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PubMed1990

Neostigmine-induced hyperglycemia is mediated by central muscarinic receptor in fed rats.

We previously reported that neostigmine injected into the third cerebral ventricle stimulated adrenal secretion of epinephrine, secretion of glucagon from the pancreas, and direct neural innervation of the liver, resulting in hepatic venous plasma hyperglycemia in anesthetized fed rats. However, receptor type of these 3 mechanisms is not known. Therefore, we examined the effects of intraventricularly injected cholinergic or adrenergic antagonists on neostigmine-induced catecholamines in intact rats, glucagon secretion which is mediated by direct neural innervation of pancreas in bilateral adrenalectomized (ADX) rats, and hepatic venous hyperglycemia which is mediated by direct neural innervation of liver in ADX rats receiving constant infusion of somatostatin from femoral vein. Atropine injected into the third cerebral ventricle suppressed epinephrine secretion and dose-dependently inhibited hepatic venous hyperglycemia induced by neostigmine in intact rats. The neostigmine-induced glucagon secretion which occurs in ADX rats was suppressed by atropine. Atropine also prevented the neostigmine-induced hyperglycemia in ADX rats receiving constant somatostatin infusion through femoral vein (ADX-Somato rats). On the other hand, phentolamine, propranolol and hexamethonium showed no significant inhibitory effect on neostigmine-induced hyperglycemia, epinephrine and glucagon secretion in intact rats, glucagon secretion in ADX rats, or hyperglycemia in ADX-Somato rats. These results suggest that neostigmine-induced epinephrine and glucagon secretion and increased hepatic glucose output stimulated by direct neural innervation to liver is mediated by central muscarinic receptor in fed rats.

Adrenergic Fibers↗
PubMed1984

Intraventricular 6-hydroxydopamine increases the adrenal cortex mitotic activity in rats.

Effects of intraventricular injections of 6-hydroxydopamine (6-OHDA) on adrenocortical cell proliferation in rats have been investigated by means of the colchicine metaphase-arrest technique. In the group of animals receiving 6-OHDA alone, an increase of mean mitotic activity rate (MMAR) was observed at 96 h and 144 h after injection. This rise of MMAR was completely inhibited by pretreatment of animals with desmethylimipramine (DMI) - a blocker of norepinephrine uptake. It is concluded that enhancement of ACTH secretion is responsible for the above mentioned increase of mitotic activity after 6-OHDA administration. This phenomenon is related to abolition of the inhibitory noradrenergic effect on ACTH secretion by 6-OHDA treatment. Additionally, the results suggest little or no involvement of dopaminergic neurons in early changes of ACTH secretion after intraventricular 6-OHDA.

Adrenal Cortex↗
PubMed1989

Role of neuromedin B in the control of the release of thyrotropin in the rat.

Neuromedin B (NB), a bombesin-like peptide, was first isolated from porcine spinal cord and subsequently found in the central nervous systems of rat, cat, and human. Immunocytochemical studies have shown that NB is present in hypothalamus and various other regions of the brain and in thyrotrophs of the anterior pituitary of the rat. The possible physiological role of NB in the hypothalamic-pituitary axis is not known. Therefore, we studied the in vivo effect of this peptide on the plasma levels of thyrotropin (TSH) after administering NB to conscious freely moving adult male rats. When injected i.v., only the highest dose of NB (50 micrograms, 44.2 nmol) significantly lowered plasma TSH levels relative to levels in saline controls. When injected intraventricularly, NB doses of 0.5 and 5 micrograms (0.44 and 4.42 nmol, respectively) lowered plasma TSH levels with a 15-min latency period. Responsiveness of the pituitary to TSH-releasing hormone (TRH) was tested after the effective dose of NB was administered i.v. The increase in plasma TSH levels after the i.v. injection of 1 microgram of TRH was not altered by NB. NB at 10(-9) to 10(-7) M also reduced TSH release from hemipituitaries incubated in vitro without decreasing the response to TRH. Consequently, NB appears to have a direct inhibitory effect on TSH release from thyrotrophs. Since the response to TRH was not depressed, NB appears to act on a separate NB thyrotroph receptor that suppresses TSH release by a TRH-independent mechanism. After antiserum directed against NB was injected into the third ventricle, there was a highly significant elevation of the plasma level of TSH, beginning at 4 hr and increasing at 6 hr, relative to initial levels and levels in normal rabbit serum-injected controls. These results indicate that NB has a tonic suppressive effect on TSH release and is a physiologically significant TSH-release-inhibitory factor.

