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PubMed1987

Phencyclidine-induced head-weaving and head-twitch through interaction with 5-HT1 and 5-HT2 receptors in reserpinized rats.

Phencyclidine mainly produced head-weaving and head-twitches at doses of 5-7.5 mg/kg and of 7.5-12.5 mg/kg, respectively. Phencyclidine-induced head-twitches and head-weaving were blocked by pretreatment with ritanserin (1 mg/kg), a selective serotonin (5-HT)2 receptor antagonist and with pindolol (20 mg/kg, s.c.), a 5-HT1 receptor antagonist, respectively. In reserpine-pretreated rats, the degree of utilization of 5-HT and the number of 5-HT1 ([3H]5-HT) and 5-HT2 ([3H]ketanserin) binding sites were significantly increased compared with the figures for the vehicle-pretreated rats. The intensity of phencyclidine-induced head-weaving (at the dose of 2.5 mg/kg) and head-twitch (at the doses of 2.5 and 5 mg/kg) was significantly increased in reserpine-pretreated rats compared with that of vehicle-pretreated rats. Furthermore, in the reserpine-pretreated rats, the intensity of phencyclidine (1.25 mg/kg)-induced head-weaving and head-twitches was increased in combination with imipramine, while the intensity of phencyclidine (2.5 mg/kg)-induced head-weaving and head-twitch was decreased by pretreatment with mianserin, a non-selective 5-HT receptor antagonist. These results indicate that phencyclidine induced head-weaving by interacting with 5-HT1 receptors, indirectly after the release of 5-HT and/or with some other mechanisms and induced head-twitch by interacting with 5-HT2 receptors directly and/or indirectly.

Animals↗

PubMed1985

Effect of nicotine and caffeine pretreatment on the gastric mucosal damage induced by aspirin, phenylbutazone, and reserpine in rats.

The effect of nicotine and caffeine pretreatment by feeding nicotine (2.5 mg %), caffeine (30 mg % base), and their combination (nicotine 2.5 mg % + caffeine 30 mg %) in drinking water ad libitum for 21 days was studied on the gastric mucosal damage induced by aspirin, phenylbutazone, and reserpine in rats. When given alone, neither nicotine nor caffeine produced any visibly discernible gastric lesions. Their concurrent administration too, did not produce any gastric mucosal injury. Pretreatment with nicotine, caffeine, and their combination resulted in significant augmentation of gastric ulcers produced by aspirin, phenylbutazone, and reserpine. However, caffeine administration produced a comparatively less profound augmentation of experimentally induced gastric lesions than that produced by nicotine pretreatment. The enhancement of gastric ulcers in the groups pretreated with the combination of nicotine and caffeine followed by one of the drugs was significantly greater than in the groups treated by either of them alone. The effect of nicotine on the mucus neck cell population of the gastric mucosa and on pancreatic bicarbonate secretion and the gastric secretory effect of caffeine may be responsible for the potentiation of the ulcerogenic effects of aspirin, phenylbutazone, and reserpine.

Administration, Oral↗

PubMed1982

Medical management of patients following a ruptured cerebral aneurysm, with epsilon-aminocaproic acid, kanamycin, and reserpine.

Patients suffering from a subarachnoid hemorrhage who were admitted to the Neurosurgical Unit of the Royal Perth Hospital during the period 1971 to 1979 were assessed with regard to the effectiveness of preoperative treatment with epsilon-aminocaproic acid, kanamycin, and reserpine. Forty-two patients who were treated with epsilon-aminocaproic acid had a rebleed rate of 2.3% compared to 1 9.7% rebleed rate in appropriately selected controls. Patients treated with kanamycin and reserpine had a preoperative cerebral vasospasm rate of 32% compared to a 26% rate in controls; however, kanamycin and reserpine were found useful for decreasing the postoperative complications of cerebral vasospasm.

Aminocaproates↗

PubMed1979

Diurnal rhythms in noradrenaline turnover and motility after reserpine and 6-hydroxydopamine.

