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PubMed1997

Acute reserpine administration elicits long-term spontaneous oral dyskinesia.

Chronic reserpine administration produces persistent oral dyskinesia accompanied by severe dopamine depletion in the caudate-putamen. The present study examined whether these behavioral and neurochemical effects would persist following acute reserpine administration. Acute administration of reserpine (1 mg/kg, s.c.) produced spontaneous oral dyskinesia that persisted above control levels for at least 84 days. Reserpine also produced a 74% depletion of dopamine in the caudate-putamen relative to vehicle treatment at 3 days post-injection, but did not significantly alter dopamine in the caudate-putamen at 84 days post-injection. The finding that reserpine-induced oral dyskinesia persisted despite repletion of dopamine in the caudate-putamen suggests that the persistent neuropathological change underlying this behavior occurs in a neural pathway other than the dopaminergic nigrostriatal pathway.

Animals↗

PubMed2000

Effects of reserpine on expression of the LDL receptor in liver and on plasma and tissue lipids, low density lipoprotein and fibrinogen in rabbits in vivo.

The effects of administering reserpine (0.1 mg/kg) or 17alpha-ethinyloestradiol (2.5 mg/kg) to New Zealand White rabbits on low density lipoprotein receptors in liver, on plasma low density lipoprotein and fibrinogen and on plasma and tissue lipids were determined. Blood pressure and heart rate were also followed. The drugs were injected subcutaneously into conscious unrestrained rabbits for 5 days. On the 6th day homologous 125I-tyramine cellobiose labelled low density lipoprotein (125I-TC-LDL) was injected intravenously and 24 h later the animals were killed. Compared to controls, reserpine significantly increased LDL receptor expression in the liver by about threefold, and reduced total cholesterol in plasma, aorta and heart, without affecting plasma triglycerides. The reductions in plasma cholesterol and heart were due to decreases in both unesterified and esterified cholesterol. Similar effects were observed with oestrogen, except that there was no change in esterified cholesterol in aorta. In liver, a decrease of 24% in total cholesterol was due mainly to decreased esterified cholesterol. In adrenal glands total cholesterol increased by 25%. Reserpine significantly accelerated the plasma clearance of intravenously injected homologous 125I-TC-LDL and reduced its accumulation in aortic wall. Neither reserpine nor oestradiol affected blood pressure, haematocrit or plasma fibrinogen. The results suggest that reserpine is an affective anti-atherogenic drug capable of decreasing cholesterol in plasma, arteries and heart by increasing high affinity LDL receptors in the liver.

Animals↗

PubMed2000

Quantitative liquid chromatographic-tandem mass spectrometric determination of reserpine in FVB/N mouse plasma using a "chelating" agent (disodium EDTA) for releasing protein-bound analytes during 96-well liquid-liquid extraction.

A sensitive, specific, accurate and reproducible analytical method employing a divalent cation chelating agent (disodium EDTA) for sample treatment was developed to quantitate reserpine in FVB/N mouse plasma. Samples pretreated with 40 microl of 2% disodium EDTA in water were extracted by a semi-automated 96-well liquid-liquid extraction (LLE) procedure to isolate reserpine and a structural analog internal standard (I.S.), rescinnamine, from mouse plasma. The extracts were analyzed by turbo ionspray liquid chromatography-tandem mass spectrometry (LC-MS-MS) in the positive ion mode. Sample preparation time for conventional LLE was dramatically reduced by the semi-automated 96-well LLE approach. The assay demonstrated a lower limit of quantitation of 0.02 ng/ml using 0.1-ml plasma sample aliquots. The calibration curves were linear from 0.02 to 10 ng/ml for reserpine. The intra- and inter-assay precision of quality control (QC) samples ranged from 1.75 to 10.9% for reserpine. The intra- and inter-assay accuracy of QC samples ranged from -8.17 to 8.61%. Reserpine and the I.S. were found to be highly bound to FVB/N mouse plasma protein. This is the first report of disodium EDTA employed as a special protein-bound release agent to recover protein-bound analytes from plasma. These matrix effects and the effects of pH in the HPLC mobile phase on the sensitivities of LC-MS-MS are discussed in this paper.