Animals↗
PubMed1991

Effect of nerve growth factor on the lesioned septohippocampal cholinergic system of aged rats.

Nerve growth factor (NGF) was injected intraventricularly into aged (24 months) rats with unilateral lesions of the lateral fimbria. The activity of choline acetyltransferase (ChAT) was determined in the septum and hippocampus from the normal unlesioned rats, lesioned and cytochrome c-treated rats (controls), and lesioned and NGF-treated rats at different times after the lesion. NGF-injection for 15 days after the lesion resulted in an increase of the ChAT activity in both the contralateral hippocampus and the entire septum, to about 130% of that in the normal animals, but resulted in a slight increase in the ipsilateral lesioned hippocampus, when compared to the activity in the ipsilateral side of the cytochrome c-treated controls. NGF-injection for 30 days after the lesion resulted in a 48% increase of the ChAT activity in the ipsilateral hippocampus as compared to cytochrome c-treated controls, but failed to result in a significant increase in the contralateral hippocampus. These findings indicate that atrophic cholinergic neurons in aged animals are similarly responsive to NGF treatment, like these in the young animals. Moreover, these findings suggest that the responses of basal forebrain cholinergic neurons to NGF treatment varies with time after the lesion and imply that the NGF administration can promote the collateral sprouting from spared cholinergic fibers after the lesion in the aged forebrain.

Acetylcholine↗
PubMed1982

Food and water intake following injection of glucose into the lateral ventricle of the brain of broiler type chicks.

The effects of glucose and 2-deoxy-D-glucose (2-DG) on food intake and water consumption were investigated in broiler chicks. Artificial cerebrospinal fluid (aCSF) containing either glucose or the glucose antimetabolite 2-DG was injected into the lateral brain ventricles of fasted and satiated chicks. The satiated chicks received 10 microliters of CSF containing either 5 or 10% 2-DG, whereas those fasted for 24 hr received CSF with 10, 20, or 30% glucose (dextrose) in 10 microliters volumes. Chicks were maintained in a thermoneutral environment with continuous lighting. Intraventricular injections of 5 or 10% 2-DG had no significant effect on food intake or water consumption in the fully-fed chicks. In the 24-hr fasted chicks, 10% glucose had no effect on food or water intake. The decrease in food intake observed following the injection of 20 and 30% glucose appeared to be an osmotic effect. Based on results obtained, it was suggested that selection for increased growth rate, such as in broilers, may have resulted in a decrease in glucoreceptor sensitivity. Such a decrease in sensitivity could lead to an increased food intake as occurs in broilers.

Animals↗
PubMed1982

Convulsant action of intracerebroventricularly administered l-kynurenine sulphate, quinolinic acid and other derivatives of succinic acid, and effects of amino acids: structure-activity relationships.

Succinic acid, and the derivatives which have been tested, i.e. phthalic, l-glutamic, l-aspartic, citric and laevulinic acids, in doses of 5,2,5,20,20 and 50 micrograms, respectively, as well as l-kynurenine sulphate and quinolinic acid, injected into the brain ventricles in mice, induced clonic seizures. When administered intraperitoneally or orally they antagonize strychnine-induced seizures. The convulsant effect of l-kynurenine sulphate was observed only when the pH of the solution was 4.0 or lower, while the actions of the other drugs tested were not dependent upon pH. Control intraventricular injections of 5 microliters of 0.06 N sulphuric acid (equivalent to 16.7 micrograms of SO4(2-), the same dose as was injected when a convulsant dose of 50 micrograms of l-kynurenine was administered) induced seizures in 25% of the mice. It is suggested that the convulsant effect of quinolinic acid and l-kynurenine sulphate is related to a moiety of succinic acid (O = C-C-C-C = O). The effect of l-kynurenine sulphate comprises the action of the cation of kynurenine and that of the anion of sulphuric acid. Reduction of the convulsant effect of l-kynurenine sulphate by alpha-amino acids and taurine is presumably related to a "shielding" of both amino- and carbonyl groups of 1-kynurenine. There is no evidence that l-kynurenine sulphate, in small doses, shares the central effects of the inhibitory amino acids.

