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PubMed1997

Glial cell line-derived neurotrophic factor: distribution and pharmacology in the rat following a bolus intraventricular injection.

Glial cell line-derived neurotrophic factor (GDNF) has been shown to increase dopaminergic parameters in vitro and in vivo and can reduce parkinsonian behaviors in animal models of the disease. This study determined the potential of the lateral ventricle as an administration route for GDNF by examining the distribution and neurochemical consequences of a single intraventricular injection. Autoradiographic analysis showed that intraventricularly administered [125I]GDNF was distributed throughout the ventricular system at 1 and 24 h following injection. The cerebral cortex, septum, diagonal band, fimbria, striatum, hippocampus, hypothalamus, substantia nigra/ventral tegmental area, and cerebellum were also labeled. At 7 days, there was still labeling throughout the ventricular system, hypothalamus, substantia nigra, and cerebellum. Twenty-four hours following an intrastriatal injection of [125I]GDNF, label was observed in the substantia nigra/ventral tegmental area, demonstrating retrograde transport. The neurochemical effects of intraventricularly administered GDNF (0.1-100 micrograms) at 7 days post injection were also examined. GDNF significantly increased striatal (approximately 28%) and nigral (up to 40%) dopamine, as well as regulated the dopamine metabolites homovanillic acid and dihydroxyphenylacetic acid. Dopamine levels were unchanged in the frontal cortex. Dopamine content was significantly increased in the hypothalamus (up to 35%), an increase which may contribute to the inhibition of weight gain seen after administration of GDNF. Additionally, dopamine turnover was decreased or unchanged across the brain regions analyzed, which may indicate that in unlesioned rats, intraventricularly administered GDNF stimulates the synthesis and storage of dopamine. This study shows that intraventricularly injected GDNF can access basal ganglia structures, most notably the midbrain dopamine cell body region, and remains present in this area for at least 7 days following a single administration. GDNF differentially increases dopaminergic tone within a variety of brain structures, including the nigrostriatal pathway. These data support the potential effectiveness of intraventricular administered GDNF as a treatment for Parkinson's disease.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Intrastriatal and intraventricular injections of oligodeoxynucleotides in the rat brain: tissue penetration, intracellular distribution and c-fos antisense effects.

We have determined the time course, the spatial spread in brain tissue, and the intracellular distribution of biotin- and fluorescein-labeled phosphorothioate oligodeoxynucleotides (ODNs) following single injections into the rat striatum or the lateral ventricle. These time and space parameters were correlated with the ability of c-fos phosphorothioate antisense ODNs to suppress the induction of Fos protein by cocaine. A rapid and dose-dependent tissue penetration of labeled ODNs was observed following either intrastriatal or intraventricular injections of a constant sample volume. Inspection of tissue sections by confocal microscopy uncovered a distinct change in the intracellular disposition of labeled ODNs during the 24 h post-injection period. At 1, 6 and 12 h, the vast majority of the fluorescent signal was confined to the interstitial spaces throughout the zone penetrated by ODNs. Neuronal nuclei displayed faint labeling along the outer portion of the nucleus at 1 and 6 h post-injection. At these time-points, ODNs were not detected in the cytoplasm. By 16 h, ODNs were barely detectable in the extracellular space and absent from neuronal nuclei. Instead, ODNs were seen in large cytoplasmic granules of neurons throughout the tissue zone penetrated by the ODNs. Experiments with intrastriatal injections of antisense ODNs to c-fos mRNA revealed Fos suppression between 3 and 12 h, but not at 16 and 24 h. This combined analysis has revealed that (1) restricted tissue penetration by ODNs limits their antisense effects on protein expression, and (2) depletion of extracellular ODNs and sequestration of c-fos antisense ODNs into large intracellular granules coincides with the loss of their biological activity.

Animals↗
PubMed1990

The distribution of serotonin immunoreactivity in the rat locus ceruleus after intraventricular injections of either 5,6- or 5,7-dihydroxytryptamine with special reference to serotonin synthesis.

The localization of serotonin-immunoreactivity (5-HT-IR) in the locus ceruleus (LC) of rats was studied by the peroxidase-anti-peroxidase method using a purified antibody obtained from a rabbit. Antibody production was performed according to the method of Grota and Brown (1974). The antibody was applied to serial cryostat sections with alternate counterstaining by cresyl violet, after intraventricular injections of 5,6-dihydroxytryptamine or 5,7-dihydroxytryptamine prior to treatment with pargyline and a precursor of 5-HT. The majority of LC neurons were immunopositive, and more than half of all LC neurons clearly showed 5-HT-IR. Although core cells were the most predominant, all types of neurons were immunopositive, and randomly scattered throughout the LC. The uptake inhibitor, Lilly 110140, administered in sufficient amounts prior to an injection of pargyline, did not reduce 5-HT-IR within the LC. The results suggest that LC neurons receive 5-hydroxytryptophan (5-HTP) through an afferent vascular-neuronal channel and/or by diffusion from blood capillaries much more than 5-HT itself. We consider from these results that all types of LC neurons throughout the nucleus are masked 5-HT cells, and that the majority of LC neurons utilize blood-borne 5-HTP as an immediate precursor for intraneuronal 5-HT synthesis.

