Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Injections, Intraventricular”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,045 records · Page 58Linked to original sources
PubMed1979

Participation of brain catecholaminergic neurons in a self-sustained circadian oscillation of plasma corticosterone in the rat.

Circadian rhythms of locomotor activity and plasma corticosterone were determined simultaneously in individual rats which were injected intraventricularly with 6-hydroxydopamine (6-OHDA), a specific depletor of catecholamines. In light-dark cycles (LD), 6-OHDA-treated rats showed essentially normal circadian rhythms of both functions. In 200 lux continuous light (LL) the locomotor activity in the drug-treated rats ran freely with a period slightly longer than 24 h: free-running parameters (mesor, amplitude and period) of the locomotor activity were the same as those control rats. The circadian rhythm of plasma corticosterone in control rats also ran freely in LL, resulting in a reversal of their phase after 12 days exposure to LL. However, the rhythm disappeared in 6-OHDA-treated rats under LL: instead in these rats 3--4 episodes of secretion were obsered over a 24 h period. These results suggest a difference in the biochemical background between the regulatory mechanism of circadian rhythm of locomotor actitivity and that of plasma corticosterone. It is also apparent that brain catecholaminergic components are indispensable for the circadian rhythm of plasma corticosterone to freerun normally in LL, but are dispensable in LD. A plausible model consisting of two oscillators is proposed to explain these findings.

Animals↗
PubMed1986

Participation of central norepinephrine in the development of two-kidney, one clip Goldblatt hypertension.

Two series of experiments were conducted to ascertain whether the central catecholamines would participate in the elevation of blood pressure in two-kidney, one clip (2K-1C) Goldblatt hypertensive rats. The effect of 6-hydroxydopamine (6-OHDA) injected intraventricularly (250 micrograms/kg.) before the induction of hypertension (acute phase) or after the establishment of hypertension (chronic phase) was examined in 2K-1C rats and sham rats. The evidence has been presented: 1) that the hypothalamic norepinephrine content of 2K-1C rats in acute phase is 50 per cent lower (p less than 0.001) than that of sham rats, but norepinephrine content in the pons is similar in these animals, 2) that the content of dopamine in hypothalamus or pons is similar in 2K-1C rats and normotensive age-matched sham rats in acute phase, 3) that the content of these monoamines either in hypothalamus or pons in 2K-1C rats in chronic phase is almost identical with that in sham rats, 4) that administration of 6-OHDA markedly reduced the development of hypertension in 2K-1C rats in the acute phase, but did not affect their sustained hypertension in the chronic phase. These findings suggest that hypothalamic norepinephrine participates in the development of hypertension in 2K-1C rats in the acute phase but is not connected with the maintenance of their established hypertension in the chronic phase.

Animals↗
PubMed1988

Hypothalamic action of delta-9-tetrahydrocannabinol to inhibit the release of prolactin and growth hormone in the rat.

The site of action of delta-9-tetrahydrocannabinol (THC) to inhibit the release of prolactin (PRL) and growth hormone (GH) was examined by in vivo and in vitro experiments. In conscious freely moving animals bearing implanted third ventricular (3V) and external jugular cannulae, THC or the diluent was microinjected into the 3V and blood samples were removed to determine the effect on plasma PRL and GH. Both the 0.4- and 4-micrograms dose injected intraventricularly resulted in a suppression of PRL and GH release as indicated by declines in plasma levels within 40-80 min which were highly significant statistically but not dose-related. The higher dose evoked a pulse of GH and/or PRL in most animals which preceded the lowering of hormonal levels. In the in vitro experiments dipersed anterior pituitary cells were incubated with 5 x 10(-8) or 5 x 10(-9)M THC or the diluent for 5 days. Fresh culture medium was added to the cells after 3 days and the cells cultured for an additional 2 days. After this period, the cells were incubated for an additional 2 h in culture medium with or without THC plus a near maximal dose of thyrotropin-releasing hormone and GH-releasing factor (50 and 10 ng/ml, respectively) or the diluent to evaluate the response of PRL and GH release, respectively. Neither dose of THC altered the release or storage of the two hormones during culture or affected the response to the releasing hormones which is suggestive that there is no direct effect of THC on either GH or PRL release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

d(CH2)5Tyr(Me)-[Orn8]vasotocin, a potent oxytocin antagonist, antagonizes penile erection and yawning induced by oxytocin and apomorphine, but not by ACTH-(1-24).