Amino Acids↗
PubMed1995

Activation of central GABAA-but not of GABAB-receptors rapidly reduces pituitary LH release and GnRH gene expression in the preoptic/anterior hypothalamic area of ovariectomized rats.

gamma-Aminobutyric acid (GABA) exerts an inhibitory action on gonadotropin-releasing hormone (GnRH) release from the hypothalamus. In vivo, this inhibitory action appears to be mediated via the GABAA receptor since in ovariectomized (ovx) rats and sheep direct application of muscimol (MUS), a GABAA agonist, into the preoptic area (POA), the site were the GnRH cell bodies are located, caused an immediate reduction of LH release. This effect may be the result of an inhibition of GnRH release but also GnRH biosynthesis may be affected. Using competitive reverse transcription-polymerase chain reaction (RT-PCR) we now addressed the question, whether an acute inhibition of the GnRH pulse generator in ovx rats by GABA involves reduction of GnRH biosynthesis as determined by GnRH mRNA levels in micropunches of the POA. To activate either the GABAA or GABAB receptor, we injected intraventricularly (icv) MUS or baclofen (BAC). Intracerebroventricular injection of 10 nmol MUS caused a rapid and lasting inhibition of LH release from about 7.5 ng/ml (pretreatment value) to approximately 1.5 ng/ml. Neither application of BAC or saline (control injections) affected LH secretion. Two hours after icv injections, rats were decapitated and GnRH mRNA levels were determined. MUS induced a pronounced decrease of GnRH levels in the POA (control rats: 2.26 pg GnRH mRNA; MUS-treated rats: 0.85 pg, n = 10/group). BAC was without any effect on GnRH mRNA levels. Thus, we confirm the inhibitory action of GABA on LH release in vivo which is exerted via the A-subtype of the receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Modulation of luteinizing hormone(LH) release by clonidine and opioid peptides in castrated male rats.

The effect of clonidine, a central alpha-adrenergic agonist, on the suppression of LH release induced by beta-endorphin or FK33-824, an endogenous opioid peptide or its synthetic analog, was investigated in castrated male rats, with or without pretreatment with reserpine. Pulsatile LH secretion was inhibited by intravenous injection of FK33-824 (400 micrograms/kg), or intraventricular injection of beta-endorphin (5 micrograms). Without pretreatment with reserpine, intraperitoneal administration of clonidine (1 mg/kg) failed to reverse the inhibition of LH release induced by these peptides. However, with pretreatment with reserpine (10 mg/kg), clonidine abolished the inhibitory effect on LH secretion induced by these peptides in castrated male rats. These data indicate that, unlike the results in ovariectomized, steroid-primed rats, pretreatment with reserpine allows the alpha-adrenergic system to act more peripherally than the opioid neuronal system in a neuronal network-regulating LH release in castrated male rats.

Animals↗
PubMed1985

Further studies on vasopressin-induced pressor responses to kainic acid injected into the nucleus tractus solitarii of the rat.

Kainic acid, an analogue of L-glutamate, was microinjected into the nucleus tractus solitarii of cordotomized rats. Kainic acid (30 ng) injected bilaterally into the nucleus elicited hypertension. The pressor response to kainic acid was restricted to sites in the intermediate one-third of the nucleus tractus solitarii. Plasma vasopressin levels were markedly increased during the kainic acid-induced pressor response. Intravenous injection of atropine sulphate or mecamylamine, or intraventricular injection of captopril did not affect the pressor response. It is concluded that in cordotomized rats the pressor response to kainic acid injected into the nucleus tractus solitarii is mainly mediated via increased release of vasopressin. It seems unlikely that the central cholinergic and angiotensin mechanisms are mainly responsible for the response to kainic acid.

Animals↗
PubMed1994

Participation of the ascending serotonergic system in the stimulation of atrial natriuretic peptide release.

