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At least 919 records · Page 51Linked to original sources
PubMed1993

Reserpine causes differential changes in the mRNA levels of chromogranin B, secretogranin II, carboxypeptidase H, alpha-amidating monooxygenase, the vesicular amine transporter and of synaptin/synaptophysin in rat brain.

Brains of rats treated with a high dose of reserpine were analyzed by in situ hybridization. The mRNA levels of several components of large dense core and small synaptic vesicles were determined. After drug treatment the secretogranin II message was elevated in the parvocellular neurons of the paraventricular nucleus, in the zona incerta, dorsal raphe, locus coeruleus and in the nucleus tractus solitarius. The levels of chromogranin B mRNA were increased in the dorsal raphe and in the substantia nigra compacta. In control animals messages for synaptin/synaptophysin could be found in most of the nuclei investigated, that of the vesicular amine transporter was only detectable in substantia nigra compacta, the dorsal raphe and the locus coeruleus whereas those of carboxypeptidase H and the alpha-amidating monooxygenase could only be determined in the paraventricular nucleus. All these messages were not changed after reserpine. We conclude that the chromogranin B/secretogranin II messages are regulated concomitantly with various neuropeptides. They represent useful general markers to identify stimulated neurons. Our results are consistent with the concept that stimulation of neurons leads to an increased synthesis of secretory peptides and consequently to large dense core vesicles filled with higher quanta of peptides.

Animals↗
PubMedDate not supplied

Quantitative changes of CRF-like immunoreactivity in eels treated with reserpine and cortisol.

Immunocytochemical techniques were applied to brain and pituitary sections of European eels after experimental manipulation of the pituitary-interrenal activity. A corticotropin-releasing factor (CRF) antiserum allowed the identification of a CRF-like peptide in the preoptic nucleus (PON) and rostral and caudal neurohypophysis (NH). CRF-immunoreactivity (ir) was not affected in solvent-injected eels compared to noninjected eels. Reserpine induced a stimulation of the pituitary interrenal axis, decreased ir-CRF in the rostral NH, but did not affect hypothalamic ir-CRF. Cortisol reduced the immunostaining of hypothalamic CRF-ir perikarya and perikarya cross-sectional area. In the rostral NH, CRF-ir fibers decreased in number and almost disappeared in long-term treated eels. The immunostaining of ACTH cells with ACTH antiserum was greatly reduced. These data suggest that cortisol induces a marked reduction in the activity of the CRF-corticotrop axis. The intensity of the ir-CRF staining observed in the caudal NH, close to the intermediate lobe (IL) was not significantly affected in reserpine-treated eels, and only slightly reduced in long-term cortisol-treated eels. The intensity of ir-CRF staining in the caudal NH did not correlate with melanocorticotropic activity or plasma cortisol level. These data suggest that immunoreactive CRF fibers in the rostral and caudal NH are differently regulated.

Anguilla↗
PubMed1991

Effects of reserpine and L-cysteine and glutathione depletion on 2-bromoethylamine hydrobromide-induced tubular necrosis in Swiss ICR mice.

Female Swiss ICR mice were injected ip with 100 or 300 mg 2-bromoethylamine hydrobromide (BEA)/kg body weight. Male Swiss ICR mice were subjected to water deprivation, or treated with 5% dextrose in water, dimethylsulphoxide, piperonyl butoxide, SKF-525A, sodium phenobarbital, beta-naphthoflavone, probenecid, reserpine, diethyl maleate, buthionine sulphoximine or L-cysteine. Urine collected sequentially from male Swiss ICR mice given 300 mg BEA/kg body weight was analysed for glucose, protein, pH and specific gravity. Female mice were less sensitive to BEA than were male mice. Diuresis, antidiuresis, treatment with cytochrome P-450 inducers and inhibitors, and the antioxidant dimethyl-sulphoxide had no effect on the incidence or severity of tubular necrosis (TN) induced by BEA. Probenecid and L-cysteine decreased the severity, but they had no effect on the incidence of TN. Glutathione depletion by diethyl maleate and inhibition of glutathione synthesis by buthionine sulphoximine decreased the dose of BEA necessary to cause TN; buthionine sulphoximine was more effective than diethyl maleate. Reserpine decreased both the incidence and severity of TN. Glycosuria, aciduria and decreased urinary specific gravity occurred before morphological changes were seen under the microscope, indicating that the functional changes precede the morphological changes. These data indicate that glutathione is important in protecting against BEA-induced TN, that BEA or a metabolite is concentrated in the tubule epithelium by way of anion transport, and that vasoconstriction contributes to the development of BEA-induced TN.

