SEARCH · PubMed Health

Results for “Injections, 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 739 records · Page 41Linked to original sources

PubMed1990

Intrathecal administration of thiorphan and bestatin enhances the antinociception and release of Met-enkephalin induced by beta-endorphin intraventricularly in anesthetized rats.

Effects of bestatin and thiorphan administered intrathecally, on inhibition of the tail-flick response and the release of Met-enkephalin induced by beta-endorphin administered intraventricularly were studied in anesthetized rats. Intrathecal pretreatment with 100 micrograms of thiorphan or bestatin potentiated the inhibition of the tail-flick response induced by beta-endorphin injected intraventricularly in pentobarbital anesthetized rats; the ED50 values for beta-endorphin were decreased 5- and 7-fold by thiorphan and bestatin, respectively. To determine if the potentiating effect was due to the inhibition of the degradation of Met-enkephalin released by intraventricular beta-endorphin, the effects of intrathecal perfusion with thiorphan or bestatin on the release of immunoreactive Met-enkephalin from the spinal cord by intraventricular injection of beta-endorphin were studied. beta-Endorphin injected into the 4th ventricle at a dose of 5 micrograms increased immunoreactive Met-enkephalin in the spinal perfusate in urethane-anesthetized rats. Thiorphan or bestatin (1 x 10(-7) to 1 x 10(-4) M each) increased the amount of immunoreactive Met-enkephalin released by intraventricular beta-endorphin in a dose-dependent manner. The results provide additional evidence for the hypothesis that antinociception induced by beta-endorphin is mediated by release of Met-enkephalin.

Aminopeptidases↗

PubMedDate not supplied

Slow-wave sleep induced in cats by extremely small amounts of synthetic and pineal vasotocin injected into the third ventricle of the brain.

A single injection of 10(-6) pg synthetic arginine vasotocin (AVT), corresponding to about 600 molecules AVT, into the third ventricle of unanesthetized cats, induced slow-wave sleep 5 min after the injection. An equivalent amount, of a partially purified pineal AVT injected into the third ventricle, produced the same effects. After incubation with trypsin, pineal AVT completely lost its ability to induce slow-wave sleep. The slow-wave sleep induced by 10(-6) pg synthetic AVT injected intraventricularly could be matched by 1 microgram synthetic AVT injected intraperitoneally. Neither synthetic arginine vasopressin, nor synthetic oxytocin, injected intraventricularly in the amount of 10(-6) pg, was able to induce slow-wave sleep. Whereas in the control animals injected with pineal AVT after incubation with trypsin, or in the control animals injected with vasopressin or oxytocin, the paradoxical sleep averaged 21.9--22.8% of the sleep time, during a total recording time of 5 hr, in the cats injected with synthetic or pineal AVT, the paradoxical sleep was completely suppressed.

Animals↗

PubMed1985

Place preference conditioning with methylphenidate and nomifensine.

The role of central catecholaminergic systems in place preference conditioning produced by methylphenidate and nomifensine was investigated. Several doses of either methylphenidate or nomifensine produced alterations in place preferences, while desipramine (10 mg/kg), a relatively selective noradrenergic uptake inhibitor, was ineffective, Haloperidol (0.15-0.5 mg/kg) did not attenuate place preferences induced with methylphenidate (2.5 and 5.0 mg/kg) or nomifensine (5.0 mg/kg), although conditioning with methylphenidate (5.0 mg/kg) was blocked after injections of a high dose of haloperidol (1.0 mg/kg). Intraventricular injections of 6-hydroxydopamine had no effect on methylphenidate (2.5 mg/kg) induced place preferences. 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). These results suggest that methylphenidate and nomifensine produce place preferences via mechanisms that are either qualitatively or quantitatively distinct from their catecholamine-dependent stimulant actions.

Animals↗

PubMed1990

Physiologically significant effect of neuropeptide Y to suppress growth hormone release by stimulating somatostatin discharge.

