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PubMed1977

Effect of reserpine on cell proliferation in the developing rat bran: a biochemical study.

Reserpine, a well-known CNS depressant which depletes central monoamine stores, was found to produce in the brains of 11-day-old rats a severe depression in cell proliferation in terms of the rate of [3H]thymidine incorporation into DNA. The effect was studied in detail 12 h after ther administration of the drug (2.5 mg/kg, s.c.) when the rate of in vivo DNA synthesis in the forebrain was about one-third of control: the decrease was less marked in the cerebellum (rate about two-thirds of control). It was possible to exclude side effects of the drug, such as restricted food intake, hypothermia and an elevation of the level of blood corticosteroids being responsible for the reduction of [3H]thymidine incorporation into DNA. Kinetic studies showed that reserpine had no marked effect on the entry of [3H]thymidine from blood to brain, but it caused some retardation in the rate of [3H]thymidine conversion into [3H]thymidine nucleotides. Nevertheless, the severe depression of DNA labelling was evident even after correcting the values on the basis of [3H]thymidine nucleotide concentrations. In contrast to these effects, thymidine kinase activity was normal in the brain of reserpine-treated animals.

Animals↗
PubMed1993

Acute effects of reserpine on tryptophan hydroxylase activity and mRNA in rat brain.

The present study examined changes in tryptophan hydroxylase (TPH) activity in the rat brainstem 1-4 days after i.p. reserpine administration. TPH enzyme activity was significantly decreased day 1 posttreatment and followed by a small but significant increase on days 2-4. Maximal TPH activity on day 4 was elevated only 42% above control level. This small increase in TPH activity was not preceded by any change of in situ hybridization signal of TPH message on day 1. In contrast, adrenal tyrosine hydroxylase (TH) activity in these same reserpinized animals was 2.5-fold higher than control on 4 day posttreatment. In addition, TH message was correspondingly increased day 1 posttreatment. Taken together, these results indicate a trend of small increase in TPH activity and no alteration in message after reserpine treatment unlike catecholaminergic systems.

Adrenal Glands↗
PubMed1995

Effects of intracerebroventricular administration of pituitary adenylate cyclase-activating polypeptide (PACAP) on the motor activity and reserpine-induced hypothermia in murines.

We investigated the effects of i.c.v. administration of pituitary adenylate cyclase-activating polypeptide (PACAP) on the spontaneous motor activity and reserpine-induced hypothermia in murines. The administration of PACAP (1 or 2 nmol) caused a dose-dependent increase in both spontaneous motor activity and rearing behavior in the rat. The peptide (0.1 or 0.2 nmol) counteracted reserpine-induced hypothermia in a dose-dependent manner in mice. On the other hand, i.c.v. injection of vasoactive intestinal polypeptide, which is structurally similar to PACAP, at a dose similar to that of PACAP (2 nmol in rats, 0.2 nmol n mice) did not show a significant effect on either behavior or body temperature. Therefore, the stimulating effect of PACAP observed here may be mediated by PACAP-specific (type I) receptors. PACAP was more potent and longer-lasting than a known potent stimulating peptide, thyrotropin-releasing hormone, in both stimulating motor activity and counteracting reserpine-induced hypothermia. Results of the present study, in combination with those of previous studies identifying endogenous PACAP in the brain, suggest that PACAP may play a important role in the CNS as a stimulant in regulating motor activity and body temperature.

Animals↗
PubMed1977

Amine repletion in the reserpinized cat: effect upon PGO waves and REM sleep.