Animals↗

PubMed2002

Catecholamine depletion by reserpine blocks the anxiolytic actions of ethanol in the rat.

Neurochemical investigations of the anti-anxiety action of ethanol demonstrate that increased dopaminergic, noradrenergic, and serotonergic activity mediates the anxiolytic actions of ethanol. Results of studies with animals and human beings also confirm an involvement of the sympathetic nervous system in the behavioral actions of ethanol. Because enhanced sympathetic activity increases the release of norepinephrine from sympathetic terminals, the interruption of normal sympathetic activity might disrupt the anxiolytic action of ethanol. The present study examined the effect of chemical sympathectomy by reserpine pretreatment on the subsequent anxiolytic action of ethanol. Seventy-one, female, Sprague-Dawley rats were administered reserpine (0 or 5 mg/kg), followed 17-19 h later by ethanol (0, 0.5, or 1.0 g/kg). Animals were then tested in the elevated plus maze. Compared with saline pretreatment, which did not attenuate the anxiolytic actions of a 1.0-g/kg dose of ethanol, reserpine pretreatment completely blocked the anxiolytic action of a 1.0-g/kg dose of ethanol. Reserpine, by itself, did not possess anxiolytic or anxiogenic actions. Because the anxiolytic action of ethanol involves increased catecholamine activity and the depletion of norepinephrine and dopamine from sympathetic nerve terminals by reserpine blocked the anxiolytic action of ethanol, it is concluded that the anxiolytic action of ethanol requires the presence of normal catecholamine activity. We suggest that prostaglandin activity normally evoked by enhanced sympathetic nervous system activity might be involved in the anxiolytic action of ethanol.

Adrenergic Uptake Inhibitors↗

PubMed2000

Effect of catecholamine depletion on oxidative energy metabolism in rat liver, brain and heart mitochondria; use of reserpine.

Regulation of mitochondrial functions in vivo by catecholamines was examined indirectly by depleting the catecholamines stores by reserpine treatments of the experimental animals. Reserpine treatment resulted in decreased respiratory activity in liver and brain mitochondria with the two NAD+-linked substrates: glutamate and pyruvate + malate with succinate ATP synthesis rate decreased in liver mitochondria only. With ascorbate + TMPD system, the ADP/O ratio and ADP phosphorylation rate decreased in brain mitochondria. For the heart mitochondria, state 3 respiration rates decreased for all substrates. In the liver mitochondria basal ATPase activity decreased by 51%, but in the presence of Mg2+ and/or DNP increased significantly. In the brain and heart mitochondria ATPase activities were unchanged. The energy of activation in high temperature range increased liver mitochondrial ATPase while in brain mitochondria reserpine treatment resulted in abolishment in phase transition. Total phospholipid (TPL) content of the brain mitochondria increased by 22%. For the heart mitochondria TPL content decreased by 19% and CHL content decreased by 34%. Tissue specific differential effects were observed for the mitochondrial phospholipid composition. Liver mitochondrial membranes were more fluidized in the reserpine-treated group. The epinephrine and norepinephrine contents in the adrenals decreased by 68 and 77% after reserpine treatment.

Adenosine Triphosphatases↗

PubMed1992

Quinolinic acid: effects on brain catecholamine and c-AMP content during L-dopa and reserpine administration.

The catecholamine content in rat brain tissue was determined following the administration of quinolinic acid alone or combined either with L-dopa and decarboxylase inhibitor or reserpine. Quinolinic acid alone decreased the levels of dopamine and noradrenaline, as well as those of c-AMP, and increased those of adrenaline. Treatment with L-dopa/decarboxylase inhibitor reversed the suppressing effect of quinolinic acid on dopamine, but not on noradrenaline. Reserpine alone depleted the contents of dopamine, noradrenaline and adrenaline. It could be concluded from the effects of quinolinic acid and reserpine given together that quinolinic acid suppresses the depletion of amines induced by reserpine. It has been demonstrated that quinolinic acid leads to injuries of nerve-cell bodies in pars compacta of the substantia nigra and in the striatum. Quinolinic acid is a natural metabolite of tryptophan, normally occurring in the liver, kidney and brain (Wolfensberger et al. 1983; Moroni et al. 1984). This compound exhibits convulsant and neuron excitant properties (Stone et al. 1987). It induces a selective pattern of neuronal degeneration both at the site of intracerebral injection (Schwarcz et al. 1983; Stone et al. 1987) and after general (intracardiac) administration (Beskid and Markiewicz 1988). The ability of quinolinic acid to produce neurotoxicity was greater in the striatum than in other parts of the brain. This prompted us to study catecholamine and c-AMP levels in rat brain tissue following quinolinic acid and L-dopa administration, as well as the influence of reserpine on quinolinic acid action.