5,6-Dihydroxytryptamine↗
PubMed1980

Suppressive effects of intraperitoneal and intraventricular injections of nicotine on muricide and shock-induced attack on conspecifics.

Rats were used to investigate the effect of nicotine on mouse-killing and foot shock-induced attack on conspecifics. It was found that intraperitoneal injections of nicotine (100-1000 micrograms/kg) suppressed mouse-killing in a dose dependent manner. The suppression of mouse-killing by nicotine was not blocked by hexamethonium (30 mg/kg), a peripheral nicotinic receptor blocking agent. Mecamylamine (30 mg/kg), a nicotinic blocking agent with central effects, did reduce the inhibition of attack produced by nicotine. Both intraperitoneal and intraventricular injections of nicotine suppressed shock-induced attack on conspecifics. Shock-elicited flinch, vocalization, and escape were not influenced by nicotine injections. These findings give further support to the view that muscarinic and nicotinic compounds produce antagonistic effects on certain types of attack behavior.

Aggression↗
PubMed1983

Intraventricular injections of drugs which inhibit phospholipase A2 suppress fever in rabbits.

Injection of two chemically dissimilar inhibitors of phospholipase A2 (mepacrine and parabromophenacylbromide) into the cerebral ventricles of rabbits inhibited the febrile response to endogenous pyrogen given by the same route. 2. The same doses of the inhibitors given intravenously did not affect the febrile response to endogenous pyrogen given into the ventricles, indicating that their action was central. 3. When given intraventricularly the inhibitors did not affect the maintenance of core temperature in a cold environment, indicating that they did not impair thermoregulatory ability. 4. The inhibitors had no effect on the temperature rise following intraventricular injection of arachidonic acid. 5. These observations are compatible with the proposition that one or more metabolic products of arachidonic acid other than prostaglandin are involved in pyrogenesis.

Acetophenones↗
PubMed1987

Effects of intraventricular injections of galanin on neuroendocrine functions in the male rat. Possible involvement of hypothalamic catecholamine neuronal systems.

Galanin-catecholamine interactions have been analysed within the hypothalamus and the anteromedial frontal cortex of male rats by means of quantitative histofluorimetrical and biochemical measurements of catecholamine fluorescence in discrete catecholamine nerve terminal systems and measurements of serum levels of adenohypophyseal hormones and corticosterone using radio-immunoassay determinations. 125I-galanin binding sites were analysed and related to the distribution of galanin-immunoreactive neuronal structures in the median eminence and paraventricular hypothalamic nucleus. The results show that intraventricular injections of galanin in the awake and unrestrained male rat produce rapid increases of prolactin and growth hormone secretion but no effects on serum luteinizing hormone, thyroid stimulating hormone or on corticosterone levels. These changes in neuroendocrine function were associated with a selective reduction of the catecholamine stores in the medial palisade zone of the median eminence at the 20 min time interval. 125I-galanin binding sites were found throughout the hypothalamus including the median eminence and the magnocellular part of the paraventricular hypothalamic nucleus with a good correspondence with galanin immuno-reactivity. It is suggested that the enhancement of prolactin secretion induced by galanin involves an interaction between galanin and dopamine in the medial palisade zone leading to a reduced synthesis and/or release of dopamine and thus to a reduced prolactin inhibitory activity and to increases in prolactin secretion. A possible involvement of hypothalamic catecholamines in the galanin-induced changes of growth hormone secretion remains to be established.

Animals↗
PubMed1985

Neonatal brain damage and recovery: intraventricular injection of NGF at time of injury alters performance of active avoidance.