Animals↗
PubMed1989

Reserpine does not prevent 3,4-methylenedioxymethamphetamine-induced neurotoxicity in the rat.

3,4-Methylenedioxymethamphetamine (MDMA; 'Ecstasy') is a known neurotoxin to 5-hydroxytryptamine (5-HT) nerve terminals. Recent studies have suggested that endogenous dopamine (DA) and/or 5-HT may mediate the MDMA-induced neurotoxicity. The central monoamine stores of rats were significantly decreased with reserpine (5 mg/kg) prior to toxic injections of MDMA. Rats given MDMA (30 mg/kg) displayed significant decreases in the density of 5-HT nerve terminals labeled by [3H]paroxetine both with (51 +/- 8%) and without (43 +/- 20%) reserpine pre-treatment. These data suggest that the degeneration of 5-HT nerve terminals following MDMA is independent of the presence of endogenous stores of DA or 5-HT.

3,4-Methylenedioxyamphetamine↗
PubMed1991

Neuropeptide Y mRNA regulation in rat sympathetic ganglia: effect of reserpine.

To study the mechanism underlying trans-synaptic neuropeptide regulation, mRNA levels of neuropeptide Y were examined in the rat stellate and superior cervical ganglia using a specific neuropeptide Y cRNA probe. Basal levels of neuropeptide Y mRNA were detectable in total RNA extracts from single ganglia. Reserpine induced a large rise in ganglion neuropeptide Y mRNA. Decentralization prevented the increase of neuropeptide Y mRNA content in the ganglia. This suggests that the reserpine induced increase in neuropeptide Y mRNA was dependent on transsynaptic stimulation. Consequently, neuropeptide mRNA levels in sympathetic ganglia may be under the control of preganglionic impulse flow.

Autonomic Fibers, Preganglionic↗
PubMed1996

Reserpine potentiates NMDA-induced c-fos mRNA expression in the mouse brain.

The systemic administration of a non-convulsant dose of N-methyl-D-aspartate (NMDA; 75 mg/kg i.p.), which was associated with motor activation, induced a regional c-fos mRNA expression in the mouse brain. The NMDA-induced c-fos mRNA expression was predominant in the dentate gyrus and in the medial mammillary nucleus and less pronounced in other hippocampal areas, cortical areas, bed nucleus of the stria terminalis and posterior amygdaloid nuclei. It is suggested that the hippocampus and/or the extended amygdala might be involved in the previously hypothesized dopamine-independent NMDA-mediated motor activation mechanism. No increase in c-fos mRNA expression was observed 21 h after reserpine treatment (5 mg/kg s.c.). However, reserpinization induced a significant potentiation of the NMDA-induced c-fos mRNA expression. These results show the existence of a strong and selective amine-dependent modulation of NMDA neurotransmission in the brain.

Animals↗
PubMed1983

Influence of chlorpromazine, reserpine and lithium carbonate upon the induction of the tyrosine aminotransferase (TAT) in the rat liver.