Animals↗

PubMed2003

Activation of group III metabotropic glutamate receptors in selected regions of the basal ganglia alleviates akinesia in the reserpine-treated rat.

1. This study examined whether group III metabotropic glutamate (mGlu) receptor agonists injected into the globus pallidus (GP), substantia nigra pars reticulata (SNr) or intracerebroventricularly (i.c.v.) could reverse reserpine-induced akinesia in the rat. 2. Male Sprague-Dawley rats, cannulated above the GP, SNr or third ventricle, were rendered akinetic with reserpine (5 mg kg(-1) s.c.). 18 h later, behavioural effects of the group III mGlu receptor agonists L-serine-O-phosphate (L-SOP) or L-(+)-2-amino-4-phosphonobutyric acid (L-AP4) were examined. 3. In reserpine-treated rats, unilateral injection of L-SOP (2000 and 2500 nmol in 2.5 microl) into the GP produced a significant increase in net contraversive rotations compared to vehicle, reaching a maximum of 83+/-21 rotations 120 min(-1) (n=8). Pretreatment with the group III mGlu receptor antagonist methyl-serine-O-phosphate (M-SOP; 250 nmol in 2.5 microl) inhibited the response to L-SOP (2000 nmol) by 77%. Unilateral injection of L-SOP (250-1000 nmol in 2.5 microl) into the SNr of reserpine-treated rats produced a dose-dependent increase in net contraversive rotations, reaching a maximum of 47+/-6 rotations 30 min(-1) (n=6). M-SOP (50 nmol in 2.5 microl) inhibited the response to L-SOP (500 nmol) by 78%. 4. Following i.c.v. injection, L-SOP (2000-2500 nmol in 2.5 microl) or L-AP4 (0.5-100 nmol in 2 microl) produced a dose-dependent reversal of akinesia, attaining a maximum of 45+/-17 (n=8) and 72+/-3 (n=9) arbitrary locomotor units 30 min(-1), respectively. 6. These studies indicate that injection of group III mGlu receptor agonists into the GP, SNr or cerebral ventricles reverses reserpine-induced akinesia, the mechanism for which remains to be established.

Aminobutyrates↗

PubMed2003

Effects of reserpine on nerve stimulation-induced constrictions in canine isolated splenic artery.

1. Our previous studies have demonstrated that peri-arterial electrical nerve stimulation (PNS) of the canine splenic artery induces a double-peaked vasoconstriction consisting of an initial transient, dominantly P2X purinoceptor-mediated constriction, followed by a prolonged, mainly alpha1-adrenoceptor-induced response. In the present study, we examined the effects of reserpine on PNS-induced double-peaked responses. 2. The vasoconstrictor response to tyramine was abolished after reserpine treatment, but the responses to noradrenaline (NA) and ATP were not significantly modified. 3. The PNS-induced second peak vasoconstrictor responses were markedly reduced in reserpinized vessels, whereas the first peak vasoconstrictor responses were not so strongly influenced (i.e. they were not significantly affected at 1 Hz, but were significantly affected at 4 and 10 Hz). 4. All reserpine-resistant responses were unaffected by treatment with prazosin, but were abolished by subsequent application of alpha,beta-methylene ATP. The exposure of reserpine-treated tissues to NA almost completely restored tyramine-induced vasoconstriction and the second neurogenic peak vasoconstrictor response, but failed to affect the first neurogenic response. 5. The present results indicate that ATP and NA are cotransmitters responsible for the double-peaked vasoconstrictor responses of canine splenic artery. In addition, it is suggested that PNS causes NA release not only from intragranular NA storage sites, but also from tyramine-sensitive cytoplasmic sites.

