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At least 865 records · Page 48Linked to original sources
PubMed1982

Effect of tyrosine on brain catecholamine turnover in reserpine-treated rats.

The injection of reserpine [2.5 mg/kg, intraperitoneally (i.p.)] increased brain concentration of tyrosine and of the major catecholamine metabolites, 3-methoxy-4-hydroxy-phenylethylene--glycol-sulfate (MHPG-SO4) in the rat. In reserpine-treated animals, tyrosine administration (200 mg/kg, i.p.) caused further increases in brain tyrosine, DOPAC, and HVA, but not in brain MHPG-SO4. The increases in DOPAC and HVA levels were observed in a dopaminergic brain region (the corpus striatum) and a noradrenergic region (the cerebellum). These results support previous observations that catecholamine synthesis and release in both dopaminergic and noradrenergic neurons can depend in part upon brain tyrosine levels.

Animals↗
PubMed1989

Noradrenergic, purinergic, and cholinergic transmission in the mouse vas deferens: influence of field-stimulation parameters, reserpinization, 6-hydroxydopamine and 4-aminopyridine.

In the field-stimulated mouse vas deferens the twitch inhibiting potency of prazosin (1 microM) and alpha,beta-methylene ATP (MeATP, 10 microM) was studied, using two types of stimulation-response curves, (a) variation of frequency from 3 to 100 Hz at a constant pulse width of 0.1 ms and (b) variation of pulse width from 0.04 to 0.8 ms at a constant frequency of 15 Hz. Prazosin and MeATP reduced the twitch response by eliminating the noradrenergic and purinergic component, respectively. After the combined application of both compounds a small third twitch component remained that was most prominent at high frequencies. Reserpinization reduced the effect of prazosin but enhanced that of MeATP and increased the cholinergic component. 6-Hydroxydopamine enhanced the effects of prazosin and MeATP to the same extent, but left the cholinergic component intact. In vasa pre-loaded with [3H]-noradrenaline, field stimulation induced a larger release of tritium at high frequency and short pulse duration (100 Hz, 0.1 ms) than at lower frequency and long pulse duration (15 Hz, 0.3 ms). Prazosin (1 microM) augmented both the spontaneous and the stimulation-induced overflow of tritium, whereas MeATP (10 microM) had only a negligible negative effect on the outflow of label. In conclusion, the twitch contraction of the mouse vas deferens has a small cholinergic component in addition to the noradrenergic and purinergic components. Adrenergic and purinergic transmission seem not to run strictly in parallel: the purinergic component dominates during stimulation at low frequency and long pulse duration, and after reserpinization; 4-aminopyridine enhances the adrenergic mechanism more than the purinergic one.

4-Aminopyridine↗
PubMed1993

Modulation of a neuronal calmodulin mRNA species in the rat brain stem by reserpine.

Reserpine evokes transsynaptic impulse activity by depleting catecholaminergic neurotransmitters in the rat brain. Previous studies suggest a relationship between catecholaminergic activity and calmodulin concentration. In this report we employ Northern blot analysis to examine the effect of a single subcutaneous injection of reserpine on levels of calmodulin mRNA species which are preferentially expressed in neurons of the rat brain. Regional differences in mRNA levels were also investigated by in situ hybridization and drug-induced changes were noted particularly in specific regions of the rat brain stem. The riboprobe used in the in situ hybridization study recognized a 4.0 kilobase neuronal calmodulin mRNA species (NGB1), which was derived from the rat CaM1 gene. A calmodulin radio-immunoassay was utilized to demonstrate a drug-induced increased in calmodulin protein levels in a region which included the brain stem.

Animals↗
PubMed1981

Reserpine prevents goldthioglucose hypothalamic lesions in mice.

In reserpinized mice the occurrence of goldthioglucose hypothalamic lesions was significantly lower than in control mice. Some protection was also conferred by serotonin-receptor blockers and by treatment with nialamide + DL-alpha-methyldopa, but the protective effect of reserpine was not reversed by serotonergic and dopaminergic agonists, alone or in combination, nor by insulin.

Animals↗
PubMed1980

Modifications of female sex chromatin (Barr body) in rat neurons after reserpine administration.