Results obtained in our laboratories have provided evidence for the participation of the hypothalamic atrial natriuretic peptide (ANP) neuronal system in the regulation of water and electrolyte homeostasis. The anterior ventral third ventricular (AV3V) region, a site of the perikarya of the ANP neurons, receives important afferent input from ascending serotoninergic axons. We hypothesized that the ascending serotoninergic tract might be involved in control of the liberation of ANP. Therefore, electrolytic lesions were produced in the mesencephalic dorsal raphé nucleus (DRN), the site of perikarya of serotonin (5-HT) neurons whose axons project to the AV3V region. Rats with sham lesions constituted the control group. In a second group of animals, the serotoninergic system was depleted of 5-HT by lateral ventricular administration of p-chlorophenylalanine (PCPA), an amino acid that causes depletion of 5-HT from the serotoninergic neurons. Control animals were injected with an equal amount of isotonic saline. The DRN lesions induced an increase of water intake and urine output beginning on the first day that lasted for 1 week after lesions were produced. There was a concomitant sodium retention that lasted for the same period of time. When water-loaded, DRN-lesioned and PCPA-injected animals showed diminished excretion of sodium, accompanied by a decrease in basal plasma ANP concentrations, and blockade of the increase in plasma ANP, which followed blood volume expansion by intraatrial injection of hypertonic saline. The results are interpreted to mean that ascending stimulatory serotoninergic input into the ANP neuronal system in the AV3V region produces a tonic stimulation of ANP release, which augments sodium excretion and inhibits water intake. Therefore, in the absence of this serotoninergic input following destruction of the serotoninergic neurons by DRN lesions or intraventricular injection of PCPA, an antinatriuretic effect is obtained that is associated with increased drinking, either because of sodium retention per se or removal of ANP-induced inhibition of release of the dipsogenic peptide, angiotensin II. The serotoninergic afferents also play an essential, stimulatory role in volume expansion-induced release of ANP and the ensuing natriuresis.

Animals↗
PubMed1981

Effects of beta-endorphin and morphine on the sleep-wakefulness behavior of cats.

The effects of beta-endorphin and of morphine SO4 (0.5 microgram and 2.0 microgram, respectively, injected intraventricularly) upon the sleep-wakefulness behavior of cats were examined. Both agents produced insomnia. Deep slow wave sleep was sharply inhibited, and rapid eye movement (REM) sleep was entirely suppressed. Light slow wave sleep, occurring in brief, isolated episodes, became the most abundant stage of sleep. The nuchal electromyogram was markedly increased after both agents. Naloxone (100 microgram/kg), injected subcutaneously 30 min before beta-endorphin or morphine SO4, entirely reversed these agents' effects on the two stages of slow wave sleep, and antagonized the exaggerated electromyogram. But naloxone did not counteract the REM-suppressant effect of either beta-endorphin or morphine SO4. Total sleep time reverted towards control values after naloxone pretreatment, but not entirely; the difference may be due to the persistent deficit of REM sleep. The data may indicate an involvement of an inner opioid in the regulation of sleep and wakefulness in the cat, and may point to a role for more than one endorphin receptor in the effects of opioids on the states of vigilance in cats.

Animals↗
PubMed1980

Stimulation of LH and FSH secretion following intraventicular injection of cysteic acid but not taurine.

Taurine and related neurally active metabolites, were tested for their ability to influence basal secretion of luteinizing hormone (LH) and follicle stimulating hormone (FSH). The animal model used was the unanesthetized, unrestrained adult rat with an indwelling catheter in the jugular vein and a cannula implanted in the right lateral cerebroventricle or anterior pituitary. The proposed inhibitory neurotransmitter traurine, and its metabolic precursor, hypotaurine, did not affect the secretion of LH or FSH following infusion of 0.2 or 2.0 mumol intraventricularly or into the pituitary. In contrast, intraventricular injection of cysteic acid, a neurally excitant amino acid, in doses of 2.0 and 0.2 mumol promoted pituitary secretion of LH in both male and female rats. FSH secretion was also increased slightly by cysteic acid (2.0 mumol). These studies provide additional evidence that excitatory amino acids have a stimulatory role in the release of pituitary gonadotropins.