Selective repletion of 5-HT and catecholamines in the reserpinized cat was used to study the role of these biogenic amines in the regulation of PGO wave activity and sleep. The results include: 1. Repletion of 5-HT, following injections of D, L and L-5-HTP, suppressed PGORes in the pons and visual system. A consistent relationship between drug dose and duration of suppression was established. D-5-HTP failed to influence PGORes. L and D, L-5-HTP also induced a state closely resembling slow wave sleep and this change corresponded, temporally, with the period of wave suppression. 2. Repletion of catecholamined, following injections of L-DOPA, often caused behavioral arousal and a conversion from PGORes to PGOW. The molar dose of L-DOPA required to block PGORes was 10-20 times greater than that of L-5-HTP required for a comparable effect. In some cases, L-DOPA failed to arouse the cat, and in each of these instances, it failed to suppress PGORes. 3. L-DOPA consistently failed to induce a premature return of REM sleep in the reserpinized animal. These results suggest that 2 neuronal systems, one employing 5-HT and the other catecholamines, play a part in the regulation of PGORes, and presumably, PGOrem. The 5-HT system may be primarily responsible for suppressing PGOrem during slow wave sleep, with the catecholamine system playing a comparable part during wakefulness. Earlier reports that L-DOPA induces REM sleep in the reserpinized animal were not confirmed, indicating that the postulated role of catecholamines in the induction of this state should be reevaluated.

5-Hydroxytryptophan↗
PubMed1985

Spontaneous cerebellar nuclei PGO-like waves in natural paradoxical sleep and under reserpine.

PGO-like spikes were described in chronically implanted cats at the cerebellar nuclei, dentatus, fastigii and interpositus, bipolarly and monopolarly recorded during natural paradoxical sleep. They showed close similarities with known PGO at occipital cortex and lateral geniculate nucleus: wave form, duration and amplitude were coincident. Moreover fast activity frequency increment in the last part of slow wave sleep also was observed at cerebellar loci. The peak-to-peak latency measurements demonstrated that the occipital cortex PGO lagged the nucleus dentatus PGO-like waves in 20-22 msec. The phasic cerebellar waves were not always related to eye movements. Acute experiments with a previous low dose of reserpine showed the PGO-like spikes when an exploring electrode penetrated a cerebellar nucleus. Chronically implanted cats, treated with reserpine, showed the phasic cerebellar waves during wakefulness and, after a few days, during the recovered paradoxical sleep. Based on electrophysiology and the reserpine experiments a common pontine generating mechanism for PGO and cerebellar PGO-like activity is proposed. It is also hypothesized that the cerebellum could participate in sleep physiology mainly related to phasic events without excluding a tonic function.

Animals↗
PubMed1975

The evaluation of anti-parkinson drugs on reserpine-induced rigidity in rats.

The effect of anti-parkinson drugs on reserpine-induced rigidity was examined using a technique which measured rigidity by hind limb palpation. Centrally acting dopaminergic and anti-cholinergic drugs were able to antagonize reserpine-induced rigidity, whereas peripherally acting drugs had no effect. Results are discussed in terms of possible modes of action. Relative potencies of the drugs studied in this model were well correlated with the dose ranges of clinically established anti-parkinson drugs. It is concluded that measurement of reserpine-induced rigidity by hind limb palpation is a rapid and sensitive technique to evaluate potential anti-parkinson drugs.

Amantadine↗
PubMed1975

Reserpine-induced catecholamine depletion from small cells in rat sympathetic ganglia.

Two reserpine dosage schedules were applied to Wistar rats (a) 5 mg/kg i.p. 6 hr before sacrifice and (b) 5 mg/kg i.p. at 36, 24 and 12 hr prior to sacrifice. Control animals were correspondingly sham-injected. The coeliac-mesenteric ganglion complex was removed and processed either for the Falck-Hillarp fluorescence histochemical technique or fixed in glutaraldehyde followed by 3.5% potassium dichromate for a chromaffin-type reaction. After a single reserpine injection there was a statistically significant (p less than 0.001) reduction in the percentage of 'chromaffin-positive' cells and a statistically significant (p less than 0.001) increase in the percentage of 'chromaffin-negative' cells compared with controls. No obvious reduction in fluorophore emission from small intensely fluorescent (SIF) cells was observed. After prolonged reserpinization (3 x 5 mg/kg) there was a highly significant reduction in the percentage of 'chromaffin-positive' small cells and also a significantly lower (by a factor of 2) level of fluorescent emission from SIF cells. The catecholamine-releasing potential of small cells is demonstrated by these results.

Animals↗
PubMed1976

The effects of chronic reserpine treatment on the contractile activity of the isolated vas deferens of the guinea pig.