Intraventricular (i.c.v.) injection of d(CH2)5-Tyr(Me)-[Orn8]vasotocin, a potent oxytocin antagonist, antagonized in a dose-dependent manner (10-100 ng) penile erection and yawning induced by the systemic injection of apomorphine (80 micrograms/kg s.c.) or by the i.c.v. injection of oxytocin (30 ng). In contrast, the oxytocin antagonist, even at the dose of 10 micrograms, did not modify penile erection and yawning induced by the i.c.v. injection of ACTH-(1-24). These results suggest that apomorphine, but not ACTH-(1-24), induce penile erection and yawning by releasing oxytocin in some brain area.

Adrenocorticotropic Hormone↗
PubMed1992

Intrathecal cholecystokinin octapeptide attenuates the antinociception and release of immunoreactive Met-enkephalin induced by intraventricular beta-endorphin in the rat.

The effects of cholecystokinin octapeptide (CCK8s) given intrathecally (i.t.) on antinociception and the release of immunoreactive Met-enkephalin in the spinal perfusate induced by intraventricular (i.vt.) injection of beta-endorphin were studied in anesthetized rats. beta-Endorphin (5 micrograms) given i.vt. inhibited the tail-flick response. The inhibition of the tail-flick response induced by beta-endorphin was blocked dose-dependently by CCK8s (0.1-7 micrograms) given i.t. The antagonistic effect of CCK8s on beta-endorphin-induced inhibition was blocked dose dependently by co-intrathecal injection of proglumide (3 and 10 micrograms), a CCK8s receptor antagonist. beta-Endorphin (5 micrograms) given i.vt. elicited a release of immunoreactive Met-enkephalin in the spinal perfusate. Repeated injections of the same dose of beta-endorphin released about the same amount of the immunoreactive Met-enkephalin in the spinal perfusate. CCK8s at concentrations from 1 x 10(-9) to 1 x 10(-6) M added into the spinal perfusate decreased the release of Met-enkephalin induced by beta-endorphin given i.vt. in a dose-dependent manner. The results suggest that CCK8s may attenuate beta-endorphin-induced inhibition of the tail-flick response by inhibiting the release of Met-enkephalin from the spinal cord.

Animals↗
PubMed1987

Differential responses of hypothalamic cAMP and cGMP to substance P and neurotensin in ovariectomized rats.

Hypothalamic cAMP and cGMP levels in ovariectomized rats were evaluated after intravenous (IV) pulse injection and/or intraventricular (IVT) injection of substance P and/or neurotensin. Intravenous substance P lowered hypothalamic cAMP concentration whereas IVT injection of 2.5 micrograms substance P produced significant increase in cAMP levels. On the other hand, IV administration of neurotensin failed to alter hypothalamic cAMP levels while IVT injection induced significant decrease in cAMP. Intravenous pulse injection of substance P elevated hypothalamic cGMP levels while IVT injection decreased cGMP concentration. Hypothalamic cGMP concentration was not modified by IV administration of neurotensin. However, IVT injection of neurotensin significantly elevated cGMP levels. Since a number of neurotransmitters/neuropeptides exert their action through cyclic nucleotides the present results indicate differential responses of cAMP and cGMP to substance P and neurotensin and implicate a mediatory role for cAMP and cGMP in the neuroendocrine action of substance P and neurotensin.

Animals↗
PubMed1983

Amphetamine-induced hyperphagia and obesity caused by intraventricular or lateral hypothalamic injections in rats.

