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PubMed1994

Effects of intraventricular injection of morphine and beta-endorphin on serotonin release from the spinal cord in rats.

Effects of intraventricular (third ventricle) injection of morphine and beta-endorphin on the release of serotonin (5-HT; 5-hydroxytryptamine) and 5-HIAA (5-hydroxy indolacetic acid) from the spinal cord were studied using urethane anesthetized spinally perfused rats. Intraventricular injection of morphine (25 micrograms) increased the 5-HT level in the perfusate about threefold. The increase of 5-HT release reached at peak between 30 and 60 min after the first injection of morphine. However, the levels of 5-HIAA, a metabolite of 5-HT, was not significantly altered by intraventricular injection of morphine. Furthermore, second intraventricular injection of morphine at the same dose did not increase 5-HT level in the spinal perfusate. In contrast to the results with morphine, beta-endorphin (10 micrograms) administered intraventricularly did not alter the release of 5-HT and 5-HIAA from the spinal cord. In addition, acute antinociceptive tolerance to intraventricular morphine induced by a prior intraventricular injection of morphine was studied in pentobarbital anesthetized rats. Acute tolerance was induced by intraventricular pretreatment with morphine (20 micrograms) for 120 min and the same dose of morphine was injected intraventricularly. The tail-flick test was used as an antinociceptive test. Pretreatment of rats with morphine intraventricularly reduced inhibition of the tail-flick response to intraventricularly injected morphine. The results support our previous hypothesis that beta-endorphin and morphine administered supraspinally activate separate descending systems. Spinopetal serotonergic descending pathway is selectively activated by intraventricularly injected morphine but not beta-endorphin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Distribution of [125I]nerve growth factor in the rat brain following a single intraventricular injection: correlation with the topographical distribution of trkA messenger RNA-expressing cells.

The present study determined the topographical distribution of [125I] nerve growth factor in rat brain at various time points following an intraventricular injection. In addition, we quantified the tissue content of nerve growth factor in various brain tissues following the injection. Autoradiographic analysis of the distribution of [125] nerve growth factor indicated that the neurotrophin is rapidly distributed within the entire ventricular system. However, penetration of nerve growth factor into the brain parenchyma was very limited. At early time points following an injection of nerve growth factor, there was an accumulation of label in the immediate vicinity of the lateral ventricle and third ventricle with predominant labeling around the septum, hypothalamus and cerebellum. By 24 h following nerve growth factor administration, there was discreet labeling of the lateral septum, medial septum, diagonal band, hypothalamus, olfactory tubercle and nucleus of the olfactory tract, and some label was present in the hippocampus and subiculum. Quantitative ELISA of nerve growth factor in brain tissues 1 h following the injection indicated a 446% and 133% increase over basal levels of nerve growth factor in the basal forebrain and hippocampus, respectively. At 24 h nerve growth factor levels measured in brain were not significantly different from endogenous basal levels as determined by ELISA, whereas there were high quantities of 125I present in the thyroid gland, suggesting that the administered [125I] nerve growth factor was rapidly degraded following the intraventricular injection. We observed a similar labeling pattern of the medial septum/diagonal band cholinergic cell body group 24 h following either an intraventricular or intrahippocampal injection of [125I] nerve growth factor. There was a good correlation between the [125I] nerve growth factor labeling pattern and the presence of trkA messenger RNA. This suggested that, at least in the septohippocampal pathway, nerve growth factor accumulated in a region which contained trkA nerve growth factor receptors. Thus, this study shows that after a single unilateral intraventricular injection of nerve growth factor into rat brain there is effective uptake by diagonal band/septal cells on both sides of the brain, and by cells whose positions correlate with the locations of cholinergic and trk A messenger RNA-expressing cells. Significant uptake was also observed in the hypothalamus and cerebellum. The very limited penetration and rapid degradation of intraventricularly administered nerve growth factor suggests that tissue penetration may be a limiting factor when attempting to influence brain neurons by exogenous neurotropic factors.

Animals↗
PubMed1972

Deficits in feeding behavior after intraventricular injection of 6-hydroxydopamine in rats.