Animals↗

PubMed2000

Reserpine pretreatment prevents increases in extracellular striatal dopamine following L-DOPA administration in rats with nigrostriatal denervation.

The influence of L-DOPA and reserpine on extracellular dopamine (DA) levels in the striatum of intact and dopaminergic denervated rats was studied using the brain microdialysis technique. In intact rats, reserpine (5 mg/kg s.c.) reduced extracellular DA levels to 4% of basal values. L-DOPA (50 mg/kg i.p.) had no effect on extracellular DA levels in reserpine-pretreated rats. In rats with 6-hydroxydopamine-induced lesion of the nigrostriatal dopaminergic system, basal levels of extracellular DA were low but markedly increased by L-DOPA (50 mg/kg i.p.). In 6-hydroxydopamine-lesioned rats, pretreatment with reserpine (5 mg/kg s.c.) diminished L-DOPA (50 mg/kg i.p.)-induced increases in extracellular DA levels to 16% of those obtained in denervated animals not pretreated with reserpine (p<0.01). These results suggest that in the intact striatum, extracellular DA stems mainly from vesicular storage sites and that in the striatum with dopaminergic denervation, a large part of the L-DOPA-derived extracellular DA is also derived from a vesicular pool that is released by an exocytosis mechanism.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1988

The effects of reserpine and LHRH or salmon GnRH analogues on gonadotropin release, ovulation and spermiation in common carp (Cyprinus carpio L.).

The effects of reserpine (catecholamine depletor) and LHRH analogues on gonadotropin secretion, spermiation and ovulation of common carp were investigated. Injections of reserpine alone at a dose of 1 or 7 mg/kg of body weight stimulated spermiation, and reserpine at a dose of 1 mg/kg of body weight in combination with (D-Arg6, Trp7, Leu8, Pro9, NEt)-LHRH (s-GnRH-A) or with (D-Ala6, Pro9)-LHRH (LHRH-A) at a dose of 50 micrograms/kg of body weight caused an increase of plasma gonadotropin levels, spermiation and ovulation in 80-90% of the females. Simultaneous injection of reserpine and LHRH analogues was as effective as injection of reserpine followed by injection of LHRH analogues 6 h later.

Animals↗

PubMed1984

Alternative modes of enkephalin biosynthesis regulation by reserpine and cyclic AMP in cultured chromaffin cells.

Exposure of bovine chromaffin cells in primary culture to 5 microM reserpine or 25 microM forskolin results in an increase in enkephalin peptide levels within 24-48 hr; 25 microM forskolin (or cholera toxin at 50 micrograms/ml) causes a 1.5- to 2-fold increase in enkephalin peptide levels, which is maximal after 48 hr of exposure and is totally blocked by addition of cycloheximide (0.5 microgram/ml). Reserpine (5 microM) elicits a 1.5- to 2-fold increase in enkephalin peptide levels within 24 hr, which is only partially blocked by cycloheximide. Chromatographic analysis of cellular extracts shows that forskolin increases levels of both [Met]enkephalin pentapeptide and high molecular weight enkephalin-containing peptides, while reserpine causes an increase in [Met]enkephalin pentapeptide and a concomitant decrease in high molecular weight enkephalin-containing peptides, suggesting enhanced conversion of enkephalin precursor(s) to the mature polypeptide hormone. Measurement of preproenkephalin messenger RNA (mRNAenk) by RNA blot hybridization with a cDNA probe for mRNAenk reveals that forskolin and cholera toxin cause a relatively rapid (less than 17 hr) 3- to 5-fold increase in mRNAenk, while exposure to reserpine elicits a gradual decrease in enkephalin mRNA (a 50%-80% decline) beginning within 24 hr and continuing over a 72-hr period. These results suggest that forskolin and reserpine differentially regulate enkephalin biosynthesis in cultured chromaffin cells, the former by increasing, presumably via a cAMP-dependent mechanism, cellular mRNA coding for preproenkephalin and the latter by a post-translational increase in proenkephalin processing.