Overeating and obesity relative to controls was produced by multiple bilateral injections of 0.5 mg of amphetamine in the lateral ventricles of female rats eating a palatable, high fat diet. This behavioral and physiological rebound following the expected period of anorexia was accompanied by long-term depletion of dopamine in the striatum and of norepinephrine in the hypothalamus. This suggested the next experiment in which 50 micrograms of amphetamine were injected repeatedly in the lateral hypothalamus; again a brief period of anorexia was followed by hyperphagia and chronic obesity. This suggests that amphetamine acts in the lateral hypothalamus not only to suppress feeding, but in high doses it may also have local neurotoxic effects that cause an upward shift in body weight maintained by overeating.

Amphetamine↗
PubMed1990

[Effect of intracerebroventricular injection of thyrotropin releasing hormone on electro-acupuncture analgesia and the content of cerebral cAMP in rats].

Experiments were performed on 42 female albino rats weighing from 180-250 gm. The pain threshold (PT) was determined by radiant heat induced tail-flick method. The cAMP contents in various regions of brain were measured by radio-immunoassay. Electro-acupuncture (EA) at bilateral "Zusanli" and "Sanyinjian" in rats significantly elevated PT, increased the content of cAMP in the hypophysis, while decreased that of septal nucleus. No effects were found in the basal PT and the cAMP contents of the hypophysis and septal nuclei after intraventricular injection of TRH. After TRH administered intraventricularly, however, EA didn't elevate PT, but still increased hypophysial cAMP with a decrease in the level of cAMP in the septal nucleus. These results suggest that the cAMP may be related to analgesic effect induced by EA in some brain regions, and TRH injected into cerebral ventricles can antagonize the analgesic effect caused by EA, but this effect seemed to have nn relation to the contents to the contents of cAMP of hypophysis, septal nucleus, caudatum, hypothalamus and thalamus.

Acupuncture Analgesia↗
PubMed1984

Inhibition of spontaneous and opiate-modified nociception by an endogenous neuropeptide with Phe-Met-Arg-Phe-NH2-like immunoreactivity.

In rats the antinociceptive actions of morphine (injected intraventricularly) or of [Met5]enkephalin-Arg6-Phe7 (YGGFMRF) (injected intrathecally) were attenuated by a pretreatment with 10 microliter of artificial cerebral spinal fluid containing 1 microM captopril/1 microM bestatin/2.5 microM Phe-Met-Arg-Phe-NH2 (FMRF-NH2) given 5 min earlier by the same route. A high molecular weight form of FMRF-NH2 purified from bovine brain attenuated the antinociceptive action of YGGFMRF. IgG, prepared from a specific FMRF-NH2 antiserum, elicited a moderate antinociception reversible by naloxone; in contrast, IgG prepared from control serum failed to change tail-flick latencies. In rats receiving morphine every 2 hr and anti-FMRF-NH2 IgG every 4 hr, the antinociceptive action was still evident after eight successive injections; in rats receiving only morphine, the antinociceptive action had disappeared after six successive injections. Morphine (1 microM) added to the perfusion fluid of the subarachnoidal spaces of rat spinal cord releases FMRF-NH2-like peptides in the perfusate.

Animals↗
PubMed1969

Facilitation of brain self-stimulation by central administration of norepinephrine.

Rats with electrodes implanted in the medial forebrain bundle stimulated their own brains at sharply reduced rates after systemic administration of disulfiram or intraventricular administration of diethyldithiocarbamate. Both drugs inhibit dopamine-beta-hydroxylase, the enzyme responsible for the final step in the biosynthesis of norepinephrine. The suppressed behavior was reinstated by intraventricular injections of 1-norepinephrine, but not by injection of its biologically inactive isomer, d-norepinephrine. Intraventricular administration of dopamine and serotonin did not restore self-stimulation. The rewarding effect of medial forebrain bundle stimulation may depend on the availability of norepinephrine as a transmitter, but not on dopamine or serotonin.