Intraventricular injections of 6-hydroxydopamine produced 95 percent depletion of telencephalic norepinephrine and 62 percent depletion of striatal dopamine in rats. Treated rats maintained body weight at subnormal levels and failed to increase food intake in response to a short-term decrease in glucose utilization. After treatment with the monoamine oxidase inhibitor pargyline, 6-hydroxydopamine produced no further norepinephrine depletion but increased the dopamnine depletion to 95 percent and produced complete aphagia. These effects are comparable to events that follow bilateral electrolytic lesions of the lateral hypothalanmus.

Animals↗
PubMed1991

[Effect of intraventricular injection of anti-beta-endorphin serum on shock after burn in rats].

Intraventricular injections of anti-beta-endorphin serum (8 microliters) at 0, 1, 2, 3 h after burn shock (20% body surface area, 100 degrees C, 20 s) in different group rats prolonged the survival time, delayed the decrease of mean arterial pressure (MAP) and heart rate, and postponed the abnormal changes of ECG. The effect was most prominent at 1 h and little at 3 h after burn.

Animals↗
PubMed1992

[Effect of intraventricular injection of 6-hydroxydopamine on the initiation of hibernation in ground squirrels].

The effect of forced depletion of brain norepinephrine (NE) on the onset of hibernation was observed in the ground squirrel (Citellus dauricus) by intraventricular injection of 6-hydroxydopamine (6-OHDA). The results showed: (1) Intraventricular injection of 100-200 micrograms 6-OHDA, which depleted 50-60% NE, markedly facilitated the onset of hibernation, i.e. the average induction period for hibernation in the treated animals was significantly shorter than that of the natural hibernating animals. (2) The average total torpor time in the treated animals was longer than that of natural hibernating animals. (3) All hibernating animals treated with 6-OHDA were able to wake up from deep hibernation spontaneously and undergo normal hibernation bouts. The results indicate the decrease of NE system activity in brain is one important factor in triggering the onset of hibernation.

Animals↗
PubMed1992

Uptake and subcellular distribution of intraventricularly injected [1-3H]dolichol in rat brain.

The uptake of C95[1-3H]dolichol in the form of liposomes into rat brain after the intracerebral and intraperitoneal injection was investigated. Efficient, time-dependent uptake of dolichol into the brain was observed exclusively after the intraventricular injection. Within 24 h after the injection about 10% of the applied dolichol was found in the brain and 1.5% in liver. The distribution of dolichol in various parts of rat brain decreased in the order: cerebellum greater than midbrain greater than grey matter and brain stem greater than white matter. Seven days after the injection total radioactivity in the brain decreased and concomitantly a significant increase was observed in blood circulating and liver of the rat. The highest activity was found in grey matter and it remained a few times higher in comparison with that in white matter. About 80% of the dolichol taken up by the brain membrane was recovered in the following subcellular fractions: crude nuclear fraction greater than microsomes greater than mitochondria greater than synaptosomes greater than myelin. These results demonstrate for the first time that dolichol is actively taken up by the brain membrane exclusively after intraventricular injection of dolichol-phosphatidylcholine in the form of liposomes; this method may be useful in studies on the role of dolichol in brain function.

Animals↗
PubMed1980

Effects of intraventricular injection of 6-hydroxydopamine in the developing kitten. III. Histochemical fluorescence and radioautographic studies of the noradrenaline hyperinnervation in the pons.

In the present study, using neonatal intraventricular injections of 6-hydroxydopamine (6-OHDA) and the fluorescence histochemical method for monoamines, it is observed that an extensive plexus of noradrenaline (NA) fibres develops in the pontine region of the cat brain subsequently to the neonatal destruction of the ascending NA bundles and of the NA innervation in the cerebral cortex by the neurotoxin. This plexus is only partly conserved 10 months after the 6-OHDA treatment. Generally, only a limited number of NA perikarya degenerate in the region of the locus coeruleus, the others (nucleus subcoeruleus senso lato) exhibiting the same strong fluorescence as the new NA fibres. Using the radioautographic method after intraventricular injections of [3H]NA, our work demonstrates also the transient disappearance (at least one month) of the uptake of [3H]NA in the pons, whose NA cell bodies and nerve terminals are no longer labeled in the same number as in control animals. The possibility of again labeling significantly NA perikarya and numerous nerve terminals occurred between 3 and 5 months of age, probably indicating both a re-establishment of normal uptake properties in the preserved NA perikarya and nerve terminals and some maturation of the uptake mechanisms in the abnormal NA fibres of the pons. This last observation is at variance with data from newborn animals showing that the uptake of NA develops in parallel with the accumulation of endogenous NA in catecholamine nerve terminals. The present results, however, do corroborate and complement previous biochemical data obtained in the cat after neonatal injection of 6-OHDA.

