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PubMed1976

Intraventricular antipyretics and bacterial pyrogen fever.

In adult fowls with cannulae chronically implanted into the IIIrd cerebral ventricle or into the hypothalamus, the effects of various hydrosoluble antipyretics, given intraventricularly, on bacterial pyrogen fever were studied. It has been shown that fever evoked by intrahypothalamic or intraventricular infusion of O somatic antigen of Shigella Dysenteriae was reduced by intraventricular administration of acetylsalicylate-lysine, indomethacin-methylglucamine or ibuprofen-lysine given during the febrile plateau. However, a 3-day intraventricular pretreatment with acetylsalicylate or indomethacin, or a single administration 30 min before, did not prevent fever by subsequent intraventricular or intrahypothalamic injection of pyrogen. On the contrary, intraventricular infusion of indomethacin or acetylsalicylate substantially reduced pyrogen fever when given after pyrogen latency period, e.g. just at the beginning of the febrile response. A possible involvement of E prostaglandins as mediator to pyrogen fever is discussed.

Analgesics↗

PubMed1989

Biochemical properties of monoamine-rich human neuroblastoma cells.

The biochemical, pharmacological and immunological characterization of cells derived from human neuroblastoma tumors recently acquired great interest, since these cells may be a putative donor source for transplantation in animal models of neurological disorders. We measured monoamine levels, tyrosine hydroxylase (TH) immunostaining, and the expression of major histocompatibility cell surface antigens (MHC) in 7 human neuroblastoma cell lines. Three cell lines (LAN5, NB69 and CHP126) had high levels of monoamines. TH immunostaining was strongly positive in CHP126 and LAN5, and NB69. MHC were not detected in any of the cells with high catecholamine levels. Treatment with neuroleptics increased the metabolism of dopamine in LAN5 but not in NB69. The implantation of LAN5 cells in immunocompetent, unilaterally 6-hydroxydopamine-lesioned rats decreased the apomorphine-induced contralateral rotation. The effect of the implant was greatest in animals in which LAN5 neuroblastoma cells, pretreated with dibutyryl cyclic adenosine monophosphate (DBcAMP) and prostaglandin E1 (PGE1, were implanted into the cerebral ventricle ipsilateral to the lesion, and then irrigated with DBcAMP administered through a totally implanted drug delivery system. The effect of the implant decreased after the second week. Neuroblastoma cells were found in approximately 50% of the implanted animals. TH immunostaining was weak or absent in the grafted animals. Inflammatory changes were present in the majority of the brains examined. Extensive tumor growth was present in one animal implanted with untreated cells. Grafting of cells treated with DBcAMP and PGE1 plus with mitomycin C and bromodeoxyuridine in animals immunosuppressed with cyclosporin A reduced the apomorphine-induced rotation to 40-60% of baseline levels and this reduction persisted beyond the period of infusion with DBcAMP. Intraventricular infusion of DBcAMP in animals injected with cell culture medium produced a transient reduction of rotation to 70% of baseline. The amphetamine-induced rotation was not significantly reduced during the 4 weeks follow up. Atypical cells, consistent with surviving neuroblastoma cells, were observed in the brain of all transplanted animals. TH immunostaining was weak or negative in most cases. Human neuroblastoma cells may be an alternative donor tissue for the study of the effects of transplantation in animal models of Parkinson's disease.

Animals↗

PubMed1975

Duration of central action of angiotensin II estimated by its interaction with csf Na+.

In pre-hydrated goats, an urge to drink persisted for approximately half an hour after combined infusions of angiotensin II and hypertonic (0.5 M) NaCl into the lateral or third cerebral ventricle. The intraventricular infusion of angiotensin/glucose solution, having no dipsogenic action of its own, markedly accentuated the dipsogenic and antidiuretic effects of the subsequent intraventricular infusion of hypertonic NaCl. The possibility is discussed that angiotensin may be bound at periventricular receptor sites where it continues to interact with Na+ in eliciting thirst and ADH release for about half an hour.