Adrenal Medulla↗

PubMed1985

Reserpine-induced changes in anesthetic action of fentanyl.

The effect of prior administration of reserpine on fentanyl dose-response curves for loss of the righting reflex and prevention of purposeful movement response to noxious stimulation was studied in rats. It was found that reserpine (5 mg X kg-1, 3 h before the tests) antagonized the effect of fentanyl on purposeful movement response to the tail clamp and, at the same time, strengthened its effect on the righting reflex. As a result, reserpine pretreatment reversed the order of fentanyl potency regarding these two effects. Reserpine changed fentanyl ED50 values for the purposeful movement response from 8.2 to 20.3 micrograms X kg-1 (P less than 0.0001) and for the righting reflex from 20.5 to 13.7 micrograms X kg-1 (P less than 0.0001). The results suggest that reserpine dissociates the analgesic action of fentanyl from its anesthetic action, defined as a loss of the righting reflex. This may be regarded as an indication that the analgesic action of narcotics may not adequately reflect their anesthetic potency.

Analgesics↗

PubMed1987

Effect of reserpine on salivary gland radioiodine uptake in thyroid cancer.

Nine patients with thyroid cancer were treated with reserpine in an attempt to reduce radiation exposure to the salivary glands from 100-150 mCi doses of I-131 therapy to thyroid remnants or metastases. Three control patients were not treated with reserpine but did receive 100-150 mCi of I-131. Parotid/background ratios of activity after radioablative doses of I-131 in patients not treated with reserpine were significantly higher than the patients treated with reserpine, and this was also true seven days after the radioablative dose. Combined therapy with reserpine, chewing gum, lemon candies, and hydration is suggested for the prevention of sialadenitis and xerostomia due to large doses of radioiodine.

Adenocarcinoma↗

PubMed1987

Functional molecular mass of binding sites for [3H]dihydrotetrabenazine and [3H]reserpine and of dopamine beta-hydroxylase and cytochrome b561 from chromaffin granule membrane as determined by radiation inactivation.

The monoamine transporter of chromaffin granule membrane has two distinct high-affinity binding sites for tetrabenazine and reserpine, which can be assayed by [3H]dihydrotetrabenazine and [3H]reserpine binding, respectively. The functional molecular mass of the components bearing these sites has been investigated by the radiation inactivation technique. The decline of [3H]dihydrotetrabenazine binding activity with increasing radiation doses followed a single exponential, from which a functional molecular mass of 68 kDa was derived for tetrabenazine binding sites. [3H]Reserpine binding activity declined in a more complex way; however, under conditions where high-affinity reserpine binding sites were specifically assayed, the decline was also exponential, corresponding to a functional molecular mass of 37 kDa for these sites. The figures obtained for high-affinity tetrabenazine and reserpine binding sites are consistent with previous values obtained by photoaffinity of tetrabenazine and serotonin binding sites, respectively. It is thus concluded that the monoamine transporter has an oligomeric structure. By the radiation inactivation technique, cytochrome b561 and dopamine beta-hydroxylase have functional molecular masses of 25 and 123 kDa, respectively. The latter value might be attributed to the dimeric form of the enzyme.

Acetylcholinesterase↗

PubMedDate not supplied

Lethal effects of reserpine plus physostigmine and neostigmine in mice.

1. The interaction between the reversible cholinesterase inhibitors, physostigmine and neostigmine and reserpine was studied. 2. A combination of reserpine plus a cholinesterase inhibitor significantly increased lethality in adult male Swiss-Webster mice above that caused by either neostigmine, physostigmine, or reserpine alone. 3. Methscopolamine completely reversed this effect. 4. It would appear that the presence of the antiadrenergic agent, reserpine, increases the toxicity of cholinomimetic agents. 5. The above results may have clinical significance, since reserpine and cholinesterase inhibitors are used in the practice of medicine.

Animals↗

PubMed1989

Effects of reserpine pretreatment on neuroeffector transmission in the vas deferens.