Aging↗
PubMed1976

Non-diffusional distribution of radioactivity in the rat median eminence after intraventricular injection of 3H-LH-RH.

The distribution of radioactivity in the rat hypothalamus after intraventricular injection of tritiated luteinizing hormone-releasing hormone (LH-RH) was studied by autoradiography and compared with that expected from Fick's second law which defines the character of ordinary diffusion. The results suggest that LH-RH penetrates through the ependyma and thin subependymal layer in the median eminence and into the suprachiasmatic area by ordinary diffusion. By contrast, concentration of radioactivity in outer layers of the median eminence is increased and, therefore, can not be explained by the diffusion law. In this region incorporation of radioactivity into cell bodies was demonstrated. In the subependymal layer of the median eminence a few rows of silver grains seemingly located in cellular processes were also observed. The diffusion coefficient in the periventricular zone was lower than that in the deeper tissue. It is suggested that the ependymal-subependymal complex of the third and lateral ventricles acts as passive membrane towards LH-RH contained in the cerebrospinal fluid. The significance of this mechanism for the intrahypothalamic transport of RH's is discussed.

Animals↗
PubMed1980

Effects of intraventricular injection of Sar1-Ala8-angiotensin II on plasma vasopressin level increased by angiotensin II and by water deprivation in conscious rats.

The effects of intraventricular injection of Sar1-Ala8-angiotensin II (A specific antagonist of angiotensin II) on the plasma vasopressin level increased by intraventricular injection of angiotensin II and by water deprivation (46 h) were examined in conscious male rats with an indwelling cannula in the third cerebral ventricle. Blood samplings were made by decapitation and the plasma level of vasopressin was determined by radioimmunoassay. Twenty-five, 50 or 100 ng of angiotensin II produced significant (P less than 0.05) increase in plasma vasopressin level 90 sec after the injection. The effect of 50 ng of angiotensin II was inhibited significantly (P less than 0.05) at least with 100 ng of Sar1-Ala8-angiotensin II given 2 min before the injection of angiotensin II. The dehydrated rats to which 1000 ng of Sar1-Ala8-angiotensin II was given 5 min before the decapitation showed the significantly (P less than 0.05) lower median plasma vasopressin level than that of the dehydrated controls. No significant difference in plasma osmolality was noted between them. These results suggest that the plasma vasopressin response to intraventricular angiotensin II is produced via angiotensin II receptors in the brain and that Sar1-Ala8-angiotensin II inhibits the effect of endogenous angiotensin II on plasma vasopressin level under dehydration.

Angiotensin II↗
PubMed1978

Direct administration of methotrexate into the central nervous system of primates. Part 1: Distribution and degradation of methotrexate in nervous and systemic tissue after intraventricular injection.

Levels of methotrexate (MTX) measured by both 3H radioactivity and dihydrofolate reductase assays were determined in cerebrospinal fluid (CSF), plasma, urine, and both neural and non-neural tissues at varying times after a single intraventricular injection into Cynomolgus monkeys (Macaca fascicularis). Clearance of the MTX from CSF was rapid after injection. A relatively constant level of 3HMTX was reached in plasma 2 1/2 hours after injection, and about 30% of the 3HMTX dose was excreted in the urine within 4 hours after injection. Maximum levels in CNS tissues were obtained by 4 hours after injection, and average concentrations of 10(-6) M MTX (moles/kg wet weight) were maintained in CSF for up to 12 hours and in brain for up to 24 hours after injection. Conversion of MTX to non-MTX products was detected in CSF between 4 and 12 hours, and in brain tissue between 12 and 24 hours after injection, and the amount of these products increased with time. Regional distribution studies in the cerebrum showed a U-shaped distribution curve for 3HMTX up to 12 hours after injection, which closely followed the 14C inulin distribution. Thus, the levels in deep cerebral tissue were less than the average level for brain, and this suggests that treatment of CNS tumors by intraventricular injection may have variable results, partly due to complex tissue distribution patterns.