Experiments were performed in male Wistar rats synchronized by controlled conditions of light (0700--1900 hr) and of darkness (1900--0700 hr). Separately in each photo-period the effects of reserpine or 6-OHDA on the cardiac noradrenaline turnover. Whereas peripheral chemical sympathectomy did not greatly affect the diurnal rhythm in the motor activity were investigated. Initial depletion of the cardiac noradrenaline after acute application of either drug was significantly greater when injected at 2000 hr compared to 0800 hr. In both photo-periods the cardiac turnover of noradrenaline was increased after peripheral chemical sympathectomy with 6-OHDA as well as after amine depletion with reserpine. Inhibition of the protein synthesis had no effect, ganglionic blockade by chlorisondamine on the other hand abolished the rhythm in the motor activity, subacute treatment with reserpine differently affected motor activity in both photo-periods, depending on the time of drug application within 24 hr of a day. The results show that diurnal variations in the levels of neuronal and of motor activity are able to influence drug effects and have thus to be taken into account in animal studies.

Animals↗

PubMed1982

Locomotor hypokinesia in the reserpine-treated rat: drug effects from the corpus striatum and nucleus accumbens.

A mechanographic method was used to assess the locomotor performance induced by apomorphine or other dopaminergic drugs in reserpine-treated rats. Reserpine was found to induce locomotor hypokinesia. The hypokinesia was dose-dependently reversed by apomorphine (APO), bromocriptine and pergolide. Locomotion was induced by microinjection of APO into the nucleus accumbens. No locomotor effect was found after injection into corpus striatum. Injection into both nuclei was not superior to accumbens only. Intra-striatal or intraaccumbens injections of trifluoperazine blocked the effect on locomotion by systematic apomorphine. The results confirmed that reserpine-induced locomotor hypokinesia is reversed by dopaminergic stimulation in the nucleus accumbens. There were indications that blockade of striatal or accumbens' dopamine receptors counteracts apomorphine-induced locomotion presumably by interaction with postural motor control. Evidence was found for separate dopaminergic control of locomotion and muscletone. This may be of importance for the development of new antiparkinson drugs.

Animals↗

PubMed1987

Reserpine-induced hypothermia: participation of beta 1 and beta 2 adrenergic receptors.

In mice, reserpine-induced hypothermia is partly antagonized by clenbuterol, a beta-adrenergic agonist specific for beta 2 receptors, and completely antagonized by dobutamine, a beta-adrenergic agonist specific for beta 1 receptors. In addition, the effects of dobutamine and of clenbuterol are impaired by betaxolol (1 and 4 mg/kg) and unchanged by ICI 118,551 (1 and 4 mg/kg) beta-blocking drugs respectively selective for beta 1 and beta 2 receptors. These results indicate that reserpine-induced hypothermia depends on the beta 1 receptors and lend support to an indirect effect of clenbuterol. After a chronic treatment, clenbuterol-induced antagonism of reserpine hypothermia is facilitated. This facilitation is impaired by ICI 118,551 and by betaxolol but, in this last case, with high doses only. So the facilitation involves beta 2 adrenergic receptors and implies an increase in the sensitivity of beta 1 receptors.

Animals↗

PubMed1990

Effect of reserpine on retention of the conditioned NK cell response.

The effect of reserpine and 6-hydroxydopamine on the learned conditioned natural killer (NK) cell response was investigated in mice. Reserpine given at 2.5 mg/kg, 24 hr prior to reexposure to camphor-conditioned stimulus on days 6 and 8 blocked the recall of conditioned NK cell response to a significant extent. In other words, the NK cell activity of conditioned mice, treated with reserpine and reexposed to the conditioned stimulus, was similar to the nonconditioned (NC) group. A conditioned increase in NK cell response was still evident in mice treated with 6-OHDA.

Animals↗

PubMed1991

CY 208-243 behaves as a typical D-1 agonist in the reserpine-treated mouse.