Amino Acids, Sulfur↗
PubMed1982

The Gordon phenomenon induced by the eosinophil cationic protein and eosinophil protein X.

Cerebellar Purkinje cell degeneration after intracerebral injection of eosinophil granulocytes or extracts thereof is known as the Gordon phenomenon. The reaction is said to be highly selective. An eosinophil-derived neurotoxin (EDN) has recently been reported to induce the Gordon phenomenon. However, we report here that two eosinophil-derived proteins, eosinophil cationic protein (ECP) and eosinophil protein X (EPX), may induce the Gordon phenomenon after intraventricular injection. The potency of ECP is far greater than that of EPX and the latter is possibly identical to EDN. The Fink-Heimer staining for degenerating nerve fibers and boutons, however, indicated that the selectivity of the Gordon phenomenon is not as specific as was previously thought, since this method revealed degeneration of all brain areas in proximity to the ventricular system.

Animals↗
PubMed1998

Neurotoxic potential of gadodiamide after injection into the lateral cerebral ventricle of rats.

PURPOSE: Results of a previous report showed that, if administered by intraventricular injection to access tissue normally protected by the blood-brain barrier, gadopentetate dimeglumine produced acute excitation, persistent ataxia, and widespread brain lesions in rats at 5-micromol/g brain but not at 3.8-micromol/g brain. The present study using gadodiamide was undertaken to see whether the effects were agent-specific. METHODS: Rats, surgically prepared with a lateral ventricular cannula, were administered a slow injection at 2 microL/min of gadodiamide into the lateral ventricle, and behavioral and neuropathologic changes were noted. RESULTS: Both gadodiamide and gadopentetate dimeglumine produced focal and generalized myoclonus over several hours. Gadodiamide did not produce the medium-term tremor or persistent ataxia seen after treatment with gadopentetate dimeglumine. Neuropathologic changes developed over 1 to 3 days and took three distinct forms: vacuolated thalamic lesions closely resembling those produced by gadopentetate dimeglumine; small but similar vacuolated symmetrical caudate lesions not produced by gadopentetate dimeglumine; and severe swelling and astrocytic hypertrophy and hyperplasia in the cerebellar vermis, again not produced by gadopentetate dimeglumine. Unlike gadopentetate dimeglumine, gadodiamide produced no spinal cord lesions. The cerebellar changes were seen at 1.25-micromol/g brain and above, behavioral changes at 2.5-micromol/g brain and above, and thalamic and caudate lesions at 10-micromol/g brain, the maximal dose used. Markedly reducing the rate of injecting the same volume over 28 hours prevented the acute excitation but did not reduce the severity of the morphologic effects. CONCLUSION: The acute excitatory effects of high intraventricular doses of gadopentetate dimeglumine and gadodiamide are similar and appear to be attributable to local action at the infusion site, but differences exist between the two agents in the character and topography of the distant morphologic changes. The cerebellum was the brain area most sensitive to gadodiamide in this experimental model. It is unlikely that gadodiamide would gain access to the brain at these tissue doses when used intravenously for conventional clinical imaging, but our experimental model suggested that it had some unexpectedly specific neuropathologic potential.

Animals↗
PubMed1987

Involvement of central alpha-pressor and beta-depressor adrenoceptors in the cardiovascular response to intracerebroventricular catecholamines in the rat.

Microinjections of catecholamines were performed into the lateral ventricle of anesthetized and unanesthetized rats and the blood pressure effects recorded prior to or after the administration of pharmacological antagonists. Injections of 20-100 micrograms normetanephrine (alpha-agonist) produced only pressor responses in both groups of animals. Injections of 10-20 micrograms of norepinephrine (preferentially an alpha-agonist) produced mainly pressor in awake and only depressor responses in anesthetized animals, whereas injections of 10-20 micrograms of epinephrine (preferentially a beta-agonist) produced only depressor responses in both groups of animals. Intracerebroventricular pretreatment with the beta-blocker propranolol (40-100 micrograms) blocked the depressor responses to the catecholamines or even reverted them into clear pressor response. Pretreatment with the alpha-blocker phentolamine (100 micrograms) reduced the pressor effects induced by the intraventricular injection of catecholamines. The existence of central alpha-pressor and beta-depressor mechanisms mediating the blood pressure responses to the intracerebroventricular administration of catecholamines is proposed.