Animals↗
PubMed1990

Glutathione and gamma-glutamyl transpeptidase in the adult female rat brain after intraventricular injection of LHRH and somatostatin.

Glutathione content and glutamyl transpeptidase activity in different regions of adult female rat brain were determined at 10 and 30 min following intraventricular injection of LHRH and somatostatin. Hypothalamic glutathione levels were significantly elevated at 10 and 30 min after a single injection of a 0.1 micrograms dose of LHRH. On the contrary, glutathione levels significantly decreased in the hypothalamus, cerebral cortex and cerebellum at 10 and 30 min after 0.5 or 1 microgram dose. However, significant decrease in brain stem glutathione was evident at 30 min after 0.5 microgram and 10 min after the 1 microgram dose. Somatostatin at doses of 0.5 microgram and 1 microgram significantly decreased glutathione levels in all four brain regions both at 10 and 30 min following injection into the 3rd ventricle. Gamma-glutamyl transpeptidase activity in the hypothalamus and cerebral cortex was significantly elevated after intraventricular injection of LHRH. However, a significant increase in gamma-glutamyl transpeptidase activity in cerebellum and brain stem was seen only with 0.5 and 1 micrograms doses of LHRH. Somatostatin also significantly increased gamma-glutamyl transpeptidase activity in hypothalamus, cerebral cortex, brain stem and cerebellum. The decrease in glutathione levels with corresponding increase in gamma-glutamyl transpeptidase activity after intraventricular administration of LHRH and somatostatin suggests a possible interaction between glutathione and hypothalamic peptides.

Animals↗
PubMed1985

Effects of intraventricular injections of 6-hydroxydopamine on amine metabolites in rat brain and urine.

The effects in rats of intraventricular injections of 6-hydroxydopamine (6-OHDA) on the urinary excretion 1-3 weeks later of 3-methoxy-4-hydroxyphenethylene glycol (MHPG), 3,4-dihydroxyphenethanol (DHPE), 3-methoxy-4-hydroxyphenethanol (MHPE), p-hydroxyphenylglycol (pHPG), homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) were examined. The excretion of MHPG was decreased to 63 and 71% of control on days 7 and 14, respectively, but had returned to control levels by day 23, even though the brain levels were decreased by 87%. Free and total HVA excretion was reduced on both days 7 and 23, but free and total DOPAC was reduced only on day 7. Based on these data, it can be estimated that about 39% of the free and 46% of the total HVA in urine originates in the CNS. The excretion of conjugated HVA was decreased by 70-80%, but this decrease does not support the notion that the conjugated form of HVA is derived principally from the brain and thus serves as a better marker of brain dopamine metabolism, since the level of this metabolite in the brain was not correspondingly decreased but was instead increased. Urinary DOPAC levels were generally more variable and derived to a greater extent from the periphery; therefore, DOPAC appears to be less suitable than HVA as a marker of brain dopamine. The results also indicate that as much as 35% of the urinary MHPG may originate in the CNS, although compensatory changes in catecholamine metabolism in either the brain or in the periphery may have somewhat influenced this estimate. The results also suggest that at least as much pHPG as MHPG in urine derives from the CNS. The data are consistent with the idea that the neutral dopamine metabolites largely derive from the brain, but the relatively small depletion in their brain levels produced by 6-OHDA prevented the exact proportion being determined accurately.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Vasopressin release from incubated in situ posterior pituitary lobe after intraventricular injection of carbachol or atropine.

The vasopressin release rate from incubated in situ rats posterior pituitary lobe as observed following intracarotid infusions of hypertonic solutions (3 x 0.1 ml/100 g b.w. contained 1.0 mmol NaCl and 0.1 mmol CaCl2 per 1 ml) was studied when influenced by intraventricular injections of 0.6 microgram carbachol or 240 microgram atropine sulphate, respectively. The increase in the release of vasopressin following intracarotid infusions of hypertonic solution augmented by intraventricular injection of carbachol was found. Atropine was shown to be effective in preventing the vasopressin release caused by hypertonic solution. The effects of carbachol and atropine indicate that mediation at synapses in the nucleus supraopticus involved in the release of vasopressin induced by osmotic stimulation is cholinergic.