The influence of chlorpromazine, reserpine, and lithium carbonate upon the induction of the tyrosine aminotransferase (TAT) in the rat liver of normal and adrenalectomized animals as well as in the presence of nicotinamide, DL-tryptophan, and L-methionine was studied. In normal animals, the TAT is significantly induced only by chlorpromazine, not, however, by reserpine and lithium carbonate. Especially the effect of chlorpromazine upon the induction is enhanced by methionine or by a combination of tryptophan and methionine. An additional administration of prednisolone slightly inhibits the induction. In adrenalectomized animals, the psychotropic substances used are very toxic. By a combination with tryptophan, a minimal induction can be observed. Prednisolone causes a complete restoration of the induction. In combination with the hormone, lithium carbonate produces the highest values. This effect can be intensified by a simultaneous administration of tryptophan.

Adrenalectomy↗
PubMed1986

Effects of two tranquilizers, reserpine and chlorpromazine, on neurosecretory cells and the ovary of the fiddler crab, Uca pugilator.

Reserpine produced alterations in neurosecretory cell types I and II in the eyestalk, brain, and thoracic ganglion, most notably a decrease in the amount of stored neurosecretory material. The ovarian index decreased, but the oocyte area increased in the reserpinized crabs. Chlorpromazine did not produce any significant changes in the structure of cell types I and II. In spite of having a normal area, the oocytes in the chlorpromazine injected crabs were devoid of yolk. Neurosecretory cell type III showed no change.

Animals↗
PubMed1989

Short- and long-term effects of reserpine on rat cardiac beta-adrenoceptors.

1. In order to explore the mechanism of reserpine-induced supersensitivity, we examined the effects of various doses of reserpine (R) on rat cardiac beta-adrenoceptors (beta AR). 2. 24 hr after a single administration of R (1 mg/kg, i.p.) beta AR were up-regulated, while with higher doses (2.5-5 mg/kg) beta AR density was not changed but beta AR coupling, evaluated by the proportion of high-affinity agonist binding states, was impaired. 3. Long-term effects of R (2.5 mg/kg/day, 2 days) included beta AR down-regulation and uncoupling 24 hr treatment (day 1), followed by up-regulation at day 7, while all parameters were similar to controls at day 14. 4. It appears that R induces either an increase or a decrease of cardiac beta AR density and coupling, dependent on the dose and the time at which beta AR are measured after treatment.

Animals↗
PubMed1991

Different effects of direct and indirect dopamine receptor agonists on immobility time in reserpine-treated mice.

1. The effects of dopamine agonists on the immobility time in mice were examined. 2. Apomorphine (APO), bupropion (BUP), bromocriptine (BRC) and quinpirole but not SKF 38393 elicited anti-immobility effect. The effect of the agonists was decreased by the D-2 antagonist sulpiride but not by the D-1 antagonist SCH 23390. 3. In animals pretreated with reserpine, the anti-immobility effects of APO and quinpirole were potentiated, while the response of BPU was decreased and that of BRC was not changed. 4. It is concluded that D-2 dopamine receptors are involved in the anti-immobility effects of dopaminergic agents, D-2 dopamine receptors may become hypersensitive by reserpine and BUP exerts its response through indirect dopaminergic if mechanism.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1995

Morphology and Fos immunoreactivity reveal two subpopulations of striatal neurotensin neurons following acute 6-hydroxydopamine lesions and reserpine administration.