3 groups of rats were sacrificed 30 min, 4 h and 24 h after reserpine (10 mg/kg i.p.) injection. Toluidine blue stained sections showed that in the motor neurons of the spinal cord the drug, at 4 h, had induced a migration of the Barr body from the nucleolus to the nuclear membrane and an increase in its size and RNA concentration. From our findings we suggest that reserpine may have an activating role on X-linked genes.

Animals↗
PubMed1994

Comparison of the effects of NMDA and AMPA antagonists on the locomotor activity induced by selective D1 and D2 dopamine agonists in reserpine-treated mice.

This study examined the interaction between various glutamate antagonists and selective D1 (SKF 38393) and D2 (RU 24213) dopamine agonists in the production of locomotion in the reserpine-treated mouse. Firstly, in normal mice, the NMDA channel blocker MK 801 (0.1-1.6 mg/kg) caused a biphasic stimulation/depression of locomotor activity, whereas the competitive NMDA antagonists CGP 40116 (0.25-8 mg/kg) and CPP (0.2-20 mg/kg), and the NMDA glycine site antagonist HA 966 (0.4-10 mg/kg) inhibited locomotion monophasically. These compounds caused varying degrees of muscle weakness and impairment of posture and gait, whilst the AMPA receptor blocker NBQX (0.2-25 mg/kg) had no significant effect on unconditioned mouse motor behaviour. None of the antagonists reversed reserpine-induced akinesia by themselves, but they all potentiated the locomotor movements induced by 30 mg/kg SKF 38393. Movements remained fluent with low doses of CPP, HA 966 and NBQX, but became ataxic with MK 801 and CGP 40116, with sedation prevailing at high doses of all the antagonists, as in normal mice. CPP and NBQX also combined synergistically with SKF 38393 to promote tonic convulsions. By contrast, RU 24213-induced locomotion was dose-dependently depressed by MK 801, CGP 40116 and HA 966, but was unaffected by CPP or NBQX. These differential effects of NMDA and AMPA antagonists on D1 and D2 motor responding in the monoamine-depleted mouse are discussed in terms of possible mechanisms and sites of action within the brain, and the implications for their putative use as adjuvants to L-dopa in antiparkinson therapy.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1994

Potentiation of dopamine-dependent locomotion by clonidine in reserpine-treated mice is restricted to D2 agonists.

Mice treated with reserpine (5 mg/kg IP), 24 h beforehand, were completely akinetic. Fluent locomotion was reinstated with the D1-selective agonist SKF 38393 (3-30 mg/kg IP), the D2-selective agonist RU 24213 (0.5-5 mg/kg SC) and the mixed D1/D2 agonist apomorphine (0.025-0.5 mg/kg SC). Clonidine (0.03125-1 mg/kg IP) caused a dose-dependent sedation in dopamine-intact mice, but had no effect by itself on the locomotor activity of monoamine-depleted mice. In drug interaction experiments, clonidine did not modify the motor stimulant action of SKF 38393, but greatly enhanced the motor responses to RU 24213 and apomorphine. These results support the hypothesis that alpha-adrenoceptor agonists facilitate dopamine D2 but not dopamine D1 motor responding in the reserpine-treated mouse model of Parkinson's disease.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Dopamine-depleting effects of MPTP and reserpine in weaver mutant mice.

The number of nigral dopamine neurons and striatal dopamine levels are reduced by 70% in the adult weaver mutant mouse (wv/wv), whereas these parameters are essentially unchanged in the heterozygote (wv/+). We hypothesized that the remaining nigral dopamine neurons and/or striatal dopamine levels in the weaver would be less sensitive to neurotoxic or dopamine-depleting agents and that nigral neurons in the heterozygote would be more vulnerable. Mice were treated with the dopaminergic neurotoxin MPTP using different injection schedules and also with reserpine. There was a similar percent decrease in striatal DA in weavers and heterozygotes compared to normal mice after these treatments. We did observe a gene-dose-related lethality to the highest dose treatment with MPTP. These results suggest that the remaining dopaminergic neurons in the weaver are not different from those in normal mice in their capacity to respond to MPTP and reserpine.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Ca-ATPase activity in salivary glands of rats treated with reserpine, isoproterenol, terbutaline or dobutamine.

