Sites of BBB disruption and hemorrhage included brain regions bordering ventricular spaces. In addition, isolated foci of protein extravasation were commonly detected in the cerebral cortex, thalamus, basal forebrain, septum and cerebellum. Pretreatment with the noncompetitive NMDA antagonist MK-801 (2 mg/kg) substantially reduced the BBB responses to NMDA. However, microvascular abnormalities were seen in NMDA-infused rats where blood pressure elevations were inhibited by blood removal. In addition to neurons, cerebral blood vessels are also acutely affected by NMDA receptor activation. Blockage of NMDA receptor channels following brain injury may potentially provide protection by attenuating BBB breakdown and subsequent brain edema.

Animals↗

PubMed1992

Intraventricular infusions of anti-neural cell adhesion molecules in a discrete posttraining period impair consolidation of a passive avoidance response in the rat.

Intraventricular infusions of anti-neural cell adhesion molecule (anti-NCAM) are demonstrated to inhibit consolidation of a passive avoidance response when administered in the 6-8 h posttraining period. Anti-NCAM was ineffective when administered during training or at any other time up to 10 h thereafter, and no amnesic effects were observed with absorbed anti-NCAM or anti-neurofilament protein. Amnesia was observed only at the 48-h recall time, and this could not be attributed to poor antibody penetration or a prolonged residence time, as studies with 125I-labelled anti-NCAM in trained animals demonstrated a rapid accumulation into all brain regions, and this was marked in the olfactory bulb and hippocampus, areas showing an inherent and paradigm-specific increase in NCAM sialylation state, respectively. The lack of an amnesic action at the 24-h recall time is attributed to anti-NCAM-impaired synapse structuring becoming apparent following the paradigm-specific increases in NCAM sialylation state.

Amnesia↗

PubMed1995

Cytoskeletal changes in rat cortical neurons induced by long-term intraventricular infusion of leupeptin.

Neurofibrillary tangles (NFTs), which are composed of paired helical filament (PHF)-like filaments, were induced by the long-term intraventricular infusion of leupeptin, a potent protease inhibitor. The fibrils composing the NFTs were 20 nm in maximal width and had periodic constrictions at 40-nm intervals. They were identical to the PHF that had been found in aged rat neurons. Dystrophic axons filled with mainly tubular structures were also abundantly found in the parietal and temporal isocortices, which were not affected in the acute or subacute phases of leupeptin treatment. An immunohistochemical study using antibodies related to the neuronal cytoskeleton showed that neuronal cytoskeletal changes accompanying ubiquitination occurred in dystrophic axons distributed widely in the isocortex as well as the hippocampal formation. The present findings suggest that long-term administration of leupeptin accelerates the neuronal ageing process in rats and causes other neuronal changes: NFT formation, such as seen in the aged brain or in neurodegenerative diseases including Alzheimer's disease, in addition to accumulation of lipofuscin granules and degeneration of neuronal processes. In other words, some disturbance of the balance between proteases and their inhibitors may play an important role in the neuronal ageing process, and some regulatory intervention in the intraneuronal protease activity may provide a new therapeutic strategy for the neurodegenerative diseases.

Alzheimer Disease↗

PubMed1997

Chronic intraventricular infusion with NGF improves LTP in old cognitively-impaired rats.

Aged (21 months) cognitively-impaired male Sprague-Dawley rats received intraventricular infusion of nerve growth factor (NGF) or cytochrome C (Cit C) for 14 or 28 days using miniosmotic pumps and were evaluated either 1 week or 3 months after treatment. Groups of untreated young, aged-impaired and aged non-impaired rats were also evaluated. Under narcose recording and stimulating electrodes were stereotactically implanted in the dentate gyrus and the perforant path. The stimulation intensity was individually adjusted to obtain a half-maximal population spike (P) for test stimuli and a quarter-maximal for tetanization. The amplitude and latency of P and the slope (S) of the field EPSP were determined before and at 2, 5, 15, 30 and 60 min after tetanization at 400 Hz. Paired stimuli at 30 ms interval were also applied before and after tetanization. Aged, cognitively impaired rats showed an absent S potentiation and a delayed P potentiation, both in amplitude and latency, while non-impaired rats behaved like the young controls. Paired pulse inhibition showed no difference among groups before or after tetanization suggesting that the impaired potentiation is not due to an increased retroactive inhibition. NGF treatment ameliorates LTP deficits to levels equivalent to non-impaired rats, while Cit C controls showed no improvement. No differences appear among NGF treated groups, but evidence suggest that the animals evaluated 3 months after treatment developed a stronger potentiation.