It was previously reported that following striatal dopamine depletion or pharmacological blockade of dopamine neurotransmission, neurotensin immunoreactivity is elicited in at least two distinct subpopulations of striatal neurons (Neuroscience Vol. 46, pp. 335-350, 1992). Recently it was shown that Fos immunoreactivity, interpreted as an indicator of enhanced neuronal activity, is appreciably co-localized in only one of the subpopulations of neurotensin-immunoreactive neurons observed following blockade of the dopamine D2 receptor (Neuroscience Vol. 57, pp. 649-660, 1993). In the present study, similar methods were used to determine the degree of co-localization of Fos and neurotensin immunoreactivity in striatal neurons in response to the dopamine-depleting effects of 6-hydroxydopamine lesions and reserpine administration. It was observed that following these treatments, a subpopulation of neurons at the small end of the medium size range exhibited light neurotensin immunoreactivity and frequent co-localization with Fos immunoreactivity. This population was predominant after reserpine administration in the dorsolateral quadrant of the striatum. Another subpopulation comprised larger neurons that exhibited intense neurotensin immunoreactivity in perikarya and proximal processes that was rarely co-localized with Fos immunoreactivity. This type of neuron was observed following all the drug treatments but was present almost to the exclusion of the smaller type of cells three days following ventral midbrain 6-hydroxydopamine lesions, being mainly located in the dorsomedial and ventrolateral portions of the striatum. The present data support the results of the preceding studies in being consistent with the existence of two subpopulations of striatal neurons that accumulate neurotensin following dopamine depletion. The possibility is considered that one subpopulation accumulates neurotensin in response to co-ordinate increases in neuronal activity and neurotensin synthesis, and the other as a result of decreased release.

Animals↗
PubMed1983

The influence of pimozide, haloperidol, alpha-methyl-p-tyrosine and reserpine on the development of morphine dependence in rats.

It was found that pimozide, haloperidol and alpha-methyl-p-tyrosine (alpha-MT), drugs inhibiting central catecholaminergic (CA) transmission, increased the development of morphine dependence measured as wet dog shakes in rats. Reserpine inhibiting CA and serotoninergic (5-HT) transmission, decreased the development of morphine dependence in rats. The inhibitory effect of reserpine was reversed by 5-hydroxytryptophan (5-HTP), but not by L-dihydroxyphenylalanine (L-DOPA). These results suggest that wet dog shakes might develop as a result of regulatory adaptation in the 5-HT neurotransmitter system.

5-Hydroxytryptophan↗
PubMed1989

Analytical oxidation of reserpine.

Electrochemical (anodic) oxidation of reserpine in an acidic medium results in the formation of 3,4-dehydroreserpine instead of the reported 10-hydroxy-reserpine. Electrochemical and chemical oxidation by sodium nitrite lead quantitatively to the same product; few by-products or consecutive products are formed if protected from light. The validity of the conditions of the spectrophotometric assay of the European Pharmacopoeia were confirmed by following the reaction using HPLC with a photodiode-array detector.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Postnatal function following prenatal reserpine exposure in rats: neurobehavioral toxicity.

Behavioral and neurochemical analyses were conducted on preweanling CD rats prenatally exposed to either 0, 0.375 or 0.750 mg/kg/day reserpine SC on gestation days 12-15. Offspring body weights were taken on test days, and pups were tested for negative geotaxis responding on postnatal day 8, developmental activity on days 12, 16 and 20, and auditory startle habituation on day 19 or 20. In addition, brains were removed from culled pups on day 1, 1 male and 1 female/litter on day 8, and animals tested for activity on day 21. Neurochemical assays were performed on whole brains from 1- and 8-day-old pups, and on caudate nucleus, frontal cortex and hippocampus of day 21 rats. Treatment resulted in dose-related decreases in maternal weight gain over gestation and mean pup weight at birth. Changes in the normal developmental activity pattern were both sex and dose dependent in treated rats. In auditory startle habituation experiments, rats exhibited a dose-related decrease in response amplitude and rate of habituation. In the day 21 females, caudate nucleus dopamine (DA) and serotonin (5-HT) concentrations and DA-receptor binding were decreased in a dose-dependent manner. Males showed less dramatic, but similar trends in caudate changes. However, hippocampal 5-HT and 5-HT receptor binding were significantly reduced only in females. Thus, sex-related behavioral alterations were accompanied by sex-related neurochemical changes, and females generally were more affected than males by prenatal reserpine treatment. The significant decrease in activity and auditory startle amplitude in the females is consistent with the suggested down regulation of the DA system in regional brain areas.

Animals↗
PubMed2005

Muscarinic receptor blockade attenuates reserpine-mediated Fos induction in the rat striatopallidal pathway.