1. The effects of reserpine pretreatment on neurotransmission in the guinea-pig vas deferens have been re-examined with a view to study the role of noradrenaline (NA) in mediating postjunctional electrical responses and, in particular, excitatory junction potentials (EJP). 2. Reserpine (5 mg/kg, i.p.) caused almost total depletion (below detection levels) of the NA content of the vas deferens. However, spontaneous and evoked excitatory junction potentials (SEJP, EJP) and currents (SEJC, EJC) could still be recorded in NA-depleted tissues. The amplitude distribution of SEJC in control and reserpinized tissues was similar. 3. Facilitation of EJP and EJC was markedly slowed in reserpinized tissues, EJP taking 50-60 pulses to facilitate fully. However the amplitudes of fully facilitated EJP were comparable to EJP recorded in control tissues. 4. EJPs in reserpinized vasa deferentia were unaffected by the NA synthesis inhibitor, alpha-methyl tyrosine, but were abolished in the presence of the stable ATP analogue alpha,beta-methylene ATP which desensitizes postjunctional P2-purinoceptors. 5. Local application of ATP, but not NA, mimicked the EJP. These results indicate that EJP are mediated by a non-noradrenergic neurotransmitter possibly ATP.

Adenosine Triphosphate↗

PubMed1992

Acute reserpine treatment increases rat brain serotonin synthesis via a nerve impulse-dependent mechanism.

Notwithstanding recent advances in the understanding of central serotonin (5-HT) function, important basic aspects of the control of brain 5-HT neuronal transmission remain incompletely elucidated. The present experiments addressed the putative mechanism(s) by which acute reserpine treatment stimulates cerebral 5-HT synthesis; also, such studies might shed further light on the relation between impulse flow and transmitter synthesis in central 5-HT neurons. Reserpine (5 mg/kg, i.p., 90 min before death) markedly elevated 5-HT synthesis [5-hydroxytryptophan (5-HTP) accumulation after decarboxylase inhibition by means of NSD 1015] in the limbic, striatal, and cortical rat brain parts. Hemitransection of ascending neuronal connections between the brainstem and the forebrain, performed immediately before reserpine injection, did not affect the 5-HT synthesis per se but completely prevented the drug response on the lesioned side. Similarly, systemic administration of the selective 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (0.1 mg/kg, s.c., 60 min before death) blocked the reserpine-induced elevation of brain 5-HT synthesis. These findings indicate that the reserpine-induced rise in axon terminal 5-HTP accumulation is dependent on intact (5-HT) neuronal impulse flow, which may or may not involve a transient impairment of somatodendritic 5-HT release and, in turn, autoreceptor tone.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1993

Reduction of dopamine synthesis inhibition by dopamine autoreceptor activation in striatal synaptosomes with in vivo reserpine administration.

In an attempt to clarify the mechanisms by which dopamine (DA) autoreceptor activation inhibits DA synthesis, the efficacy and potency of the D2 DA agonists bromocriptine, lisuride, and pergolide, and the D1-D2 DA agonist apomorphine were studied in rat striatal synaptosomes, in which the rate of DA synthesis (formation of 14CO2 from L-[1-14C]tyrosine) was increased 103% by treating the animals from which the synaptosomes were obtained with reserpine (5 mg/kg i.p. twice, 24 and 2 h before they were killed), using the striatal total homogenate as the standard synaptosomal preparation. The increase in DA synthesis evoked by reserpine was additive with that produced by treatment of the synaptosomes with dibutyryl cyclic AMP, suggesting that, not a cyclic AMP-dependent, but possibly a Ca(2+)-dependent mechanism was involved. The DA agonists showed a concentration-dependent inhibition of DA synthesis in the control synaptosomes, which was antagonized by the selective D2 DA antagonist (-)-sulpiride. In the synaptosomes with increased rate of DA synthesis obtained from the rats treated with reserpine, the concentration-response curves of DA synthesis inhibition for the other DA agonists were shifted to the right, and the effect of bromocriptine was completely eliminated, whereas bromocriptine antagonized the effect of apomorphine. The increased rate of DA synthesis was not preserved in the striatal P1 + P2 fraction obtained from the reserpine-treated rats, but the effects of the DA agonists were still reduced to the same degree as those in the total homogenate. (-)-Sulpiride did not enhance DA synthesis in synaptosomes from the reserpine-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