Aging↗

PubMed1975

Fine structure of labelled axons in the cerebellar cortex and nuclei of rodents and primates after intraventricular infusions with tritiated serotonin.

The cerebellar cortex and deep cerebellar nuclei in rats and rhesus monkey were studied after treatment with monoamine oxidase inhibitor and continuous intraventricular infusion with 10(-5) M serotonin-3H. Autoradiographs were prepared for light and electron microscopy. The cerebellum contained no labelled cells. Labelled unmyelinated axons arrive from the brain stem via the periventricular zones of the aqueduct and fourth ventricle. In the parafloccular cortex about 1 per cent of the mossy fibers are labelled, together with a small number of fine varicose axons in the molecular layer that run parallel to the folial axes (less than 0.1%). In the paravermal and vermal cortex there are few labelled fibers in the granular layer and a five-fold greater number of labelled axons in the molecular layer (about 0.5%). Apparently three systems of serotonin-containing axons are present in the cortex: mossy fibers, parallel fiber-like, and a diffuse system in granular and molecular layers. The fastigial (medial), interpositus, and dentate (lateral) nuclei, lateral vestibular and other vestibular nuclei all have numerous labelled axons. The dentate and interpositus nuclei receive labelled fibers which arrive through the superior cerebellar peduncle as well as from the periventricular area. Six morphologically different classes of labelled axon terminals have been differentiated. Class 1a, the mossy fiber rosettes, and class 1b, the CAT2 axons, have small, round, clear synaptic vesicles and large granular vesicles (lgv); class 2 axons have a distinctive collection of round granular vesicles; class 3 boutons have numerous tubular profiles, a few containing dense dots, packed in a dark axoplasmic matrix; class 4 axons have tiny 250 A granular vesicles, clear tubular profiles and occasional LGV; class 5 terminals have numerous LGV, both round and elongated, with clear round and tubular profiles; class 6 terminals have LGV, clear and granular synaptic vesicles and clear tubular profiles. All these axons have LGV 900 A in diameter with 500-600 A variably dense centers that do not fill the vesicle, and Gray's type 1 axodendritic or axasomatic synapses on postsynaptic locations in the cortex and nuclei. Labelled axons in the cortex end as mossy fibers upon granule cell dendrites in glomeruli (Class 1a) or upon dendrites of cortical interneurons, e.g. Golgi cells, basket and stellate cells, and not on Purkinje cells. ...

Animals↗

PubMed1975

Ovulation induced by the intraventricular infusion of norepinephrine in rats made anovulatory by neonatal administration of various doses of testosterone.

Gradually increasing doses of neonatal TP decrease the rate of ovulation induced by intraventricular infusion of 100 mug of NE. This finding suggests that the reduced functional capacity of the LH-RH-producing neurons in androgen-sterilized rats may account for the difference between the ovulatory action of NE in anterior hypothalamus-lesioned and androgen-sterilized rat.

Animals↗

PubMed1985

An intraventricular infusion model for inducing morphine dependence in rats: quantitative assessment of precipitated withdrawal.