Chronic reserpine treatment of guinea pigs during 5 days (1 mg/kg/day) induces postjunctional supersensitivity in the isolated vas deferens. It has been previously proposed that postjunctional supersensitivity occurs as a result of an ionic and/or membrane mechanism. Contrasting with previous observations in vascular smooth muscle the present results demonstrate that chronic reserpine treatment did not increase the sensitivity of the depolarized vas deferens to calcium. Experiments on drug responsiveness show that the supersensitive depolarized tissues have a greater and slower rate of loss of responsiveness than do control vasa deferentia. However, in a Ca2+-free Krebs solution responsiveness of supersensitive vasa deferentia did not differ from that of control tissues. These findings suggest that, in the guinea-pig vas deferens, reserpine-induced supersensitivity could be at least partially dependent on the increased availability of a calcium store(s) probably located at the cell membrane and/or cytoplasmic compartments.

Acetylcholine↗
PubMed1982

Reserpine and sympathetic denervation cause an increase of postsynaptic alpha 2-adrenoceptors.

The changes in alpha-adrenoceptors in rat vasa deferentia after injections of reserpine and 6-hydroxydopamine (6-OHDA) were examined in binding studies with [3H]WB4101 and [3H]clonidine. On intraperitoneal injection of reserpine (0.5 mg/kg body weight per day, 2 days), [3H]clonidine binding sites increased by about 2.0 pmol/g wet weight; the binding sites were not detectable in vasa from control rats. [3H]WB4101 binding sites showed no apparent change in amount. After a single injection of 6-OHDA (30 mg/kg body weight), [3H]clonidine binding sites amounted to about 1.1 pmol/g wet weight. The data suggest that both reserpine treatment and incomplete chemical denervation with 6-OHDA cause an increase of [3H]clonidine binding sites in the postsynaptic region of rat vasa deferentia. The possibility was tested by completely denervating rat vasa deferentia by chemical treatment and operation. The treatments increased the binding sites to about 0.9 and 1.0 pmol/g wet weight, respectively over the control level. The results imply that the binding sites indeed also increased in the postsynaptic area.

Animals↗
PubMed1984

Dissociation of supraspinal and spinal morphine analgesia by reserpine.

Reserpine antagonized systemic morphine analgesia as measured by tail-flick latency but the antagonism was surmountable by increasing the morphine dose. Reserpine had no effect on the intrathecal morphine analgesia while the analgesic action of intraventricular morphine was practically eliminated by reserpine.

Animals↗
PubMed1987

Sympathetic nerve-mediated release of ATP from the guinea-pig vas deferens is unaffected by reserpine.

The release of ATP from the guinea-pig vas deferens was measured using the luciferin-luciferase assay. The effects of reserpine, tetrodotoxin, 6-hydroxydopamine and guanethidine on this efflux were investigated. Reserpine, which produced extensive loss of noradrenaline (NA) (about 99%) and eliminated the second phase of the nerve-mediated contraction, failed to impair either ATP release from the vas deferens or the concomitant 'twitch' contraction; in fact both were increased. Therefore the neurotransmitter mediating the twitch cannot be NA, thus excluding the gamma-receptor hypothesis. Furthermore, since the release of ATP is unaffected by reserpine, it is unlikely that ATP is being released from smooth muscle as a consequence of the post-junctional actions of NA. Tetrodotoxin, 6-hydroxydopamine and guanethidine substantially reduced or abolished the release of ATP and both phases of the nerve-mediated response. To conclude, in the guinea-pig vas deferens, ATP co-released with NA from sympathetic nerves, mediates the twitch phase of the contraction and its underlying electrical events.

Adenosine Triphosphate↗
PubMed1988

Use of reserpine and 6-hydroxydopamine supports evidence for purinergic cotransmission in the rabbit ear artery.

The relative roles of noradrenaline and ATP in the contractile response of the rabbit central ear artery following electrical stimulation of the sympathetic perivascular nerves were investigated after treatment with reserpine and 6-hydroxydopamine. In control tissues, electrical stimulation produced frequency-dependent contractile responses that were reduced, but not abolished, following incubation with the alpha 1-adrenoceptor antagonist prazosin (10(-6) M). Desensitisation of the P2X-purinoceptor by alpha,beta-methylene ATP (10(-6) M) abolished the prazosin-resistant component of the response. Tissues removed from reserpine-pretreated animals responded to electrical stimulation with small, frequency-dependent contractions, despite a dramatically reduced tissue noradrenaline content. Prazosin (10(-6) M) had no significant effect on these contractile responses. Following P2X-purinoceptor desensitisation, the neurogenic responses were virtually abolished. Tissues that had been incubated with 6-hydroxydopamine failed to respond to electrical stimulation at the parameters used in the control and reserpine-pretreated vessels. This study provides supporting evidence for the involvement of noradrenaline and ATP in sympathetic cotransmission in the rabbit central ear artery.