Acute administration of the dopamine-depleting agent reserpine (10 mg/kg) induces Fos expression in striatopallidal neurons of intact rats-an effect that is blocked by pretreatment with the D2 agonist quinpirole (0.5 mg/kg). Systemic administration of the muscarinic antagonist scopolamine (50 mg/kg) partially attenuates reserpine-mediated striatal Fos expression. These data suggest that muscarinic receptors, either within the striatum or in extrastriatal sites, regulate D2 receptor-mediated Fos expression in rat striatopallidal neurons.

Adrenergic Uptake Inhibitors↗
PubMed1998

Reserpine does not induce orofacial dyskinesia in spontaneously hypertensive rats.

The nigrostriatal dopaminergic system seems to be involved in both reserpine-induced orofacial dyskinesia in normal rats and in the pathogenesis of hypertension in spontaneously hypertensive rats. In the present study, repeated reserpine administration (1.0 mg/kg, s.c., every other day, for 3 days) increased tongue protrusion and vacuous chewing frequencies as well as the duration of facial twitching in Wistar normotensive but not in spontaneously hypertensive rats. These results suggest that genetic hypertension and drug-induced orofacial movements may be inversely modulated by similar mechanisms in the nigrostriatal dopaminergic system.

Analysis of Variance↗
PubMed1976

A new gas chromatographic method for the estimation of reserpine and rescinnamine.

Under the conditions described for alkaline hydrolysis of reserpine and rescinnamine in absolute and aqueous methanol, and after esterification (with diazomethane) of the resulting acid fraction, methyl 3,4,5-trimethoxybenzoate was quantitatively recovered, whereas methyl trans-3,4,5-trimethoxycinnamate, in normal lighting conditions, was either partly isomerized to methyl cis-trimethoxycinnamate or formed an adduct with a molecule of methanol, yielding methyl 3-methoxy-3-(3,4,5-trimethoxyphenyl)propionate. The structures of the products were established by synthesis, nuclear magnetic resonance studies and mass spectrometry. This investigation of the hydrolytic conditions allowed a reliable and rapid gas chromatographic determination of reserpine and/or rescinnamine in amounts down to 500 and 2000 mug, respectively, to be devised.

Chromatography, Gas↗
PubMed2002

Pharmacological properties of the anti-Parkinson drug rasagiline; modification of endogenous brain amines, reserpine reversal, serotonergic and dopaminergic behaviours.

Rasagiline [N-propargyl-1R(+)-aminoindan; TVP1012] is a potent irreversible monoamine oxidase (MAO) inhibitor with selectivity for type B of the enzyme, which is being developed for treatment of Parkinson's disease. In this study we examined effects of rasagiline on CNS monoamine levels, modification of behavioural response to L-tryptophan, fluoxetine and L-DOPA, and reversal of reserpine syndrome. Reserpine-induced ptosis was reversed by rasagiline at doses above 2 mg x kg(-1) i.p., which inhibit MAO-A as well as MAO-B, but not at MAO-B-selective doses. However, combination of rasagiline (10 mg x kg(-1) i.p.) with L-DOPA or L-tryptophan (50 mg x kg(-1) i.p.), or rasagiline (10 mg x kg(-1) p.o.) with fluoxetine (10 mg x kg(-1) p.o.), did not induce the behavioural hyperactivity syndrome which is seen following inhibition of both MAO-A and MAO-B by tranylcypromine together with the monoamine precursors. Following oral administration, levels of noradrenaline (NA), 5-hydroxytryptamine (5-HT) and dopamine (DA) were unaffected in hippocampus and striatum after single doses of rasagiline up to 2 mg x kg(-1). Following chronic oral administration (21 days, one dose daily), levels of NA, 5-HT and DA in hippocampus and striatum were unaffected by rasagiline at doses up to 1 mg x kg(-1). Rasagiline does not modify CNS monoamine tissue levels or monoamine-induced behavioural syndromes at doses which selectively inhibit MAO-B but not MAO-A.

Animals↗