Angiotensin II↗

PubMed1999

Treatment of neoplastic meningeal xenografts by intraventricular administration of an antiganglioside monoclonal antibody, 3F8.

Leptomeningeal (LM) neoplastic metastases are painful, debilitating and inevitably lethal. Intrathecal (IT) anti-tumor antibodies may have therapeutic potential. We evaluated 3F8, an anti-G(D2) murine IgG(3) monoclonal antibody (MAb) in the treatment of human melanoma (SKMEL-1) and neuroblastoma (NMB7) xenografts in athymic rats. Both tumors were lysed efficiently in vitro by 3F8 in the presence of rat neutrophils or rat complement. Antibody-dependent cellular cytotoxicity (ADCC) was not augmented by recombinant human GM-CSF (rhGM-CSF), rhG-CSF, recombinant rat MIP-2 (rrMIP-2) or lipopolysaccharide (LPS). In vivo, continuous intraventricular administration of 3F8 and LPS prevented tumor engraftment, retarded tumor growth and eradicated 3-day-old established xenografts whereas 3F8 alone, LPS alone or F(ab)'(2) plus LPS had no or only marginal effects. Tumor establishment in brain was completely prevented in 36% of animals implanted with SKMEL-1 and 65% of animals implanted with NMB7. Twenty percent of established xenografts around the brain were eradicated but all animals had persistent tumor in the lumbosacral meninges despite treatment. Continuous intraventricular infusion of LPS produced a variable polymorphonuclear (PMN) pleocytosis that was dose-dependent. Continuous intraventricular infusion of 3F8 produced immunohistochemically detectable attachment to 86% of persistent brain deposits of tumor but <1% of spinal lumbosacral deposits. We conclude that regional therapy with anti-G(D2) MAb could target neutrophils to inhibit LM tumor growth. However, optimal activation and mobilization of neutrophils into the cerebrospinal fluid (CSF) and improved penetration of MAb to tumor sites remain critical variables.

Animals↗

PubMed2002

Adeno-associated virus-mediated gene transfer to the neonatal brain.

For many metabolic diseases, early treatment is necessary to prevent irreversible developmental damage. This is particularly true for childhood diseases that affect the central nervous system (CNS). The development of effective techniques for gene transfer to the neonatal brain would provide a new set of therapeutic options for many of these disorders. Vectors based on adeno-associated virus (AAV) have shown promise as agents for neonatal CNS transduction. In preclinical animal models, a single treatment with AAV vectors at birth has been shown to produce persistent CNS expression of transduced genes into adulthood. Transduction of the neonatal brain has been accomplished by a variety of methods, including direct intraparenchymal injection, intraventricular infusion, and intravenous administration. Of these methods, intraparenchymal injection provides the highest levels of localized activity, while intraventricular infusion results in a more widespread distribution of activity when performed in the neonate. Here we describe a method for direct, intraparenchymal injection of AAV into the neonatal brain. This technique provides a method for investigators to evaluate the effects of in vivo expression of exogenous genes on the process of early brain development.

Adenoviridae↗

PubMed1995

Centrally infused anions alter body temperature in conscious rats.

Central anionic influences on the regulation of body temperature were studied in 42 conscious male rats. The animals were divided into seven equal groups and were given intraventricular infusions of either chloride or bicarbonate solution of sodium, calcium, or potassium. Infusions were made in the unanesthetized and unrestrained animals through stainless steel cannulae, chronically implanted into the anteroventral part of third ventricle. Control rats received intraventricular infusions of artificial cerebrospinal fluid. All of the chloride solutions, irrespective of the associated cations, elicited hyperthermia, whereas bicarbonates had hypothermic effect. Responses of chloride and bicarbonate solutions varied significantly (p < 0.001). There was, however, cationic modification of the anionic responses. Thus, sodium ions manifested hyperthermic modifications, accentuating hyperthermia of chloride and attenuating hypothermic effect of bicarbonate. Calcium and potassium ions exerted hypothermic modulation. The results suggest that anionic concentration of intraventricular CSF is crucial for central regulation of body temperature in unanesthetized conscious rats. The cations probably have only modulatory influences.