Rats were given lesions of either the ventromedial hypothalamus (VMH) or septal nucleus at 7 days of age and then were tested repeatedly in an active avoidance task (A.A.) from 20 to 80 days. VMH rats were consistently impaired on the A.A. task beginning at 40 days of age. The animals with septal lesions performed the A.A. task consistently better than VMH or control animals throughout the entire test period, the septal syndrome becoming more pronounced as the rats reached maturity. In intact rats a single, intraventricular injection of NGF given at 7 days of age resulted in a greater reactivity, especially as the rats approached maturity. NGF, given at time of surgery, also improved performance of the A.A. task in VMH-damaged rats tested at 40-80 days. In rats given septal lesions, NGF treatment at time of injury attenuated the septal syndrome of improved A.A. performance. The data indicate that NGF treatment, given to neonatal rats, can produce long-lasting effects on CNS functions and can contribute to functional recovery from brain lesions.

Animals↗
PubMedDate not supplied

Feeding following intraventricular injection of CA++, MG++ or pentobarbital in pigs.

The effects on food intake, of injections into the lateral ventricle of Ca++, Mg++ or equimolar mixtures of the 2 ions have been studied in pigs. The chloride salts were made up in normal saline which together with 1.35 percent NaC1 was used as a control injection. Dosages of 12.5 mumoles, 25 mumoles, or 50 mumoles either Ca++ or Mg++ elicited increased food intake in the 30 min following the injection and there was a predominantly linear feeding response to increasing concentration of the two ions. Ca++ was more effective in eliciting increased food intake than Mg++. Equimolar mixtures of Ca++ and Mg++ of 6.5 + 6.5 mumoles, 12.5 + 12.5 mumoles or 25 + 25 mumoles also increased food intake linearly and the mixture of ions was more effective than equivalent concentrations of Ca++ or Mg++ alone. No antagonism between Ca++ and Mg++ was seen with respect to food intake. Intraventricular injections of 16 mumoles of sodium pentobarbital also elicited increased food intake in the 30 min following injection. It is suggested that the ions and the barbiturate probably act by deression of periventricular neurons, particularly in the medial hypothalamus which is adjacent to the third ventricle.

Animals↗
PubMed1986

Increase in plasma catecholamines by intraventricular injection of histamine in conscious rats.

Intraventricular administration of histamine (HA; 2.5 and 5 micrograms) caused a significant increase of plasma adrenaline and noradrenaline levels in conscious, freely-moving male rats. The increase of adrenaline was more rapid (5 min after injection) and greater than that of noradrenaline. The plasma adrenaline increase observed 15 min after HA administration was dose-dependent. In contrast, plasma noradrenaline increased maximally in response to the low dose and reached similar values after the largest dose studied. Receptor mediation was examined by means of selective HA antagonists. Pretreatment with mepyramine blunted the adrenaline response at 15 min which suggests mediation at H1 receptors. In contrast, it was ineffective on plasma adrenaline at 5 min and plasma noradrenaline increase. Ranitidine, an H2-receptor antagonist, did not modify adrenaline response but enhanced the HA-induced increase of plasma noradrenaline. These findings suggest that HA activates the central drive to the adrenal medulla and to the peripheral sympathetic system. A participation of peripheral catecholamine secretion in the acute cardiovascular changes induced in rats by centrally injected HA is postulated.

Animals↗
PubMed1978

Effects of intraventricular injections of norepinephrine on brain-pituitary-ovarian function in the rabbit.

In estrous estrogen-primed female rabbits with electrodes chronically implanted in various subcortical regions of the brain, the intraventricular injection of an ovulation-inducing dose of norepinephrine (NE) stimulated a prolonged episode of high amplitude 40-60 cps electroencephalographic (EEG) activity in the olfactory bulb (OB) and its projections. This activity, which started usually between 30 and 60 min after NE injection and was maintained continously for periods up to an hour thereafter, was regularly absent in the same rabbits when they were pseudopregnant and non-ovulatory to NE. Similar OB-EEG activity and ovulation had been observed earlier in response to intraventricular histamine under light pentobarbital anesthesia. The ovulatory response to histamine was eliminated by massive midbrain lesions or removal of the olfactory bulb, but intraventricular NE still induced ovulation after such losses. The ovulatory effectiveness of NE was blocked, however, by low doses of pentobarbital or high doses of atropine, neither of which inhibited the ovulatory response to intraventricular epinephrine. Atropine and alpha-adrenergic blocking agents also prevented the ovulatory response to intraventricular histamine. It is suggested that histamine activates pituitary-ovarian function by stimulating central noradrenergic elements and that NE has more of the physiological-pharmacological characteristics of a natural central nervous activator of luteinizing hormone-releasing hormone than has epinephrine.

Animals↗
PubMed1992

[Alterations of pulmonary arterial pressure following intraventricular injection of histamine in rabbits].