Neuropeptide Y (NPY) is a peptide found in a variety of hypothalamic loci which is frequently colocalized with catecholamines. It is also secreted into hypophyseal portal vessels. The injection of NPY into the third ventricle (3V) lowered plasma GH levels in conscious, freely moving male rats. To determine the physiological significance of the hypothalamic inhibitory action of the peptide, highly specific antiserum directed against NPY was injected into the 3V of conscious rats. 3V injection of the antiserum evoked a significant elevation of plasma GH within 2 h on comparison to values in normal rabbit serum-injected, ovariectomized rats. The difference increased and reached a maximum at 6 h after injection. On the other hand, there was no effect of the antiserum in ovariectomized, estrogen, progesterone-blocked rats. Intraventricular injection of the anti-NPY serum also caused a significant elevation of plasma GH within 2 h in normal male rats and the increases above values in normal rat serum-injected control animals became even more significant at 3 and 4 h. To determine the mechanism by which NPY lowers GH after its intraventricular injection, its effect on the release of somatostatin (SRIF) from median eminence fragments incubated in vitro was examined. NPY stimulated SRIF release with a highly significant effect at a concentration of 10(-9) M. Borderline stimulation was observed at doses as low as 10(-11) M. The curve was bell-shaped with a declining release at 10(-8) M and 10(-7) M. The releasing action of NPY was blocked by either the alpha 1-receptor blocker, prazosin (10(-6) M), or the beta-receptor blocker, propranolol (10(-6) M), but was not affected by the alpha 2-receptor blocker, yohimbine (10(-6) M). We conclude that NPY has a physiologically significant inhibitory action within the hypothalamus to suppress GH release in ovariectomized female and intact male rats by stimulation of SRIF release by alpha 1 and beta-adrenergic receptor-mediated mechanisms.

Animals↗

PubMed1989

Effect of leukotriene D4 on blood flow to cerebrum and choroid plexus.

The purpose of this study was to examine effects of leukotriene D4 on blood flow to the cerebrum and choroid plexus. Blood flow was measured with microspheres in anesthetized rabbits. Under control conditions, blood flow to the cerebrum was 37 +/- 4 ml. min-1.100 g-1 (mean +/- SE) and blood flow to the choroid plexus was 428 +/- 52 ml.min-1.100 g-1. Intra-atrial infusion of leukotriene D4 at 0.1 and 1.0 microgram.kg-1.min-1 did not alter blood flow to the brain or choroid plexus, but produced a 49 +/- 3% and 69 +/- 5% decrease in blood flow to the bowel. We also examined effects of intracerebroventricular administration of leukotriene D4. Intraventricular injection of 1.0 microgram of leukotriene D4 did not affect blood flow to the cerebrum or choroid plexus. In contrast, intraventricular injection of 1.0 microgram of angiotensin II produced a 42 +/- 4% decrease in blood flow to the choroid plexus. In summary, neither intravascular nor intraventricular administration of leukotriene D4 affects blood flow to the brain or choroid plexus.

Angiotensin II↗

PubMed1977

Behavior of rats in various stages of the sexual cycle after injection of noradrenaline into the lateral ventricle of the brain.

The influence of intraventricular injection of 50 microng of noradrenaline (NA) on behavior of female Wistar rats in various phases of the sexual cycle, and the influence of 17-beta-estradiol and progesterone in castrated female rats were studied. Changes in motor and exploratory activity were observed in the course of the sexual cycle in female rats. Sensitivity to NA injected intraventricular varied significantly in different phases of the sexual cycle. Castration depressed the action of NA on motor and exploratory activities in rats, and progesterone prevented the depressive effect of NA in castrated rats.

Animals↗

PubMed1977

Neurotoxicity of apamin and MCD peptide upon central application.

Besides apamin, the structurally related MCD peptide (mast cell degranulating peptide; peptide 401) is another centrally acting peptide from bee venom. In contrast to apamin, it is hardly neurotoxic upon intravenous injection in mice. Following intraventricular injection, as little as 0.3 microgram/animal produce convulsions and respiratory arrest in mice. The clinical picture differs from that elicited by apamin, and apamin is about 10 times more potent than MCD peptide when given intraventricularly. Apamin and MCD peptide injected into the spinal cord of rats in nanogram amounts, produce circumscript hyperexcitation lasting more than one day, however with complete recovery following sublethal doses. Local apamin poisoning differs from local tetanus (elicited by the same way) by its faster time course.