Animals↗

PubMed1988

Intraventricular bethanechol infusion for Alzheimer's disease: results of double-blind and escalating-dose trials.

Ten patients with biopsy-proven Alzheimer's disease (AD) received low-dose (0.35 mg/d) intraventricular bethanechol, a muscarinic agonist, and saline placebo in a 24-week double-blind crossover design. Eight of these ten patients later participated in an open escalating-dose (to 1.75 mg/d) trial of bethanechol. Patients' drug responses were assessed by neuropsychological examination and informant measures of activities of daily living, mood disturbance, and abnormal behavior. Bethanechol appears to have a narrow therapeutic window for positive effects; low doses did not reliably alter patient functioning, moderately increased doses appeared to have a palliative effect on patient mood and behavior, and the highest dose was detrimental to patient functioning. Bethanechol does not appear to ameliorate the dementia of AD, but may exert a mildly positive effect on patient behavior and mood.

Aged↗

PubMed1994

Estrogen dependence of cholinergic systems that regulate lordosis in cycling female rats.

Previous evidence indicated that physostigmine, an acetylcholinesterase inhibitor, facilitated lordosis behavior when administered intraventricularly to cycling female rats on proestrus prior to the onset of natural sexual receptivity, but not when administered to rats on mid-diestrus or diestrus II. In the present experiments, intraventricular infusion of physostigmine (10 micrograms bilaterally) facilitated lordosis on mid-diestrus and diestrus II if females were primed with two injections of estradiol (0.2, 0.1, or 0.05 micrograms) administered 20 h and 32 h prior to infusion of physostigmine. Despite unequal levels of endogenous progesterone, physostigmine facilitated lordosis equally on mid-diestrus and diestrus II following estradiol priming. Finally, intraventricular infusion of the muscarinic receptor blocker scopolamine (20 micrograms bilaterally) reduced the incidence of lordosis in females that displayed lordosis on mid-diestrus following estrogen priming. Results confirm that cholinergic mechanisms influence sexual behavior displayed by cycling female rats. Data further indicate that sufficient estrogen stimulation is necessary for cholinergic neurons to facilitate lordosis. However, progesterone does not play a major role in the regulation of lordosis by cholinergic systems.

Animals↗

PubMed2006

Growth factor-stimulated generation of new cortical tissue and functional recovery after stroke damage to the motor cortex of rats.

Recent studies suggest that proliferation in the adult forebrain subventricular zone increases in response to a forebrain stroke and intraventricular infusions of growth factors enhance this response. The potential for growth factor infusions to regenerate the damaged motor cortex and promote recovery of motor function after stroke has not been examined. Here, we report that intraventricular infusions of epidermal growth factor and erythropoietin together, but not individually, promote substantial regeneration of the damaged cerebral cortex and reverse impairments in spontaneous and skilled motor tasks, in a rat model of stroke. Cortical regeneration and functional recovery occurred even when growth factor administration was delayed for up to 7 days after the stroke-induced lesion. Cell tracking demonstrated the contribution of neural precursors originating in the forebrain subventricular zone to the regenerated cortex. Strikingly, removal of the regenerated cortical tissue reversed the growth factor-induced functional recovery. These findings reveal that specific combinations of growth factors can mobilize endogenous adult neural stem cells to promote cortical tissue re-growth and functional recovery after stroke.

Animals↗

PubMed1989

Distribution of a somatostatin analog after continuous intraventricular administration.

Decreased somatostatin in the brains of patients with Alzheimer's disease has led to an investigation of the efficacy of neurotransmitter replacement therapy. The distribution of a somatostatin analog, octreotide, was determined after 2 to 6 days of continuous intraventricular infusion at 40 micrograms/h in dogs. The tissue concentration was greater than 100 ng/g wet weight in all parts of the brain, which is greater than the normal concentration of native somatostatin. There was no reduction in native somatostatin production because of the infusion of the analog. The cerebrospinal fluid octreotide concentration was 1000 times greater than the plasma concentration. The results demonstrate that neurotransmitter replacement for somatostatin can be achieved by chronic intraventricular infusion of a metabolically stable analog.