The object of this study was to determine if the newly developed phenanthridine derivative, CY 208-243, retains its apparent in vivo preference for dopamine D-1 receptors under conditions of dopamine depletion, as a starting point to understanding why CY 208-243 possesses antiparkinson activity and the selective D-1 agonist SKF 38393 does not. Three hours after receiving reserpine (5 mg/kg), mice were strongly sedated and completely unresponsive to the motor stimulant effects of CY 208-243 (0.1-10 mg/kg) or the selective D-2 agonist RU 24213 (0.5-5 mg/kg) administered alone. After 24 h reserpine, the akinesia was partially and dose-dependent reversed by both CY 208-243 (0.1-10 mg/kg) and RU 24213 (0.5-5 mg/kg) alone. CY 208-243 also stimulated rearing and grooming, while RU 24213 gave rise to strong head-down sniffing. The response to 1 mg/kg CY 208-243 was practically abolished by pretreatment with the D-1 antagonist SCH 23390 (0.2 mg/kg). On the other hand, blocking D-2 receptors with metoclopramide (0.25 mg/kg) unexpectedly facilitated CY 208-243-induced locomotion and rearing, but suppressed grooming. When CY 208-243 (1 mg/kg) was injected together with RU 24213 (0.5-5 mg/kg), the two drugs interacted synergistically to stimulate locomotion at all times after reserpine. These animals also exhibited a greater preponderance of grooming, sniffing, gnawing and oral dyskinesia. Apart from the potentiation of some elements of CY 208-243-stimulated motor behaviour by D-2 blockade, these results are qualitatively indistinguishable from those previously obtained with the prototype D-1 agonist SKF 38393.(ABSTRACT TRUNCATED AT 250 WORDS)

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

PubMed1993

Effects of acute haloperidol and reserpine administration on vacuous jaw movements in three different age groups of rats.

In these experiments three different age groups of rats were tested for vacuous jaw movements. The age groups included rats aged 3 months, rats aged 6-9 months, and rats aged 12-15 months. In the first experiment, rats were given a single IP injection of either 0.3% tartaric acid vehicle or 0.4 mg/kg haloperidol. In the second experiment, rats were given injections of vehicle or 5.0 mg/kg reserpine. Haloperidol and reserpine significantly increased vacuous jaw movements. There were significant effects of age on vacuous jaw movements, with rats aged 6-9 months and rats aged 12-15 months showing more jaw movements than 3-month-old rats. In both experiments, the drug x age interaction was not significant, indicating that the combined effects of age and neuroleptic treatment were additive and not synergistic. Haloperidol and reserpine also reduced rearing behavior in all age groups. It is concluded that age is an important variable in studies of vacuous jaw movements.

Aging↗

PubMed1991

Neuropeptide Y and tyrosine hydroxylase mRNA levels in the locus coeruleus show similar increases after reserpine treatment.

In situ hybridisation histochemistry was used to study the effect of intra-peritoneal reserpine administration on messenger RNA (mRNA) levels in the locus coeruleus (LC) of the rat. 48h after injection, levels of mRNA encoding tyrosine hydroxylase (TH) and neuropeptide Y (NPY) in the LC increased to approximately 250% of control values (p less than 0.05). The level of beta-tubulin mRNA was unaffected by reserpine administration. The similar and selective increase in TH and NPY mRNA in the LC following reserpine administration suggests that NPY may play a role in the neurotransmitter function of this catecholaminergic nucleus.

Animals↗

PubMed1981

The prolactin-stimulating potency of reserpine in man.

The prolactin (PRL) response to 0.5 mg i.m. of reserpine was compared to 0.5 mg i.m. of haloperidol in eight young men. The fact that reserpine was found to be a potent releaser of PRL--significantly greater than haloperidol--suggests a major role of storage pool dopamine in regulating PRL Secretion. Since the PRL response to neuroleptics is highly correlated with clinical potency, reserpine could be a potent antipsychotic, and further clinical trials are indicated.

Adult↗

PubMed1995

Effect of reserpine treatment on enkephalin mRNA level in the rat striatum: an in situ hybridization study.

We investigated the molecular mechanisms responsible for the preproenkephalin A mRNA increase following catecholamine depletion by reserpine using quantitative in situ hybridization at the cellular level. Macroscopic analysis showed that short term reserpine treatment increases the preproenkephalin A mRNA level in the rat striatum to +40.2 +/- 9%. Microautoradiography analysis demonstrated different increases in the preproenkephalin A mRNA level in different parts of the striatum: +124 +/- 22% in the dorso-median striatum, +131 +/- 19% in the dorso-lateral striatum, +119 +/- 8% in the ventro-lateral striatum and +75 +/- 6% in the ventro-median striatum. We found no difference in the number of cells expressing PPA mRNA in reserpine treated rats suggesting that these increases are only due to an increase in the number of mRNA expressed by cell.