Animals↗

PubMed1989

[The influence of GABA injected into cerebral ventricle on electrical activities of pain-excitation neurons and pain-inhibition neurons in nucleus parafascicularis of the thalamus of rats].

The influence of intraventricular injection of GABA on electrical activities of PEN and PIN in nucleus parafascicularis of the thalamus of rats was studied. The results showed that GABA could significantly inhibit the electrical discharges of PEN and increase the electrical discharges of PIN. So it was believed that intraventricularly injected GABA could antagonize or partly antagonize the excitatory action of noxious stimuli and might thus produce analgesia.

Animals↗

PubMed1985

Intertectal neuronal plasticity in Xenopus laevis: persistence despite catecholamine depletion.

In normal Xenopus, the tectum receives a direct projection from the contralateral retina and an indirect projection, via the intertectal system, from the ipsilateral eye. The two maps of binocular visual space, at each tectum, are in register. If one eye is rotated during larval development, the ipsilateral visuotectal projection compensates by changing its orientation. Rearrangement of the intertectal system brings the ipsilateral map back into register with the contralateral map. We sought to determine whether this intertectal plasticity required normal levels of brain monoamines. Animals received an eye rotation between stages 55-63 of larval life and were then placed in one of 3 groups. A first control group received no further treatment. A second control group was given intraventricular injections of ascorbate vehicle. The experimental group was given intraventricular injections of 6-hydroxydopamine in ascorbate vehicle. Two to 3 months after metamorphosis, visuotectal projections were mapped electrophysiologically and the brains were assayed for monoamines. Intertectal plasticity occurred in all 3 groups of animals, including animals in which brain catecholamine levels were severely reduced. We conclude that normal levels of brain catecholamines are not required for this form of neural plasticity.

Animals↗

PubMed1979

Intracerebral adrenocorticotropic hormone mediates novelty-induced grooming in the rat.

Intact male rats exhibited more grooming in unfamiliar testing chambers than in their home cages. Hypophysectomized rats showed a much reduced increase in grooming in these testing chambers. Intraventricular injections of antiserum to adrenocorticotropic hormone to intact rats decreased the grooming usually observed in the novel situation, whereas a similar injection of control serum did not produce this effect. Peripheral injections of the antiserum did not affect grooming. Since intraventricularly injected adrenocorticotropic hormone induces excessive grooming, these results suggest that the increased grooming observed in the novel environment may be at least partly due to the release of this hormone directly into the cerebral ventricular system.

Adrenocorticotropic Hormone↗

PubMed1991

Post- and presynaptic lesions in the CA1 region of hippocampus: effect on [3H]forskolin and [3H]phorboldibutyrate ester binding.

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. Four days after transient four vessel occlusion a 80% loss of [3H]FOR and a 35% loss of [3H]PDBU binding could be measured in the CA1 stratum radiatum of operated Wistar rats as compared to control rats. Four days after intraventricular injection of kainic acid only a marginal loss of [3H]FOR and a 30% increase of [3H]PDBU binding was seen in the CA1 stratum radiatum while in the CA3 stratum lucidum and radiatum respectively a 30% loss of [3H]FOR and no significant change in [3H]PDBU binding was observed. As transient cerebral ischemia and intraventricular kainic acid injection are depleting the hippocampal CA1 region of CA1 pyramidal cells and axons of CA3 pyramidal cells respectively in rat brain, these findings strongly suggest that both adenylate cyclase and protein kinase C are localized in CA1 pyramidal cells of rat hippocampus.

Adenylyl Cyclases↗

PubMed2005

Through central arginine vasopressin, not oxytocin and endogenous opiate peptides, glutamate sodium induces hypothalamic paraventricular nucleus enhancing acupuncture analgesia in the rat.