An experimental model of morphine dependence, in which rats were made dependent upon morphine by intraventricular infusion, is described. Morphine dependence was assessed and quantified by a series of withdrawal signs that were induced by the intraperitoneal administration of the morphine antagonist naloxone. The infusion of different concentrations of morphine resulted in the production of physical dependence, the severity of which was directly correlated with the concentration of morphine infused. A weak to moderate degree of dependence characterized by such withdrawal signs as teeth chattering, whole-body shakes, and vocalization was produced by infusions of morphine less than 5 micrograms/hr. A strong degree of physical dependence characterized by additional dominant withdrawal signs such as jumping and launching was produced by the infusion of 50 micrograms/hr morphine. The morphine pellet model that most closely approximated this degree of dependence was a three-pellet model in which a single 75-mg morphine pellet was implanted at 48-hr intervals. Abstinence precipitated by removal of the morphine-containing osmotic minipumps was characterized primarily by teeth chattering and whole-body shakes which persisted for at least 48 hr.

Animals↗

PubMed1989

Intraventricular infusion of Dopamine in Parkinson's disease.

A patient with severe end-stage Parkinson's disease and troublesome fluctuations in motor function was treated with a long-term intraventricular infusion of dopamine. There was modest improvement in speech and mentation and there was smoother control of motor symptoms that was superior to that achieved by conventional oral medications.

Adult↗

PubMed1991

Treatment of leptomeningeal carcinomatosis with continuous intraventricular infusion of recombinant interleukin-2.

A 42-year-old man developed leptomeningeal carcinomatosis 6 years after treatment of a malignant melanoma. He was treated with two courses of recombinant interleukin-2, administered as a continuous intraventricular infusion (6 X 10E5 U/24 h) during 5 days. During the first day of the first course he also received 5 X 10E9 lymphokine-activated killer cells intraventricularly. This gave rise to a severe elevation of intracranial pressure, with headaches and meningismus. During the second course no LAK cells were administered. This course was tolerated much better. The neurological status did not change during the treatment. Recombinant interleukin-2 levels were maintained at about 300 U/mL during both courses.

Adult↗

PubMed1996

Intraventricular infusion of basic fibroblast growth factor (bFGF) in the MPTP-treated common marmoset.

Basic fibroblast growth factor (bFGF) prevents damage to the nigrostriatal system in rodents. We now report the effects of bFGF administered by intraventricular infusion to adult common marmosets (Callithrix jacchus) previously rendered parkinsonian by the administration of 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Infusion commenced 10 weeks after MPTP treatment and the animals received bFGF in low (1.8 micrograms/l), medium (18 micrograms/l), or high (180 micrograms/l) doses over a 28-day period. At weekly intervals, automated activity measurements, behavioral disability scoring, and videotape analyses were made. There was no improvement in the motor deficits exhibited by MPTP-treated common marmosets receiving bFGF infusion compared to vehicle-treated controls. Three of five high dose animals showed neurological impairment prior to the end of the study. No significant differences were found between control and bFGF-infused MPTP-treated common marmosets with respect to nigral tyrosine hydroxylase immunoreactive cell counts and striatal [3H]mazindol binding. All high dose animals showed hydrocephalus which was also observed in four other animals receiving bFGF. Histological examination revealed proliferation of the choroid plexus and ependyma which was most marked in the high dose animals. Adverse effects, in the form of hydrocephalus and neurological deterioration, were presumably secondary to an ependymal and choroid plexus reaction induced by bFGF.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1999

Intraventricular infusion of the histamine H(1) receptor antagonist chlorpheniramine improves maze performance and has anxiolytic-like effects in aged hybrid Fischer 344xBrown Norway rats.

In the present study we analyzed the effect of continuous intraventricular infusion of the histamine H(1) receptor antagonist d-chlorpheniramine on the performance of 32-month-old Fischer 344/Brown Norway F1 hybrid rats in the place version of the Morris water maze and in two different tests of anxiety (open field and black-and-white exploration). Control groups included vehicle-infused old and adult (3-month-old) F1 hybrids. Chronic infusion of chlorpheniramine improved the maze performance of the old rats and reduced fear-related behaviors in the open field and black-and-white box. Furthermore, long-term administration of chlorpheniramine was found to diminish age-related deficits in motor capacities. The findings substantiate that histamine H(1)-receptive sites are involved in learning and fear-related processes and indicate that hypomnesia and hyperanxiety seen in the course of brain aging may be based, in part, on hyperactivation of the central histaminergic neuron system. Furthermore, the data contribute to the behavioral characterization of the Fischer 344/Brown Norway F1 hybrid rat in the context of behavioral gerontopharmacology.