Animals↗
PubMedDate not supplied

Anxiolytic- and antidepressant-like effects of group III metabotropic glutamate agonist (1S,3R,4S)-1-aminocyclopentane-1,3,4-tricarboxylic acid (ACPT-I) in rats.

We examined the anxiolytic-like activity of (1S,3R,4S)-1-aminocyclopentane-1,3,4-tricarboxylic acid (ACPT-I) using the Vogel conflict drinking test, while antidepressant-like effects of this compound were evaluated using Porsolt's test. ACPT-I, a selective group III mGlu receptor agonist, produced a dose-dependent anticonflict effect after intrahippocampal injections and antidepressant-like effect in rats after intraventricular injections. These data suggest that selective group III mGlu receptor agonists may become a new class of anxiolytics and/or antidepressants.

Animals↗
PubMed1992

Evidence that cholecystokinin-enhanced retention is mediated by changes in opioid activity in the amygdala.

Mice, partially trained to avoid footshock in a T-maze, showed enhanced retention relative to vehicle-injected mice when treated peripherally with arecoline, D-amphetamine, cholecystokinin octapeptide (CCK-8), epinephrine or naloxone. Both intra-amygdaloid and intraventricular injections of beta-endorphin resulted in amnesia. D-amphetamine and arecoline blocked the amnestic effect of beta-endorphin administered into the amygdala but it required higher doses for CCK-8, epinephrine and naloxone to block the amnestic effect of beta-endorphin. The effects of CCK-8, epinephrine and naloxone showed a differential ability to block amnesia induced by beta-endorphin intraventricularly with epinephrine and naloxone preventing amnesia but CCK-8 not improving retention. This data suggests that the memory enhancement produced by peripherally administered CCK-8 involves the amygdala and that both CCK-8 and epinephrine interact with opioid amnestic mechanisms within the amygdala to alter memory processing.

Amygdala↗
PubMed1981

Enkephalin receptors in the emetic chemoreceptor trigger zone of the dog.

1 The emetic action of Met-enkephalin, morphine and naloxone was studied following their administration into the cerebral ventricles of dogs through chronically implanted cannulae and the effect on the responses of ablating the chemorceptor trigger zone (CTZ) was investigated. The opiate antagonist, naloxone, was used to determine the role of enkephalin receptors in emetic responses.2 Administration of Met-enkephalin (1.0 mug/kg) into the IVth ventricle regularly evoked emesis with an average latency of 35 s. A dose of morphine (2.5 mug/kg) which was five times larger was required for a consistent emetic response when introduced into the lateral cerebral ventricle (i.c.v.) as compared to the dose required by the IVth ventricular route. The latency of emetic responses by the latter route of injection of morphine was shorter. This is in accord with an action of morphine on the emetic CTZ.3 After bilateral ablation of the CTZ, intraventricular injections of Met-enkephalin and morphine failed to produce emesis even when given in doses that were 5 to 10 times the dose which regularly elicited emesis in animals with intact CTZ. The emesis produced in dogs by intraventricular Met-enkephalin and morphine is thus fully accounted for by an action on the CTZ.4 Naloxone (i.c.v.) in doses up to 10.0 mug/kg did not cause emesis. However, higher doses of naloxone elicited dose-dependent emesis in dogs. The 100% emetic dose of naloxone was found to be 160 mug/kg and the latency of emesis was 180 s. Unlike Met-enkephalin and morphine, naloxone continued to elicit emesis in CTZ-ablated animals.5 Pretreatment with intraventricular naloxone (1 to 8 mug/kg) blocked the emetic responses induced by intraventricular Met-enkephalin and morphine but not that to apomorphine. The selective protective action of the opiate antagonist against Met-enkephalin and morphine supports the presence of enkephalin receptors in the emetic CTZ.