Our previous study proved that the hypothalamic paraventricular nucleus (PVH) plays an important role in acupuncture analgesia. The neuropeptides involving in the PVH regulation of acupuncture analgesia was investigated in the rat. The changes of pain threshold, which was induced by electrical acupuncture of "Zusanli" points (St. 36), were measured as acupuncture analgesia. Microinjection of l-glutamate sodium into the PVH, which only excites the PVH neurons, could dose-dependently enhance the acupuncture analgesia, but microinjection of l-glutamate sodium into the area nearby the PVH did not alter acupuncture analgesia. Removing pituitary did not influence this effect of l-glutamate sodium. Microinjection of l-glutamate sodium into the PVH only increased the arginine vasopressin (AVP), not oxytocin (OXT), leucine enkephaline (L-Ek), beta-endorphine (beta-Ep) and dynorphinA(1-13) (DynA(1-13)) concentrations in the PVH perfuse liquid using radioimmunoassay. Intraventricular injection of anti-arginine vasopressin serum (AAVPS) could completely reverse the effect of microinjection of l-glutamate sodium into the PVH enhancing acupuncture analgesia. Intraventricular injection of naloxone, one opiate peptide antagonist, partly attenuated this effect of l-glutamate sodium, and intraventricular of anti-oxytocin serum (AOXTS) did not change this effect of l-glutamate sodium. The results suggested that l-glutamate sodium induces the PVH enhancing acupuncture analgesia only through AVP, not OXT and endogenous opiate peptides in central nervous system.

Acupuncture Analgesia↗

PubMed1976

Evidence that brain prostaglandin synthesis is not essential in fever.

1. We have tested the hypothesis that a fever caused by pyrogen depends upon the synthesis of prostaglandin E in the brain and that the prostaglandin in turn acts on the hypothalamus to produce fever. 2. In rabbits, fever was produced by the injection of leucocyte pyrogen in a lateral cerebral ventricle. The latency, rate of rise and magnitude of the fever was unaffected by the simultaneous intraventricular injection of two prostaglandin antagonists, SC 19220 and HR 546. 3. Both antagonists effectively attenuated the fever caused by the intraventricular injection of prostaglandin E2. 4. This evidence is not consistent with the hypothesis that prostaglandin E is the principal mediator of fever.

Animals↗

PubMed1988

Beta-endorphin-(1-27) antagonizes beta-endorphin- but not morphine-, D-Pen2-D-Pen5-enkephalin- and U50, 488H-induced analgesia in mice.

beta-Endorphin-(1-27), administered intraventricularly has been previously reported to block the analgesia induced by beta-endorphin injected intraventricularly. The present study was to determine if the blocking effect of beta-endorphin-(1-27) was specific to beta-endorphin which stimulates epsilon receptors, but not to other opioids with activity at different opioid receptors. The antagonistic effects of beta-endorphin-(1-27) on the analgesia induced by beta-endorphin (epsilon-opioid receptor agonist), D-Ala2-NMePhe4-Gly-ol-enkephalin(DAGO) and morphine, (mu-opioid receptor agonists), D-Pen2-D-Pen5-enkephalin(DPDPE) and D-Ala2-D-Leu5-enkephalin(DADLE) (delta-opioid receptor agonists) and U-50, 488H (kappa-opioid receptor agonist) were studied. beta-Endorphin-(1-27) injected intraventricularly, at doses which, when injected alone did not produce analgesia, antagonized the analgesia induced by beta-endorphin given intraventricularly. However, the analgesia induced by DAGO, morphine, DPDPE, DADLE and U-50, 488H given intraventricularly was not antagonized by beta-endorphin-(1-27). The data suggest that beta-endorphin-(1-27) selectively blocks the analgesia induced by the stimulation of epsilon receptors but not by the stimulation of mu, delta, and kappa receptors. The results support the previously proposed hypothesis that beta-endorphin produces its analgesia by stimulating specific epsilon receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed2001

Release of [Met5]enkephalin from the spinal cord by intraventricularly administered endomorphin-2, but not endomorphin-1 in the anesthetized rat.

Effects of intraventricular injection of endomorphin-1, endomorphin-2 and beta-endorphin on the release of immunoreactive [Met(5)]enkephalin from the spinal cord were studied in pentobarbital anesthetized rats. Intraventricular injection of endomorphin-2, but not endomorphin-1, caused an increased release of immunoreactive [Met(5)]enkephalin in the spinal perfusates. Beta-endorphin given intraventricularly also increased the release of immunoreactive [Met(5)]enkephalin in an amount 15-fold higher than that produced by endomorphin-2. The increase of the release of immunoreactive [Met(5)]enkephalin induced by endomorphin-2 was blocked by mu-opioid receptor antagonist CTOP. Our result suggests that endomorphin-2 stimulates another subtype of mu-opioid receptor different from that acted by endomorphin-1 at the supraspinal site and subsequently increases the release of [Met(5)]enkephalin from the spinal cord.