Adenosine Triphosphate↗
PubMed1990

Increase in galanin and neuropeptide Y mRNA in locus coeruleus following acute reserpine treatment.

Galanin and neuropeptide Y are known to coexist with noradrenaline in neurones of the locus coeruleus. Furthermore, reserpine depletes noradrenaline from, and increases the synthesis and activity of the catecholamine-synthesizing enzyme tyrosine hydroxylase in, this nucleus. We have found by in situ hybridization of specific 35S-labelled oligonucleotide probes that a single dose of reserpine (10 mg/kg) induced a significant (70-145%) and long-lasting (up to at least 3 days) increase in the amount of galanin and neuropeptide Y mRNA in the locus coeruleus (along with the characteristic increase in tyrosine hydroxylase mRNA). These results suggest a similar reserpine-sensitive mechanism of galanin, neuropeptide Y and tyrosine hydroxylase gene regulation.

Animals↗
PubMed1991

Postsynaptic dopamine/adenosine interaction: II. Postsynaptic dopamine agonism and adenosine antagonism of methylxanthines in short-term reserpinized mice.

Caffeine and its first-stage metabolites (paraxanthine, theophylline and theobromine) caused a significant potentiation of the locomotor activity induced by bromocriptine, 5 mg/kg, in mice pretreated with reserpine, 5 mg/kg (4h prior to the start of motor activity recordings). None of these substances significantly enhanced locomotor activity in reserpinized mice when administered alone. The rank order of potency was caffeine greater than paraxanthine greater than theophylline greater than theobromine. A high dose of a D-2 antagonist (sulpiride 100 mg/kg) caused a marked inhibition of the locomotor activity induced by bromocriptine, 5 mg/kg, plus 25 mg/kg of caffeine, paraxanthine or theophylline. However, a high dose of a D-1 antagonist (SCH-23390 1 mg/kg) caused a significant decrease of the locomotor activity induced by bromocriptine 5 mg/kg, plus 25 mg/kg of caffeine or paraxanthine, but did not change the locomotor activity caused by bromocriptine, 5 mg/kg, plus theophylline 25 mg/kg. The inhibitory effect of 5'-(N-ethyl)carboxamido-adenosine (NECA), 0.025 mg/kg, on bromocriptine-induced locomotor activation in reserpinized mice was reversed by the simultaneous administration of 10, 25 and 50 mg/kg of caffeine, paraxanthine or theophylline. The rank order of potency for reversal was theophylline greater than paraxanthine = caffeine. We suggest that methylxanthines act postsynaptically by potentiating the effects of D-2 stimulation and that this potentiation can be produced by D-1 agonism (paraxanthine or caffeine) and by adenosine antagonism (theophylline, paraxanthine or caffeine), most probably involving A-2 receptors.

Adenosine↗
PubMed1991

Differential response of striatal dopamine and muscarinic cholinergic receptor subtypes to the loss of dopamine. II. Effects of 6-hydroxydopamine or colchicine microinjections into the VTA or reserpine treatment.