Animals↗

PubMedDate not supplied

Feeding and body temperature in the rat: diencephalic localization of changes produced by excess calcium ions.

In the unanesthetized rat, Ca++ ions in solutions ranging from 2.6 to 112.0 mM in excess of the normal level in CSF were applied at different sites in the brain and by three separate procedures, Colonic temperature was monitored and in certain experiments, the amount of food pellets and water consumed was measured simultaneously following the administration of excess Ca++ ions. An infusion into the lateral cerebral ventricle of excess calcium in a volume of 5.0 mul produced a concentration-dependent hypothermia, This fall in temperature was not attenuated by a prior intraventricular infusion of mecamylamine and often enhanced by atropine. Depending on the site, a microinjection of excess Ca++ ions in a volume of 0.5 to 1.0 mul directly into the hypothalamus produced hypothermia or feeding. The sites of maximum sensitivity at which excess calcium caused a decline in temperature were clustered in the caudal hypothalamus, whereas those at which calcium elicited feeding were distributed widely in caudo-lateral, medial and rostral hypothalamic areas. Push-pull perfusions at a rate of 20 to 25 mul per min for 10 to 20 min at homologous sites caused similar responses but the cation concentration required to evoke feeding or hypothermia was significantly less than that of either microinjection or intraventricular infusion. These findings demonstrate species continuity in the rat concerning anatomical localization of the postulated set-point mechanism for body temperature. Several different pathways in the feeding system are affected by an alteration in the hypothalamic level of calcium.

Animals↗

PubMed1999

Complement-derived anaphylatoxin C5a protects against glutamate-mediated neurotoxicity.

Previous work from this laboratory indicates a role for the complement component C5 in neuroprotection against excitotoxicity. In the present study, we tested the hypothesis that the C5-derived anaphylatoxin C5a protects against kainic acid (KA)-induced neurodegeneration and investigated the mechanism of C5a neuronal activity in vitro. Brain intraventricular infusion of KA into adult mice caused neuronal morphological features of apoptosis in the pyramidal layer of the hippocampal formation as indicated by counts of neurons with pyknotic/condensed nuclei associated with cytoplasmic eosinophilia. Co-intraventricular infusion of human recombinant C5a with KA resulted in a marked reduction of morphological features of apoptotic neuronal death. In vitro studies confirmed C5a neuroprotection: treatment of primary murine corticohippocampal neurons with human or mouse recombinant C5a reduced glutamate neurotoxicity, as measured by trypan blue exclusion assay. This protection concurred with inhibition of glutamate-mediated induction of the caspase-3-related cysteine protease and coincided with marked reduction of neurons with morphological features of apoptosis, as found in vivo. Our studies indicate that C5a may inhibit glutamate-mediated neuronal death through partial inhibition of caspase-3 activity. These findings suggest a novel noninflammatory role for C5a in modulating neuronal responses to excitotoxins.

Alzheimer Disease↗

PubMed1994

Suppression of ischemia-induced fos expression and AP-1 activity by an antisense oligodeoxynucleotide to c-fos mRNA.

Activation of c-fos, an immediate early gene, and the subsequent expression of the Fos protein have been noted following focal cerebral ischemia. Fos and Jun form a heterodimer as activator protein 1 (AP-1), which transregulates the expression of several genes. To study the postischemic events related to c-fos expression, we suppressed the expression of c-fos by intraventricular infusion of an antisense oligodeoxynucleotide (anti-rncfosr115) of c-fos mRNA. The effectiveness of anti-rncfosr115 was confirmed first by its capability to block in vitro c-fos mRNA translation. In vivo, after intraventricular infusion of 32P-labeled anti-rncfosr115, the oligodeoxynucleotide was internalized within 6 hours and detectable also in the nucleic acids fraction up to 41 hours. Treatment of the recovered nucleic acids with RNase H separated the labeled oligodeoxynucleotide from the nucleic acid fraction, indicating an association of the antisense oligodeoxynucleotide and cellular RNA after uptake. When focal cerebral ischemia was induced 16 hours after the infusion of anti-rncfosr115, the postischemic increase in Fos expression and AP-1 binding activity were suppressed. Specificity of the effect of anti-rncfosr115 was suggested by its failure to suppress the DNA binding activity of nuclear cyclic AMP response elements. These results support the hypothesis that increased AP-1 binding activity following focal cerebral ischemia is dependent on Fos expression and can be inhibited in vivo by antisense c-fos oligodeoxynucleotides.