Animals↗
PubMed1985

The effects of histamine and some related compounds on conditioned avoidance response in rats.

When histamine (Hi) and other agonists were applied intraventricularly, Hi caused a dose-dependent inhibition of the avoidance response in rats; its ED50 was 3.60 micrograms. 1-methylHi, 1-methylimidazole acetic acid and imidazole acetic acid which are major metabolites of Hi produced no inhibitory effect even at 50 micrograms. H1-agonists (2-methylHi and 2-thiazolylethylamine) also depressed the avoidance response; their dose-response lines run parallel to that of Hi. The depressant effects of H2-agonists (4-methylHi and dimaprit) were relatively weak; their dose-response lines were not parallel to that of Hi. When antagonists were pretreated intravenously, Hi action was clearly antagonized by diphehydramine and pyrilamine, but not by cimetidine or ranitidine. Intraventricular injection of Hi mixed with cimetidine or ranitidine did not change the effect induced by Hi alone. The avoidance response was not affected by noradrenaline, dopamine or 5-hydroxytryptamine. Although acetylcholine (ACh) suppressed the avoidance response dose-dependently, its effect was much weaker than that of Hi. Pretreatment with cholinergic blocking drugs (atropine and scopolamine) antagonized ACh action but not Hi action. From these results, it is assumed that the inhibitory effect of Hi on the avoidance response is preferentially linked to the H1-receptor. After intraventricular application of 3H-Hi, the highest radioactivity was determined in the hypothalamus.

Acetylcholine↗
PubMedDate not supplied

Gamma aminobutyric acid effect on acetylcholine level and metabolism in rat cerebral cortex.

Gamma aminobutyric acid injected into the lateral brain ventricle of white rats in doses of 0.6, 0.8 and 1.6 mg raised the level of acetylcholine and in doses of 0.2, 0.4, 0.6, 0.8 and 1.6 mg increased acetylcholine synthesis. The effects were greatest 15 minutes after injection. Gamma aminobutyric acid injected intraventricularly in doses of 0.6 mg increased the activity of choline acetyltransferase but had no effect on the activity of choline esterase.

Acetylcholine↗
PubMed1996

Neuroendocrine and cardiovascular effects of serotonin: selective role of brain angiotensin on vasopressin.

Central serotonin (5-HT) and angiotensin (ANG II) stimulate arginine vasopressin (AVP), oxytocin (OT), and adrenocorticotropin (ACTH) secretion and increase blood pressure. Studies were conducted in conscious rats to determine whether neuroendocrine activation by 5-HT requires a brain angiotensinergic intermediate pathway. In the first study, ANG II formation was inhibited by the angiotensin-converting enzyme inhibitor enalapril before injection of the 5-HT releaser/uptake inhibitor d-fenfluramine. Fenfluramine (2 mg/kg ip) stimulated AVP, OT, corticosterone, and prolactin (PRL) secretion (P<0.01). Enalapril (60 mg/l in drinking water for 4 days and 10 mg/kg ip 2 h before the rats were killed) inhibited only the AVP response (P<0.01) to d-fenfluramine. In the second study, the effect of intracerebroventricular injection of the 5-HT2A/2C antagonist LY-53857 (10 microgram), or the ANG II AT1 antagonist DuP-753 (10 microgram), on intracerebroventricular 5-HT (10 microgram)-stimulated AVP, OT, ACTH, PRL, renin secretion, mean arterial pressure (MAP) and heart rate (HR) was tested. LY-53857 inhibited the AVP, OT, and ACTH responses to 5-HT (P<0.01), whereas DuP-753 inhibited only the AVP response (P<0.01). Intraventricular injection of 5-HT increased MAP and decreased HR. The MAP response was not affected by LY-53857 or DuP-753, and at no time did MAP decline below starting levels. The decreased HR was inhibited by LY-53857 but not by DuP-753. These results demonstrate that 5-HT-induced AVP secretion is mediated selectively via brain angiotensinergic mechanisms by way of the AT1 receptor.

Adrenocorticotropic Hormone↗