Animals↗
PubMed1969

The interactions of noradnamine and imipramine-like antidepressant drugs.

1. The hypothesis of Roberts & Broadley (1965) that noradnamine formation in the brain is responsible for endogenous depression has been investigated in mice.2. Injections of noradnamine given directly into the lateral ventricles caused convulsions and profound hypothermia, but were without effect if given subcutaneously.3. The hypothermia, but not the convulsions, induced by noradnamine was reversed by imipramine-like antidepressant drugs given before or after the injection of noradnamine. The convulsions but not the hypothermia were abolished by phenobarbitone.4. Increasing doses of nortriptyline produced a parallel shift of the hypothermic log dose-response curve for intraventricular injections of noradnamine to the right.5 The minimal effective dose of nortriptyline required to reverse noradnamine hypothermia was the same whether the nortriptyline was injected directly into the lateral ventricle or subcutaneously.6. No evidence was found to substantiate the claim that reserpine hypothermia is mediated by noradnamine formation in the brain.7. Intraventricular, but not intraperitoneal, injection of noradnamine caused a depletion of brain noradrenaline and an increase in brain 5-hydroxytryptamine. These changes did not result from the convulsive activity and were not modified by pretreatment with nortriptyline. No effect on heart noradrenaline levels was recorded.8. Noradrenaline, given subcutaneously, also antagonized the hypothermic response to noradnamine.9. The reversal of noradnamine hypothermia by both noradrenaline given subcutaneously and nortriptyline was blocked by alpha and beta-adrenoceptive receptor blocking agents.10. It is considered that the mode of action of the antagonism of noradnamine hypothermia by imipramine-like antidepressant drugs is a peripheral and not a central mechanism and probably results from a potentiation of the effects of circulating noradrenaline released by noradnamine.

Animals↗
PubMed1984

Intrahypothalamic action of corticotrophin-releasing factor (CRF) to inhibit growth hormone and LH release in the rat.

The effects of intravenous or intraventricular injection of synthetic ovine corticotrophin-releasing factor (oCRF) on plasma levels of anterior pituitary hormones were studied in conscious, ovariectomized (OVX) female rats and compared with the actions of the peptide on dispersed anterior pituitary cells from OVX female rats incubated in the presence of CRF. Third ventricular injection of oCRF in freely moving rats caused a significant increase in plasma levels of ACTH in a dose-related manner with a minimal effective dose of less than 0.5 micrograms (0.1 nmol). The effect was observable at 5 min after injection and persisted for the 60 min duration of the experiment. In contrast, growth hormone levels were significantly depressed within 15 min with a minimal effective intraventricular dose of 0.5 micrograms. The suppression persisted for the duration of the experiment but there was no additional effect of the higher dose of 5 micrograms. Plasma LH levels were also lowered by the highest dose of 5 micrograms (1.0 nmol) of oCRF, with the first significant lowering at 30 min. Lower doses had no effect on plasma LH. Plasma TSH levels were not significantly altered. Control injections of the 0.9% NaCl diluent were without effect on the levels of any of the hormones. Intravenous injection of similar doses of oCRF had no effect on plasma levels of GH or LH. The ACTH-releasing action of the oCRF preparation was confirmed by in vitro incubation of the peptide with dispersed anterior pituitary cells for 2 h. A dose-related release of ACTH occurred in doses ranging from 0.1-10 nM, but there were no effects on the release of the other anterior pituitary hormones. The results suggest that oCRF may act within the hypothalamus to suppress the release of GH and to a lesser extent LH. The stimulation of ACTH release following intraventricular CRF is presumably related to its uptake by portal blood vessels with delivery to the pituitary and stimulation of the corticotrophs.

Adrenocorticotropic Hormone↗
PubMed1985

Effect of various drugs producing convulsive seizures on rat brain glycerolipid metabolism.