The changes of the pulmonary arterial pressure (PAP) following microinjection of histamine (HA) into the lateral ventricle in the rabbit were investigated. It was found that (1) Intraventricular injection of HA (50 micrograms) induced either an increase (in the majority) or a decrease in PAP and cardiac output (CO), or a biphasic response characterized by a decrease followed by an increase. Slowing down of heart rate (HR) and elevation of carotid arterial pressure (CAP) were observed accordingly. (2) After bilateral cervical vagotomy or fixing the heart rate by cardiac pacing, drop in CO and PAP in response to HA was no longer observed. Instead, they even showed some constant increase. The pressor response of PAP and CAP to HA could be partially blocked by phentolamine applied intravenously without affecting the increment of CO. On the other hand, intravenous injection of propranolol could totally block the HA-induced increment of CO, but not affect the pressor responses of PAP and CAP. Intravenous injection of hexamethonium or combined application of phentolamine and propranolol could completely abolish all the increment responses in CO, PAP and CAP to HA. (3) The cardiovascular responses to HA could be blocked by the H1 receptor blocker-chlorpheniramine, but not by H2 receptor blocker-cimetidine. It is thus assumed that HA applied intraventricularly can activate the central H1 receptor, thus inducing an increase in the cardiac output and vasoconstriction of pulmonary and peripheral vessels giving rise to an elevation of both PAP and CAP by way of sympathetic nerve. Central application of HA also induces bradycardia by activating vagus nerve.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Central action of drugs acting on the cholinergic muscarinic receptor. III. Influence of atropine and scopolamine injected intraventricularly on behavior and levels of biogenic amines in the rat brain.

Atropine (At) and scopolamine (Sc) in low doses intensify basic activity, increase amphetamine stereotypy, and suppress catalepsy induced by injection of haloperidol. High doses lower body temperature, antagonize amphetamine stereotypy, and intensify the hypnotic action of chloral hydrate. Doses of about 1/2 LD50 induce narcotic sleep. Both At and Sc in a wide range of dosage protect against the tonic phase of convulsions produced by electroshock. Sc depresses content of acetylcholine in the brain proportionally to its dosage; At had a similar effect only at the lower of the two doses that were used. Both compounds had no effect on levels of noradrenaline and dopamine in the brain. The results indicate that low doses of blockers of the cholinergic muscarinic receptor, injected intraventricularly, produce strong central stimulation, whereas high doses produce depression of the central nervous system.

Acetylcholine↗
PubMed1972

thermoregulatory effects of intraventricular injection of noradrenaline in the mouse and the influence of ambient temperature.

1. At an ambient temperature of 20 degrees C, intraventricular injection of noradrenaline in the mouse resulted in hypothermia accompanied by a fall in metabolic rate and by cutaneous vasodilatation. Subcutaneous injection of noradrenaline resulted in hyperthermia with raised metabolic rate and cutaneous vasodilatation.2. The hypothermia and fall in oxygen consumption rate following intraventricular noradrenaline were prevented by pre-treatment with subcutaneous propranolol, while the cutaneous vasodilatation was un-affected. However, the effects of subcutaneously injected noradrenaline were completely abolished by subcutaneous propranolol. Intraventricular propranolol did not modify the hypothermic effect of intraventricular noradrenaline.3. The direction of the effect on body temperature of intraventricular noradrenaline was dependent upon ambient temperature; hypothermia occurring at low (15 degrees C) and hyperthermia at high (36 degrees C) ambient temperatures. However, when the possibility of any peripheral action of noradrenaline escaping into the systemic circulation was prevented by prior subcutaneous injection of propranolol, significant hypothermia could be detected at temperatures as high as 32 degrees C.4. The possibility that the effects of intraventricular noradrenaline could be due to complete abolition of central temperature regulation was further excluded by the occurrence of thermal salivation in all animals during experiments performed at 36 degrees C.5. It is suggested that, in the mouse, the hypothermic actions of intraventricular noradrenaline are due to a central effect, while its hyperthermic effects at high ambient temperature are due to escape of noradrenaline into the peripheral circulation. The hypothermia could be the result of selective activation of central heat loss mechanisms.6. Intraventricular noradrenaline was without effect on brain plasma-space although exposure to 100% oxygen caused a detectable fall.

Animals↗
PubMed1975

Effects of an intraventricular injection of synthetic ACTH on plasma testosterone, progesterone and LH levels and on sexual behavior in male and female rabbits.

Sexual behavior and elevation of gonadal steroids were induced in both male and female New Zealand white rabbits following injection of synthetic beta (1-24) ACTH into the lateral cerebral ventricle. In blood assays collected by cardiac puncture, testosterone, progesterone and corticosterone were all increased above both resting levels and samples were taken after a control intraventricular injection of physiological saline. Parallel increases of plasma LH were also demonstrated. The results were interpreted to indicate that intraventricular ACTH, through LH release, influences sex hormone levels and sexual behavior by 'centrally', probably within the hypothalamus.