Analgesics, Opioid↗

PubMed1987

Central action of interleukin-1 in altering the release of TSH, growth hormone, and prolactin in the male rat.

In order to determine the possible effects of interleukin-1 on the release of pituitary hormones by direct action on the brain, the peptide was injected into the third brain ventricle of conscious, unrestrained male rats and the effects on hormone release were compared with effects on rectal temperature. The procedure of blood sampling and intraventricular injection resulted in a significant decline in body temperature and a decrease in plasma growth hormone without alteration in the plasma level of thyroid stimulating hormone (TSH) and prolactin. Interleukin-1 injected intraventricularly at a dose of 5 ng (0.3 pmol) prevented the decline in body temperature that occurred in the saline-injected controls and resulted in a significant elevation of plasma growth hormone levels that became apparent within 15 min of injection, as well as a highly variable but significant elevation of plasma prolactin and a significant decline in plasma TSH that was observed at 30 min. The results were similar when areas under the release curves for the various hormones were calculated. On the other hand, the higher dose of 25 ng (1.5 pmole) of interleukin-1, although producing a frank pyrexia, was associated with smaller changes in hormone values, which were no longer significant for any of the three hormones. The results indicate that interleukin-1 can act in minute doses, presumably on structures near the third ventricle, to stimulate growth hormone and prolactin release and to inhibit TSH release. Apparently when frank febrile responses occur, these hormonal responses are muted for reasons that are yet to be determined. In view of the minute doses injected we favor a hypothalamic site for these effects.

Animals↗

PubMed1983

Benzodiazepine receptors in the rat hippocampal formation: action of catecholaminergic, serotoninergic and commissural denervation.

The problem of benzodiazepine receptor localization in the rat hippocampal formation has been approached using several methods of selective deafferentation, followed by [3H]flunitrazepam binding studies. The intraventricular injection of 6-hydroxydopamine reduced, after 14 days, the norepinephrine content of the hippocampal formation by 68.4%, and decreased the number of binding sites by 32%, without change in affinity. The intraventricular injection of 5,6 dihydroxytryptamine reduced the serotonin content by 61.5% but did not alter the [3H]flunitrazepam binding. The intraventricular bilateral injection of 0.5 micrograms kainic acid selectively destroyed the pyramidal neurons in area CA3 of both hippocampi and produced an increase of 28% in [3H]flunitrazepam binding, without change in affinity. These results are discussed in relation to our previous observations about benzodiazepine receptor changes after fimbria-fornix transection. The reduction in [3H]flunitrazepam binding after administration of 6-hydroxydopamine suggests the possible localization of the benzodiazepine receptors on adrenergic presynaptic terminals. The increase in binding sites after destruction of CA3 pyramidal cells, which are the site of origin of commissural fibers, is tentatively interpreted as resulting from the sprouting of mossy fibers that replace the associational-commissural projections.

5,6-Dihydroxytryptamine↗

PubMed1986

Inhibitory roles of the hypothalamic atrial natriuretic polypeptide on the vasopressin release in the sodium-loaded rats.

Implication of the brain atrial natriuretic polypeptide on the vasopressin release was investigated using rats fed with a high-sodium containing diet. Sodium loading increased not only the blood pressure but also the urinary output of vasopressin significantly. The plasma vasopressin concentration increased about 10 times after the intracerebroventricular injections of angiotensin II. Thereby, magnitude of the response was significantly smaller in the rat fed with a high sodium diet than in rats with the regular-diet. The hypothalamic content of both vasopressin and atrial natriuretic polypeptide was significantly larger in the high-salt group than the regular-salt. The intraventricular injections of atrial natriuretic polypeptide abolished the vasopressin release induced by the intraventricular injections of angiotensin II. These results indicate that the vasopressin production in the hypothalamus is increased, but the release is relatively suppressed in the sodium-loaded rats, and that increased hypothalamic atrial natriuretic polypeptide is involved in the suppression of the vasopressin release and in decreasing their sodium appetite to avoid the high sodium environment.

Angiotensin II↗