Aging↗

PubMed1979

Enhanced responsiveness to intraventricular infusion of amphetamine following its repeated systemic administration.

Previous studies have demonstrated that long-term administration of d-amphetamine produces a progressive augmentation of behavior. In the present experiment, rats receiving repeated systemic injections responded to an intraventricular infusion of d-amphetamine with an augmented increase in locomotor activity. These results indicate that central mechanisms, rather than peripheral dispositional factors, subserve the enhanced behavioral response to repeated amphetamine administration.

Animals↗

PubMed1996

The effect of continuous intraventricular infusion of L1 and NCAM antibodies on spatial learning in rats.

Recent studies suggest a role of the neural cell adhesion molecules L1 and NCAM in mechanisms of memory storage. In the present study we analyzed the effect of continuous intraventricular infusion of polyclonal antibodies directed against L1 (antiL1) or NCAM (antiNCAM) on the performance of male Wistar rats during the acquisition and retention of a spatial learning task (Morris water-maze). In this task animals have to learn the spatial position of a hidden escape platform in a water tank to escape onto it. During acquisition of the task animals with continuous infusion of antiNCAM - but not those infused with antiL1 - showed day-dependent attenuated learning in comparison to controls (P = 0.001). Control animals were either injected with vehicle (PBS) or with polyclonal antibodies raised against liver cell membrane. When the escape platform was removed during the retention test (transfer test), the performance of animals continuously infused with antiL1 as well as those continuously infused with antiNCAM showed an impaired search pattern when compared with the performance of control animals (P = 0.001 and 0.04, respectively). Whereas control animals spent up to 46% of their time searching for the platform in the correct quadrant, the time antiL1- and antiNCAM-infused animals spent in this quadrant was closer to chance level (30.5% and 36.5%), respectively). The present data provide additional support for an involvement of the two adhesion molecules L1 and NCAM in synaptic plasticity underlying memory storage.

Animals↗

PubMed1992

Effects of intraventricular infusion of the N-methyl-D-aspartate (NMDA) receptor antagonist AP5 on spatial memory of rats in a radial arm maze.

Rats were trained to asymptotic performance in an 8-arm radial maze. They then received chronic intraventricular infusion of either artificial CSF or the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5- phosphonopentanoic acid (AP5), at a concentration (30 mM) that has been shown previously to prevent the induction of long-term potentiation in the dentate gyrus of the hippocampus in vivo. Subsequently the rats received another 9 trials in the maze in a quasi-random order, 3 uninterrupted trials, and another 6 trials each with mid-trial delays of 5, 20 or 60 min during which the animals were placed in their home cage. The mean number of errors for the AP5 rats did not differ significantly from that of the controls in the uninterrupted trials throughout the experiment, nor did it differ from that of the controls in any of the 3 delayed trials when these were first introduced. However, the control animals performed better at the longer delays when these were introduced for the second time, whilst there was no such improvement (but rather a deterioration) for the AP5 animals. The impairment of performance in the AP5 rats during the second block of delayed trials was significant, and independent of the length of the delay. These results show that NMDA receptor blockade does not impair working memory in the radial maze per se, but that it does prevent an improvement of working memory persistence with further training.

2-Amino-5-phosphonovalerate↗

PubMed1987

Changes of cholinergic, noradrenergic and serotonergic synaptic transmission indices elicited by ethylcholine aziridinium ion (AF64A) infused intraventricularly.