Ca-ATPase activity (mol Pi/mg protein per min) of submandibular and parotid glands after injection of single or multiple (over seven days) 0.5 mg/kg doses of reserpine was the same as in untreated glands. Twice daily doses (50 mg/kg body wt) of the non-selective beta-adrenergic agonist, isoproterenol, for six days, increased Ca-ATPase specific activity of parotid gland by 17 per cent but that of submandibular gland was the same as controls; with dobutamine, the same dosage caused a 53 per cent decrease in submandibular activity and a 31 per cent decrease in parotid. The activity of the entire parotid gland was markedly increased by all three beta-agonists, and this was generally a reflection of the induced increase in gland size. The submandibular gland had an increase in total Ca-ATPase activity only with isoproterenol. As gland weight did not change after reserpine, total glandular Ca-ATPase activity was also not altered by it. Thus, calcium accumulation and reduction in Ca-ATPase activity are not necessarily related. However, the dobutamine-induced decrease in Ca-ATPase activity of both glands suggests that there is a beta 1-mediated regulation of this enzyme.

Animals↗
PubMed1982

Effects of haloperidol and apomorphine on catecholamine metabolism in brain slices. Reserpine-like effects of haloperidol.

The accumulation, release and catabolism of [3H]dopamine (DA) and [3H]norepinephrine (NE) synthesized from [3H]tyrosine were measured in mouse striatal and substantia nigral slices. Apomorphine inhibited both [3H]NE and [3H]DA accumulation (IC50 less than 10(-6) M), presumably by acting on a presynaptic receptor. Haloperidol (10-8M) caused a small, but significant increase in [3H]DA accumulation from [3H]tyrosine in the presence of 26 mM K+, possible reflecting blockade of presynaptic receptors activated by release DA. However, at higher concentrations (10(-6) to 10(-5) M), haloperidol inhibited [3H]DA and [3H]NE accumulation. Reserpine also potently inhibited catecholamine synthesis; chlorpromazine had only a weak effect, and fluphenazine was ineffective. Both haloperidol (10(-5) M) and reserpine (10(-7) M), but not chlorpromazine and fluphenazine, markedly increased the formation of labeled dihydroxyphenylacetic acid (DOPAC) and increased the spontaneous release of labeled DA from striatal slices preloaded with [3H]tyrosine or [14C]DA. These data suggest that haloperidol has some direct effects on DA metabolism that are unrelated to DA-receptor blockade. Because the effects of haloperidol are apparently independent of DA release, haloperidol may elevate cytoplasmic DA by altering its vesicular storage. This would, in turn, increase the spontaneous release of labeled DA by diffusion, the oxidation of DA to DOPAC by monoamine oxidase, and the end-product inhibition of tyrosine hydroxylase.

Animals↗
PubMed1985

Effect of apomorphine, alpha-methylparatyrosine, haloperidol and reserpine on DOPA production in clonal cell lines (PC-12 and N1E-115).

The effect of various drugs on DOPA production in the pheochromocytoma clone PC-12 and the neuroblastoma clone N1E-115 was studied. The N1E-115 cells contain only very low amounts of dopamine due to a lack of the aromatic L-amino acid decarboxylase, whereas the PC-12 cells are rich in dopamine. alpha-Methyl-p-tyrosine and apomorphine blocked DOPA production in both cell clones. Reserpine and haloperidol reduced the intracellular dopamine in the PC-12 cells and simultaneously induced a blockade of cellular DOPA production. The released dopamine was primarily recovered as 3,4-dihydroxyphenylacetic acid indicating a release of dopamine into the cytoplasm. This transient increase of cytoplasmic dopamine by reserpine or haloperidol brings about the inhibition of DOPA production in the PC-12 cells. Our results show that the PC-12 clone especially reacts to various drugs like other in vitro systems and may serve as an additional model for studying drug effects on catecholamine biosynthesis and metabolism.

Adrenal Gland Neoplasms↗
PubMed1975

Ontogeny of the induction of tyrosine hydroxylase by reserpine in the superior cervical ganglion, nucleus locus coeruleus and adrenal gland.