Animals↗
PubMed1990

Intraventricular injection of neurotensin reduces dopamine D2 agonist binding in rat forebrain and intermediate lobe of the pituitary gland. Relationship to serum hormone levels and nerve terminal coexistence.

In order to investigate neurotensin-dopamine receptor interactions in vivo, the effects of intraventricular injection of neurotensin were analyzed on S(-)[N-propyl-3H(N)]propylnorapomorphine [( 3H]NPA) binding in cryostat sections of the forebrain, hypothalamus and pituitary gland, and on serum levels of prolactin, luteinizing hormone and corticosterone in the male rat. The relationship of modulation of [3H]NPA binding with neurotensin-dopamine coexistence in nerve terminals was analyzed by investigating coexistence of neurotensin and tyrosine hydroxylase (TH) immunoreactive nerve terminals in various brain areas, using a double immunohistofluorescence procedure. Intraventricular injections of neurotensin (0.03-3 nmol, 30 min) reduced dose-dependently specific [3H]NPA binding (0.25 nM) in the caudate-putamen (-38 +/- 4%), nucleus accumbens (-42 +/- 5%), tuberculum olfactorium (-52 +/- 7%) and in the intermediate lobe of the pituitary gland (-17 +/- 2%). Coexistence of neurotensin and TH was demonstrated in nerve terminals in the prefrontal, cingulate, piriform and entorhinal cortex and in the cortical and deep nuclei of the amygdaloid cortex. It was not possible to demonstrate coexistence in the caudate-putamen, nucleus accumbens, tuberculum olfactorium and median eminence, in view of the high density of dopamine nerve terminals present in relation to the few visualized neurotensin terminals. Nor could coexistence be demonstrated in the few remaining TH-positive nerve terminals following unilateral 6-hydroxydopamine lesions (8 micrograms per 4 microliters; one week) in spite of increased numbers of neurotensin-containing cell bodies and terminals in the ipsilateral dorsomedial caudate. Neurotensin injection markedly decreased serum prolactin levels and increased serum corticosterone levels by about 60%, whereas serum levels of luteinizing hormone were unaffected. The present study indicates that central dopamine D2 receptors may be regulated by neurotensin in vivo and that the neurotensin involved most likely is released from nerve terminals not containing dopamine, since fibers showing coexistence were only found in prefrontal and limbic cortical areas.

Animals↗
PubMed1982

Delay of cancer anorexia following intraventricular injection of para-chlorophenylalanine.

Serotonergic mediation of cancer anorexia was investigated in immature female rats following the intraventricular injection of para-chlorophenylalanine (PCPA) or normal saline. Significant anorexia developed 6 days after the induction (IM) of Walker 256 carcinosarcomas in saline-treated rats. Although tumor-bearing rats treated with PCPA ate less than PCPA-injected controls by day 7, their feeding response was significantly greater than that of saline-treated tumor-bearing rats on days 5, 6 and 7. The PCPA treatment had no significant effect on food intake in nontumor-bearing rats. Biochemical analysis revealed significant elevations in plasma free tryptophan, brain tryptophan and brain 5-hydroxyindoleacetic acid in saline-treated tumor-bearing rats. Brain serotonin, 5-hydroxyindoleacetic acid and norepinephrine levels were decreased in PCPA-treated rats. Although these data may provide some support for a serotonergic mediation of cancer anorexia, additional mechanisms are clearly indicated.

Animals↗
PubMed1976

Sites of action of morphine involved in the development of physical dependence in rats. I. Comparison of precipitated morphine withdrawal after intraperitoneal and intraventricular injection of morphine antagonists.

In rats made dependent on morphine by implantation of morphine pellets, withdrawal, as precipitated by intraventricular injection of morphine antagonists, was compared to withdrawal as precipitated by systemic antagonist application. The results, most clearly those obtained with a hydrophilic compound, diallyl-nor-morphinium-bromide, point to periventricularly located sites of action for the release of most withdrawal signs by antagonists. Jumping, reaching only low levels after i.ventr. injection of levallorphan and nalorphine, was very pronounced when the benzomorphane derivative SH 254, was used. In the case of writhing and diarrhea, the situation is more complicated. Possibly, central as well as peripheral mechanisms are involved in the expression of these signs.

Animals↗