Convulsive seizures were elicited in the rat by the injection of several different drugs (pyridoxal phosphate, bicuculline, penicillin and ouabain). Glycerolipid metabolism was studied after the intraventricular injection of [2-3H]glycerol, which was incorporated into rat brain glycerides. The percentage of total lipid label found in each lipid class (phosphatidylethanolamine, PE; phosphatidylcholine, PC; phosphatidylserine, PS; phosphatidic acid, PA; phosphatidylinositol, PI; diacylglycerol (+ monoacylglycerol), DG and triacylglycerol, TG) depended on the time elapsed from the injection of the labeled precursor. The percent of total lipid radioactivity as PE and PC increased with time (3-60 min), whereas the opposite was true for the radioactivity of DG and PA. The radioactivity of other lipid classes did not appreciably vary between 3 and 60 min from the injection of the labeled glycerol. The intraventricular administration of pyridoxal phosphate together with labeled glycerol decreased the percent of lipid radioactivity as PE and increased that as DG. This 'lipid effect' was detected also after the administration of other convulsants, such as ouabain and penicillin. The intraperitoneal administration of bicuculline affected lipid metabolism in cerebellum.

Animals↗
PubMed1989

Hypothalamic action of cachectin to alter pituitary hormone release.

Cachectin (tumor necrosis factor, TNF) is a macrophage hormone which is released during infection and after injection of bacterial lipopolysaccharides. We have already demonstrated that the peptide has direct action on the pituitary to alter pituitary hormone release in vitro. To evaluate its action in vivo, we injected it into the third ventricle (3V) of conscious, male rats and measured its effect on various anterior pituitary hormones. The peptide produced an elevation in rectal temperature measurable on first measurement at 1 hour postinjection which was maintained for 3 hours. The maximal increase in body temperature was 1-1.5 degrees C and maximal effect was obtained by a dose as low as 1 ng (0.3 pmol) of the peptide. Preinjection of indomethacin into the 3V 1 hour prior to injection of TNF completely blocked the effect on body temperature without producing an alteration in rectal temperature itself which suggests that the elevation in body temperature may be mediated by prostaglandins. Following the intraventricular injection of various doses of TNF, there was no significant effect on plasma adrenocorticotropin (ACTH) except with the highest, 100 ng dose tested, which evoked a small but significant increase in plasma ACTH with a delay of 1 to 2 hours. Thus, the dose necessary to release ACTH was much higher than that required to elevate body temperature. The effect was no longer significant in indomethacin-pretreated animals suggesting a role for prostaglandins in the effect. This highest dose of intraventricularly administered TNF also produced a relatively modest, but significant, delayed increase in plasma GH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Antidiuresis produced by injection of renin into the third cerebral ventricle of the dog.

The purpose of this study was to determine whether centrally administered renin stimulated vasopressin secretion. Vasopressin was not measured directly, but, instead, changes in urinary water excretion in anesthesized dogs undergoing a water excretion in anesthetized dogs undergoing a water diuresis were used as an index of changes in vasopressin secretion. Intraventricular injection of hog renin in a dose of 0.1 Goldblatt unit produced a marked decrease in urine flow which was associated with a decrease in free water clearance and an increase in urinary osmolatiy with no change in osmolar clearance. Sodium excretion increased significantly but there was no change in potassium excretion. These effects, which closely resemble those resulting from an increase in vasopressin secretion, were prevented by hypophysectomy. The antidiuretic effect clearly resulted from an action of renin in the central nervous system since renin had no effect on urine flow or osmolality when administered intravenously. Intraventricular administration of saralasin acetate, a specific antagonist of angiotensin II, completely blocked the effects of intraventricular renin indicating that these effects were mediated via the formation of angiotensin II. The data therefore indicate that there is an interaction between injected renin, brain angiotensinogen, and converting enzyme resulting in the formation of angiotensin II which stimulates the secretion of vasopressin. Additional studies are required to determine whether the brain renin-angiotensin system plays a physiological role in the regulation of a vasopressin secretion.

Animals↗