In the previous paper it was demonstrated that striatal dopamine (DA) D1 and D2 receptor subtypes and muscarinic M1 and M2 receptor subtypes show differing responses to lesions of the mesostriatal DA system. To examine this differential regulation further rats were given unilateral injections of 6-hydroxydopamine (6-OHDA) or colchicine into the ventral tegmental area (VTA), or treated chronically with reserpine or saline. Two weeks later the animals were tested for their behavioral response to a subthreshold dose of apomorphine and 24 h later their brains were removed and processed for quantitative autoradiography or for analysis of DA levels by high-performance liquid chromatography. The 6-OHDA-lesioned animals showed a supersensitive rotational response to apomorphine. The loss of DA, loss of DA uptake sites, regulation of DA D1 and D2 receptors and regulation of the muscarinic cholinergic system was similar to the previous paper. Injection of colchicine in the VTA resulted in incomplete loss of striatal DA (50%), [3H]mazindol binding (50%), and no behavioral supersensitivity to apomorphine. There was a small loss of presynaptically located D2 receptors (13%). Similar to the 6-OHDA lesions there was a loss of D1 (12%) and M1 receptors. Reserpine treatment produced an 86% decrease in DA levels, an enhanced stereotyped responsiveness to apomorphine, and an increase of both D2 (28%) and D1 receptors (26%). There was a loss of muscarinic M1 but not M2 receptors. Thus removal of DA terminals or blockade of transport of proteins in the mesostriatal axons can lead to a reduction in D1 receptor density in the striatum. In contrast, loss of DA without removal of DA terminals leads to a significant up-regulation of the D1 receptor. D2 receptors show increases following removal of DA or of DA terminals. Alteration in the muscarinic cholinergic system following damage to the mesostriatal DA system is a complex response not mimicked by either reserpine or colchicine treatment.

Animals↗
PubMedDate not supplied

Comparative effects of prolactin, perphenazine and reserpine on non-arteriosclerotic (virgin) vs arteriosclerotic (breeder) rats.

Non-arteriosclerotic, virgin and arteriosclerotic breeder rats were subjected to chronic treatment with prolactin or prolactin-releasing drugs such as perphenazine and reserpine for 12 weeks. Males and females responded to the prolactin as evidenced by increased milk secretion, adrenal hyperplasia and thymus gland involution. Although the prolactin- and reserpine-treated animals gained weight and manifested pituitary gland basophilia, the perphenazine-treated animals showed considerable loss of body weight as well as involution of the pituitary gland, ovaries and testes, suggesting a condition of induced hypopituitarism. Chronic treatment with prolactin, both directly and indirectly, caused uniform increases in serum enzymes, e.g., CPK, SGOT, SGPT and LDH, lipids, e.g., triglycerides, free fatty acids and cholesterol, glucose and BUN. Corticosterone production was enhanced by prolactin, reduced by perphenazine and unaffected by reserpine. Prolactin did not induce any arterial disease in the arteriosclerosis-resistant, virgin rats but it did cause eracerbation of the usual severity of arteriosclerosis in the hilar renal arteries of the arteries sclerosis-prone, breeder rats as well as an increased incidence of "old" and "new" foci of myocardial necrosis, characteristically found in breeder rats. It is suggested that hypothalamic control of prolactin as well as ACTH release may play a role in the spontaneous arteriosclerosis which develops in repeatedly-bred, male and female rats.

Alanine Transaminase↗
PubMed1983

Lithium attenuates dopamine depleting effects of reserpine and tetrabenazine but not that of alpha methyl-p-tyrosine.

Concurrent administration of lithium (Li) significantly attenuates the dopamine (DA) depleting effects of reserpine and tetrabenazine, but does not change alpha-methyl-p-tyrosine (AMPT) induced DA depletion in rat brain. This effect of Li is probably mediated, in part, by inhibiting the magnesium-dependent binding of both reserpine and tetrabenazine to their specific receptor sites. Such interaction between these drugs may attenuate the beneficial effects of tetrabenazine and reserpine on patients with tardive dyskinesia or tardive dystonia who are treated concurrently with lithium for their psychiatric disorder.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

The effect of nicotine pretreatment on the gastric mucosal damage induced by aspirin and reserpine in rats.

The effect of nicotine pretreatment by feeding nicotine (5mcg/ml) in drinking water ad libitum for 10 days was studied on the aspirin and reserpine induced gastric mucosal damage in rats. The administration of nicotine resulted in the significant augmentation of aspirin (P less than 0.01) and reserpine (P less than 0.05) induced gastric ulcers. The mechanism(s) involving the sensitization of gastric mucosa towards the ulcerogenic effect of aspirin and reserpine may be responsible for the increased intensity of gastric ulcers in both the groups. The study indicates the possibility of a similar interaction in heavy smokers who ingest these drugs.

Animals↗