Animals↗

PubMed2002

Acute and chronic administration of melanin-concentrating hormone enhances food intake and body weight in Wistar and Sprague-Dawley rats.

AIM: Although melanin-concentrating hormone (MCH) is believed to be an important regulator of feeding behavior, both its acute and chronic effects on food intake as well as its interaction with other brain peptides involved in the control of appetite remain unclear. Therefore, the acute effects of MCH on food intake and the chronic effect of MCH on food intake and the gene expression of various hypothalamic peptides involved in the control of appetite were studied in rats. METHODS AND RESULTS: Either the acute or the continuous intraventricular infusion of MCH for 12 days stimulated feeding in both Wistar or Sprague-Dawley rats. Removal of the hypothalamus at the end of the chronic infusion studies allowed measurement of the expression of mRNAs encoding for MCH, neuropeptide Y (NPY), orexin, agouti gene-related peptide, cocaine and amphetamine-related transcript and neurotensin-neuropeptides involved in the control of appetite. Chronic intraventricular infusion of MCH activated only NPY mRNA synthesis in Sprague-Dawley rats. The increase in food intake in response to MCH in Sprague-Dawley rats did not appear to be due to the release of NPY since combination studies demonstrated consistently additive effects of the two peptides on food intake at maximum or near maximum doses. CONCLUSIONS: These results strongly suggest that MCH is an orexigenic peptide involved in the control of both short- and long term food intake in satiated rats and further indicate that the MCH pathway is a possible target for the control of food intake and obesity.

Agouti-Related Protein↗

PubMed2003

Olivocerebellar projections are necessary for exogenous trophic factors to delay heredo-Purkinje cell degeneration.

The temporally protracted heredodegeneration of cerebellar Purkinje cells in shaker mutant rats can be modified: ablation of the inferior olive accelerates their degeneration whereas chronic intraventricular infusion of trophic factors extends their survival. The present study sought to determine if chronic trophic factor infusion could block the accelerated degeneration of Purkinje cells due to inferior olivary chemoablation thereby focusing on possible mechanisms for the amelioration of heredo-Purkinje cell death. When the inferior olive was chemically ablated with 3-acetylpyridine at the midpoint of 2 weeks of conjoint intraventricular infusion of glial cell line-derived trophic factor (GDNF) and insulin like growth factor type I (IGF-1) Purkinje cells were not protected by the exogenous trophic factors, but rather degenerated prematurely consistent with chemoablation alone. These findings support the conclusion that when the inferior olive is ablated, Purkinje cell heredodegeneration progresses through a mechanism not significantly affected by the action of these trophic factors.

Animals↗

PubMed1997

Anticonvulsive and neuroprotective actions of a potent agonist (DCG-IV) for group II metabotropic glutamate receptors against intraventricular kainate in the rat.