Bilateral (3 nmol/side) i.c.v. infusion of ethylcholine aziridinium ion (AF64A) causes a 70% decrease of hippocampal acetylcholine content lasting for longer than 30 days without changing the density of hippocampal recognition sites for muscarinic ligands. In hippocampal slices prepared from rats receiving i.c.v. AF64A, the activation of phosphoinositide turnover or the inhibition of cyclic AMP accumulation elicited by muscarinic receptor agonists is facilitated. This AF64A treatment also causes a long-lasting decrease of hippocampal norepinephrine and serotonin (5-HT) content. Even a smaller dose of AF64A (1.5 nmol/side) reduces the hippocampal 5-HT content. The number of alpha-1 adrenoceptor recognition sites is slightly increased by 3 nmol/side of AF64A and the stimulation of phosphoinositide turnover by norepinephrine is facilitated. In contrast the decrease of hippocampal 5-HT concentration elicited by AF64A fails to change the 5-HT receptor indices that were measured. These results indicate that in rat hippocampus muscarinic receptors and alpha-1 adrenoceptors are denervated by AF64A and that this denervation promotes a receptor supersensitivity. These results also suggest that we could not find appropriate conditions to express a complete specificity of AF64A in destroying cholinergic axons and therefore this drug cannot be used readily to induce a selective deficiency of central cholinergic transmission.

Acetylcholine↗

PubMed1994

Anti-ubiquitin immunoreactivity associates with pyramidal cell death induced by intraventricular infusion of leupeptin in rat hippocampus.

Pathological studies on several neurodegenerative diseases including Alzheimer's disease have revealed common deposition of ubiquitin in many inclusion bodies. This implies a possible association of ubiquitin with neurodegeneration. To address this possibility, we examined histochemically the effect of intraventricular infusion of leupeptin, a thiol proteinase inhibitor, which is known to elevate anti-ubiquitin immunoreactivity in rat Purkinje cells. In the leupeptin-infused rat, an intense anti-ubiquitin immunoreactivity in the cytoplasm of neurons occurred not only in cerebellar Purkinje cells but also elsewhere in a wide area of the rat brain. The increase in the immunoreactivity was followed by a gradual depletion of pyramidal neurons in the hippocampal CA1 and CA3 subfields. The immunoreactive neurons disappeared concurrently. The number of anti-ubiquitin immunoreactive neurons was negatively correlated with that of surviving neurons when the duration of leupeptin infusion was varied. These results suggest that increased anti-ubiquitin immunoreactivity associates with neuronal death in leupeptin-treated rat brain.

Animals↗

PubMed1975

Strain differences during intraventricular infusion of norepinephrine: possible role of receptor sensitivity.

Two rat strains previously shown to differ with respect to behavioral activity, regional brain tyrosine hydroxylase activity, and norepinephrine-elicited accumulation of adenosine 3', 5'-monophosphate exhibited differential behavioral responsiveness during the intraventricular infusion of norepinephrine. The results are interpreted in terms of differential catecholamine receptor sensitivity.

Amphetamine↗

PubMed1982

Inhibition of lordosis behavior in the female rat by intraventricular infusion of prolactin and by chronic hyperprolactinemia.

The role of prolactin (PRL) in the control of the lordosis reflex of female rats was investigated. In the initial series of experiments, the normal high level of sexual receptivity observed in the ovariectomized, estrogen-progesterone (E-P) primed female rat was suppressed by intraventricular infusion of 100 ng PRL. Mating behavior remained suppressed 2, 3, and 5 hours following a single infusion of PRL into the third ventricle. In contrast, infusions of either an equal volume of the solvent vehicle (saline) or 100 ng of adrenocorticotropic hormone (ACTH) were ineffective in modulating the level of mating behavior in hormone-primed female rats. In a second series of experiments, chronic hyperprolactinemia was induced by pituitary transplants under the renal capsule in intact, normal cycle diestrus rats (N=12). A significant decrement in E-P induced mating behavior was observed at 12 and 14 weeks posttransplantation but not at 4 weeks. Sham-operated animals (N=12) displayed the characteristic pattern of behavior normally observed under exogenous E-P therapy. In summary, transient exposure as well as chronic exposure to high levels of PRL can suppress mating behavior, thus suggesting a possible role for PRL in the mediation of reproductive behavior in the female rat.

Adrenocorticotropic Hormone↗