The ontogeny of the induction of tyrosine hydroxylase by reserpine has been studied in the superior cervical ganglion, adrenal gland and nucleus locus coeruleus of the rat. The inductive response developed gradually over a period of days in all 3 areas. However, the onset of induction occurred at markedly different times in these regions, being present from day 2 of life, the earilest time tested, in the adrenal, day 6 in the locus coeruleus and day 24 in the ganglion. In the ganglion even extremely high, toxic doses of reserpine failed to induce the enzyme during the first 3 weeks of life. Decentralization studies indicated that the ganglion was functionally innervated at this time. Moreover, the onset of induction was not time-locked to a specific phase of the postnatal development of tyrosine hydroxylase activity in the areas examined. It is probable that the development of inducibility reflects maturation of mechanisms intrinsic to the adrenergic cell, and this timetable is different for cells in different areas.

Adrenal Glands↗
PubMed1977

Effect of reserpine on cell proliferation in the developing rat brain: a quantivative histological study.

Rats aged 11 days were injected with reserpine (2.5 mg/kg body wt.) and the rate of [3H]thymidine incorporation into brain DNA was followed over a period of 36h. In the forebrain this was significantly depressed by 2h, and it reached a nadir of about 30% of the control level at 4h, at which it remained for another 26h. A partial recovery occurred by 36h. The effect was less pronounced in the cerebellum. On the basis of this information brains of rats were examined histologically and by autoradiography between 7 and 36 h after reserpine to obtain estimates of cell cycle parameters and of rates of cell proliferation and cell loss. In the forebrain lateral ventricular subependymal layer the labelling index was markedly reduced in comparison withe controls. Cell cycle time was prolonged by 50% and turnover time increased by 60%. In the cerebellar external granular layer, the mitotic index was reduced and increased numbers of degenerate postmitotic nuclei were found, notably in the latter part of the experimental period. These effects are potentially of functional and clinical significance.

Animals↗
PubMed1983

Reserpine-induced depletion of corticoliberin (CRF)-like immunoreactivity in the zona externa of the rat median eminence.

An acute reserpine treatment has the same selective and marked depleting effect on corticoliberin-like immunoreactivity as on vasopressin-like immunoreactivity in the rat zona externa of the median eminence. Somatostatin and gonadoliberin immunoreactivities appear unmodified. Reserpine effect is blocked by pretreatment with monoamine oxidase inhibitors (pargyline or tranylcypromine). Present results support the notion of an inhibitory role of monoamines, particularly catecholamines, on the release of corticoliberin.

Animals↗
PubMed1985

Effect of chronic reserpine and desmethylimipramine treatment on CRF-like immunoreactivity of discrete brain areas of rat.

The corticotropin releasing factor-like immunoreactivity (CRF-LI) of discrete areas of rat brain were measured following reserpine (2 mg/kg i.p. for 3 days) or chronic desmethylimipramine (DMI) (20 mg/kg i.p. for 14 days) treatment. Reserpine caused a 40% and 36% reduction in the (CRF-LI) of the median eminence (ME) and posterior pituitary respectively, while DMI caused a 61% rise in CRF-LI of the posterior pituitary only. The results support the role of monoaminergic regulation of CRF release from the ME and further suggest an interaction between monoaminergic and CRF neurons in the posterior pituitary.

Animals↗
PubMed1986

Effects of serotonin, cyproheptadine and reserpine on corticotropin-releasing factor release from the rat hypothalamus in vitro.

We investigated the effects of serotonin, cyproheptadine and reserpine on corticotropin-releasing factor (CRF) release from the rat hypothalamus, and the effect of cyproheptadine on CRF-induced adrenocorticotropic hormone (ACTH) secretion from the anterior pituitary (AP) in vitro using a perifusion system for rat hypothalami and AP, and a rat CRF radioimmunoassay. Cyproheptadine, 10(-8) M, had a direct inhibitory effect on both basal and 10(-9) M CRF-induced ACTH secretion from the rat AP in vitro. In addition, 10(-9)-10(-7) M cyproheptadine inhibited basal CRF release in a dose-dependent fashion, and also suppressed serotonin- and KCl-induced CRF release. Conversely, 10(-9)-10(-7) M reserpine failed to influence CRF release from the rat hypothalamus. These results indicate that a serotonergic mechanism may be involved in the CRF-releasing mechanism, and inhibition of depolarization-dependent calcium entry into cells and/or nerve endings. In addition an anti-serotonergic mechanism is involved in the inhibitory action of cyproheptadine.

Adrenocorticotropic Hormone↗