Anticonvulsive and neuroprotective effects of (2S,1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl) glycine (DCG-IV), a potent agonist for Group II metabotropic glutamate receptors, were examined in vivo against the excitotoxicity of kainic acid in the rat. Intraventricular injection of kainic acid (2 nmol) induced circling behavior and wet-dog shakes soon after injection, followed by episodes of limbic motor seizures at intervals of several minutes (sporadic limbic motor seizures). The frequency of sporadic limbic motor seizures gradually increased until seizures occurred incessantly (continuous limbic motor seizures). Intraventricular kainic acid also caused severe selective neuron damage in the hippocampal CA3 region, limbic lobe and medial geniculate body. Prolonged intraventricular infusion of DCG-IV (24-240 pmol/h) for 17 h before and 7 h after the application of kainic acid decreased the incidence of the continuous limbic motor seizures and the degree of neuronal damage in circumscribed brain areas. However, the behavioral changes observed immediately after the administration of kainic acid were unaffected by prolonged intraventricular infusion with DCG-IV (8-2400 pmol/h). Similarly, the occurrence of sporadic limbic motor seizures was only slightly reduced by the administration of DCG-IV (8-800 pmol/h). High doses of DCG-IV, greater than 800 pmol/h, afforded no protection against kainate-induced lesions; rather, the degradation of hippocampal CA1 pyramidal neurons was increased under such conditions. Single injections of DCG-IV (10-300 pmol/rat) in the lateral ventricle did not affect kainate neurotoxicity. Thus, prolonged infusion of DCG-IV showed a bell-shaped doso-response relationship with regard to protection against kainate-induced neurotoxicity.

Animals↗

PubMed1986

Gonadotropin secretion following intraventricular norepinephrine infusion into neonatally androgenized female rats.

To determine whether norepinephrine (NE) will stimulate gonadotropin secretion in androgenized female rats, we administered NE (0.3 microM in 2 microliter saline; pH 6.0-6.5) into the third ventricle of females which had been treated neonatally with two different doses of testosterone propionate (TP; 10 or 100 micrograms) on day 5 of life. This treatment rendered these animals anovulatory as evidenced by polyfollicular ovaries and a persistent vaginal estrus condition which occurred by 100 days of age. Those females which were determined to be anovulatory were ovariectomized 4 weeks prior to the stereotaxic implantation of an intracerebroventricular (ICV) cannula. Ten to twelve days following cannula placement, animals were primed with either estradiol benzoate (EB; 30 micrograms) or EB and progesterone (P; 5 mg). Two days following steroid priming, NE was infused into the third ventricle at 15.00 h and blood samples were taken via an intra-atrial catheter at 15-min intervals for 2 h before and 2 h after administration. In both TP-treated groups, NE caused rapid and significant (p less than 0.01) elevations in plasma luteinizing hormone (LH) concentrations when animals were primed with EB as compared with control females given acid saline infusions (pH 6.0-6.5). Similar responses to NE were seen after additional priming with P at the same time as EB. Follicle-stimulating hormone (FSH) values did not increase following NE or saline infusion to any of the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Adenovirus-mediated gene transfer of fibroblast growth factor-2 increases BrdU-positive cells after forebrain ischemia in gerbils.

BACKGROUND AND PURPOSE: Progenitor cells continue to generate neurons in the adult mammalian brain, and cerebral ischemia induces neurogenesis. We examined the efficacy of the intraventricular injection of a recombinant adenovirus-expressing fibroblast growth factor-2 (FGF-2) (AxCAMAssbFGF) on neurogenesis in both normal and ischemic brains. METHODS: We used a gerbil model of transient global ischemia and counted the number of BrdU-positive cells after injection of AxCAMAssbFGF into the brain with or without ischemia. RESULTS: Intraventricular AxCAMAssbFGF produced robust FGF-2 protein increases in diverse regions of the brain and markedly increased FGF-2 concentrations in cerebrospinal fluid 2 days after administration and evoked significant proliferation of BrdU-positive cells not only in the subventricular zone and dentate gyrus of the hippocampus but also in the cerebral cortex, and some BrdU-positive cells differentiated into neurons. Continuous intraventricular infusion of FGF-2 protein increased FGF-2 concentration in cerebrospinal fluid but not in brain tissues and produced BrdU-positive cell proliferation only in the subventricular zone of the lateral ventricle. CONCLUSIONS: Adenovirally mediated transfer of the FGF-2 gene promoted progenitor cell proliferation more efficiently in widespread regions of the brain after transient global ischemia than continuous intraventricular infusion of FGF-2 protein.

Adenoviridae↗