Disease relevance of Injections, Intraventricular

• Hyperphagia and increased growth in rats after intraventricular injection of 5,7-dihydroxytryptamine [1].
• In addition, the destruction of the central noradrenergic system by intraventricular injection of 6-hydroxydopamine abolishes the effect of ischemia on capillary beta-adrenergic receptor function in both hemispheres [2].
• A single intraventricular injection into adult rats of 100 mouse lethal doses of tetanus toxin (TeTox) produces a marked intracellular redistribution of Ca2+/phosphatidylserine (PtdSer)-dependent protein kinase C (PKC) activity [3].
• 1 The hypothermia produced by intraventricular injections of thyrotropin releasing hormone (TRH) in unanaesthetized cats has been investigated [4].
• Myoclonus or convulsions occurred at various times after the intraventricular injection of cis-2,3-piperidine dicarboxylic acid, trans-2,3-, cis-2,4-, cis-2,5- and cis-2,6-, piperidine dicarboxylic acids, and after the intraperitoneal injection of trans-2,3-piperidine dicarboxylic acid [5].

Psychiatry related information on Injections, Intraventricular

• The intraventricular injection of D-alanine-methionine-enkephalinamide (D-Ala2-Met-enkephalinamide), a synthetic analog of Met-enkephalin that is resistant to enzymatic degradation, inhibits copulatory behavior in sexually vigorous male rats in doses which do not influence motor activity or feeding behavior [6].
• Antinociception induced by CCK 8 (which did not appear to be associated with reduced locomotor activity) was evident 5 min after intraventricular injection and was maximal at 10 min, the effect lasting over a 30-45 min period [7].
• Finally, in Experiment 3, the three DBH inhibitors reduced self-stimulation (a behavior dependent upon catecholamines) in a dose-related manner and intraventricular injections of 1-norepinephrine reinstated normal rates of self-stimulation [8].

High impact information on Injections, Intraventricular

• In particular, intraventricular injections or infusions of NGF in young adult rats have been shown to prevent retrograde neuronal cell death and promote behavioural recovery after damage to the septo-hippocampal connections [9].
• Neither its peripheral injection, nor the intraventricular injection of the inactive CRF analog des-Glu to Arg ovine CRF was effective [10].
• The inhibitory effects of a short-day photoperiod on testicular function were prevented by nighttime, but not daytime, intraventricular injections of carbachol, a cholinergic agonist [11].
• Compensatory increase in tyrosine hydroxylase activity in rat brain after intraventricular injections of 6-hydroxydopamine [12].
• The intraventricular injection of methionine-enkephalin (50 to 100 micrograms) or [d-Ala2]-methionine-enkephalinamide (1.5 to 12 micrograms), a synthetic enkephalin analog resistant to enzyme degradation, caused a marked dose-dependent increase in dihydroxyphenylacetic acid and homovanillic acid concentrations in the rat striatum [13].

Chemical compound and disease context of Injections, Intraventricular

• Thus a possible role of zinc in causing neuronal death in the brain needs to be fully investigated. intraventricular injections of calcium EDTA have already been shown to reduce neuronal death after a period of ischemia [14].
• It has been reported that intraventricular injection of chlorpromazine methiodide (CPZMI), a quaternary ammonium derivative of chlorpromazine, in rats induces abnormal, twisting postures which may serve as an experimental model of the human movement disorder dystonia [15].
• Adult male rats received a daily intraventricular injection of partially purified nicotinic acetylcholine receptor antibodies (anti-AChR) obtained from a female patient with myasthenia gravis, for 5 consecutive days [16].
• In contrast, pretreatment with haloperidol (0.2 mg/kg) or intraventricular injections of 6-hydroxydopamine attenuated locomotor activity induced by methylphenidate (5.0 mg/kg) [17].
• The effect of transient cerebral ischemia and intraventricular injection of kainic acid on adenylate cyclase and protein kinase C as labeled by [3H]forskolin ([3H]FOR) and [3H]phorboldibutyrate ester ([3H]PDBU) in several rat brain microregions was investigated in a quantitative autoradiographic study [18].