Adrenocorticotropic Hormone↗
PubMed1983

Acute inhibition of PRL and TSH secretion after intraventricular injection of PRL in ovariectomized rats.

Prolactin (PRL) is under short-loop inhibitory control via the hypothalamus. However, earlier studies evaluated the effects on PRL secretion of PRL levels elevated for periods of days. In this study we evaluated the acute effects of intraventricular and systemic injection of PRL on the release of a variety of pituitary hormones. Ovariectomized (OVX) rats, bearing implanted third ventricular and jugular cannulas were used. Blood was withdrawn in unanesthetized, freely moving animals before and after intraventricular injection of 0.9% NaCl or 1 or 3 micrograms of bovine (b) or ovine (o) PRL. Prolactin was also administered intravenously in doses of 3 or 6 micrograms. No effect on plasma levels of any of the pituitary hormones occurred after intraventricular or systemic injection of saline. Intraventricular injection of both doses of bPRL or oPRL significantly lowered plasma PRL within 15-30 min. In animals with elevated initial PRL values because of stress or estradiol (E) priming, greater lowering of PRL occurred. Inconsistent reductions in plasma PRL occurred after intravenous injection of oPRL but not bPRL, which elevated PRL values via cross-reaction in the immunoassay. In contrast, only small and inconsistent declines in luteinizing hormone (LH) were seen after intraventricular injection of PRL in either OVX or OVX E-primed rats. Plasma follicle-stimulating hormone (FSH) and growth hormone (GH) were not affected by PRL in any of the experiments; however, a significant lowering of thyrotropin (TSH) occurred in OVX or OVX E-primed rats within 30 min after intravenous injection of 3 micrograms of oPRL, but no change occurred after intravenous PRL. The data indicate that PRL can acutely inhibit PRL and TSH release via a hypothalamic action, whereas release of LH is only slightly inhibited and that of FSH and GH is unaltered.

Animals↗
PubMed1981

[Effects of intraventricular injection of 5,7-dihydroxytryptamine on monoamines and sleep in the kitten (author's transl)].

Intraventricular injections of 5,7-DHT (.15 mg/g of brain weight) were performed in kittens aged 5 or 30 days. The neurotoxin induced a significant decrease of 5-HT and NA levels in the forebrain in both age groups, whereas a slight increase of each amine was observed respectively in the raphe and lateral brain stem of the younger group (Fig. 1). Pretreatment with desmethylimipramine (20 mg/kg I.P.) resulted in a protection of the noradrenergic system from the neurotoxin (Fig. 2). From the neurophysiological standpoint, 5,7-DHT induced a major paradoxical sleep (PS) insomnia in the one-month-old group, whereas no alteration of PS was observed in the younger group (Fig. 3). The DMI pre-treatment did not modify these results. The hypothesis of brain stem sprouting is discussed, and it is concluded that the serotoninergic system does not mediate the sleep regulation in the early post-natal period.

5,7-Dihydroxytryptamine↗
PubMed1975

Effects of intraventricularly injected 6-hydroxydopamine on carotid sinus baroreceptor reflex in rabbits.

Effects of 6-hydroxydopamine (6-OH-DA) injected into the lateral brain ventricle on the carotid sinus baroreceptor reflex were studied in rabbits anesthetized with alpha-chloralose and urethane. As short term effects, injection of 500 mug/kg of 6-OH-DA caused a fall in blood pressure and heart rate, enhanced the depressor and bradycardia responses to electrical stimulation of the carotid sinus nerve (CSN), and inhibited the pressor response to carotid occlusion. These effects reached the maximum with 2 hrs and disappeared by the 4th hr. Intraventricular injection of noradrenaline (NA) could mimic most of these effects. At 4.5 hrs after injection of 6-OH-DA, NA content of the brain was definitely reduced: 21% of control in the hypothalamus and 14% in the pons-medulla. Rabbits treated with 6-OH-DA under penthobarbital anesthesia 24 hrs before showed a slight fall in resting blood pressure and almost normal baroreceptor function. Intraventricular application of phentolamine abolished the responses to CSN stimulation in 6-OH-DA pretreated as well as normal animals. These results suggest that the acute effects of 6-OH-DA are based on the increased release of NA from the affected nerve terminals and that noradrenergic neurons are involved in the central pathway of baroreceptor reflex. Moreover, the relfex may be functionally maintained by a small portion of brain NA content, even when noradrenergic neurons are greatly affected by 6-OH-DA.

Animals↗