Biological context of Injections, Intraventricular

• The intraventricular injection of 42 mumol unlabeled uridine with the [3H]uridine decreased the phosphorylation of [3H]uridine in brain significantly and also decreased the clearance of [3H]uridine from the CSF [19].
• Ovulation was restored by the intraventricular injection of NE, but not of dopamine [20].
• Nicotinic cholinergic receptor binding sites labeled by [3H]acetylcholine were measured in the cerebral cortices, thalami, striata, and hypothalami of rats lesioned by intraventricular injection of either 6-hydroxydopamine or 5, 7-dihydroxytryptamine [21].
• The methylation of water-soluble ethanolamine compounds de novo was further confirmed by experiments performed in vivo by intraventricular injection of [3H]ethanolamine [22].
• Further, intraventricular injection of FSH elicits a selective increase in serum FSH during estrus by influencing this LHRH-dependent system [23].

Anatomical context of Injections, Intraventricular

• In the median eminence, neostriatum, and frontal cortex, intraventricular injection of [D-Ala2,D-Leu5]-enkephalin (25 micrograms) or beta-endorphin (15 micrograms) produced the same effects on dopamine turnover as morphine [24].
• Systemic administration of hormone prevents, in a time- and dose-dependent manner, the activation of microglia and the recruitment of peripheral monocytes induced by intraventricular injection of lipopolysaccharide [25].
• Intracellular recordings were performed in the CA1 region of the rat hippocampus following an ipsilateral intraventricular injection of kainic acid [26].
• Specific labelling by LNC 1 was decreased if synaptosomes were prepared from rats that had received intraventricular injections of 6-hydroxydopamine [27].
• For intraventricular injections, hGH (0.1 U/10 microliter) or SmC (500 ng/10 microliter) were injected into the lateral ventricle 2 h before the experiments [28].

Associations of Injections, Intraventricular with chemical compounds

• Intraventricular injections of carbachol, a cholinergic agonist, can mimic both of these effects [29].
• The embryonically expressed ShcA proteins were functionally active, since p52(ShcA) became phosphorylated on tyrosine and associated with Grb2 following intraventricular injection of epidermal growth factor in the embryonic brain [30].
• Intraventricular injection of the diluent had no effect on gonadotropin release [31].
• But, in striking contrast with the blockade of the response to volume expansion induced by intraventricular injection of methylatropine, the response to volume expansion was markedly enhanced by i.p. injection of methylatropine [32].
• Our results demonstrated that intraventricular injection of 130 ng deferoxamine to rats prior to 250 micrograms of 6-OHDA partially prevented the decrease in striatal dopamine content caused by 6-OHDA (56% reduction vs 90%, respectively) [33].

Gene context of Injections, Intraventricular

• Distribution of brain derived neurotrophic factor (BDNF) following intraventricular injection is minimal due to the binding to the trkB receptor along the ventricular wall [34].
• Intraventricular injection of recombinant human IL-1 beta did not affect hybridization to aFGF mRNA but did induce significant and widespread increases in hybridization to bFGF mRNA [35].
• Earlier studies in ovariectomized and intact male rats have shown that intraventricular injection of NPY inhibits release of growth hormone (GH) and luteinizing hormone (LH) without producing significant modification of plasma follicle stimulating hormone (FSH) and thyrotropin stimulating hormone (TSH) [36].
• Intraventricular injection of a nonspecific tetrapeptide caspase inhibitor or a specific tetrapeptide inhibitor of caspase-3 just after SCI reduced enzyme activity at 7 days [37].
• The intraventricular injection of PGE1 (1 and 5 micrograms/rat) resulted in a dose-related increase in peripheral plasma PRL levels in the rat [38].

Analytical, diagnostic and therapeutic context of Injections, Intraventricular

• In contrast with the results with intraventricular injection of the peptide, intravenous injection of 30 or 300 pmol of galanin produced small, brief, dose-related increases in plasma GH [39].
• In in vivo studies, following intraventricular injections of NGF cDNA complexed with DC-Chol liposomes, ELISA detected nine- to 12-fold increases of NGF in rat CSF [40].
• By contrast, intraventricular injection of the neurotoxin 5,7-dihydroxytryptamine (75 microgram free base, for 10 days) caused a 77% depletion of brain serotonin and attenuated the rise in beta-END-LI levels in response to immobilization (3.28 +/- 0.20 vs. 1.83 +/- 0.25 ng/ml) [41].
• However, generalized destruction of CNS 5-HT nerves produced by intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) or selective destruction of spinal 5-HT nerves produced by intraspinal injection of 5,7-DHT reduced the magnitude of the antinociceptive responses to electrical stimulation [42].
• Neither intraventricular injection nor injection into the periaqueductal grey of high doses of substance P (30 nmol) induced analgesia, whereas beta-endorphin (1 nmol) and morphine (15 nmol) were effective [43].

References