Animals↗

PubMed1984

Depletion and recovery of neuronal monoamine storage in rats of different ages treated with reserpine.

The effect of reserpine on dopamine, noradrenaline, adrenaline and serotonin concentrations in different brain regions, and the recovery of normal levels of these monoamines after such treatment were studied in rats aged 5, 15 and 27 months. In a preliminary experiment we found that distribution of the drug was not altered in the aged rats. Then we observed that a single dose of reserpine (5 mg/kg IP) had a similar depleting effect on all the brain monoamines, in all the brain regions considered in all three age groups. The curves expressing recovery of monoamine storage in all the nerve terminals, several days after treatment, were superimposable. These results suggest that in the rat, age does not influence the effect of reserpine on the storage mechanism of brain monoamines. Moreover, as restoration of this mechanism depends on the synthesis of new vesicles, the similarity in the rates of recovery in adult, old and very old rats indicated indirectly that synthesis of these neuronal organelles is not affected by aging.

Aging↗

PubMed1989

The effects of posture changes on blood pressure and heart rate of anesthetized and reserpinized sloths.

1. Tilting sloths anesthetized with chloralose from erect to supine or supine to erect produced little or no effect on heart rate. 2. Tilting anesthetized sloths from erect to supine increased both systolic and diastolic pressures significantly and by about the same amounts. The maximum effect was produced in 20 sec. 3. Pressures stabilized at a higher level than in the erect posture but below the maximum reached in tilting. 4. Tilting these sloths from the supine to the erect posture resulted in a rapid (20 sec) and dramatic fall in pressures to below the initial erect pressure levels. Return to initial erect levels took place slowly. 5. Tilting reserpinized sloths from erect to supine or supine to erect produced little or no effect on heart rate. 6. Tilting reserpinized sloths from erect to supine increased both systolic and diastolic pressures materially and by similar amounts. The maximum effect took 50 sec. 7. Pressures stabilized at higher levels than in the erect posture but less than maximum reached with tilting. 8. Tilting these sloths from supine to erect caused significant falls in pressure to slightly below the initial erect pressure, with maximum effect reached in 30 sec and eventual return to control level. 9. Pressure changes were almost entirely the result of altered venous return. 10. Neither chloralose nor reserpine completely blocked vascular control but reduced it materially.

Anesthesia↗

PubMed1985

Reserpine-induced potentiation of the inhibitory action of neuropeptide Y on the rat vas deferens neurotransmission.

The inhibitory action of neuropeptide Y (NPY) on the muscular activity of the prostatic end of the rat vas deferens elicited by transmural electrical stimulation was examined in control and in reserpinized rats. Pretreatment with 1 mg/kg reserpine for 48 h induced a 6-fold increase in NPY potency. Likewise, the potency of clonidine to inhibit the electrically induced muscular activity or noradrenaline to contract the ductus musculature was also potentiated. It is hypothesized that reserpine via a denervation super-sensitivity-like process increases the density of the NPY receptors. The functional significance of NPY in the motor activity of the vas deferens is discussed.

Animals↗

PubMed1986

Reserpine-induced up-regulation of dopamine D2 receptors in the rat striatum is enhanced by denervation but not by chronic receptor blockade.

Compensatory increases in the density of dopamine (DA) D2 receptors in the rat striatum occur following chronic interruption of dopaminergic neurotransmission. Substantia nigra lesions, DA depletion with reserpine and D2 receptor blockade by neuroleptics increase the number of striatal D2 receptors as identified with the D2 ligand, [3H]spiperone [( 3H]SPIP). Chronic administration of haloperidol to substantia nigra-lesioned rats causes an additive increase in binding over levels obtained with one treatment alone. In this study we have found a similar response when lesioned animals are treated with reserpine. However, compensatory increases in the number of [3H]SPIP binding sites found after combined administration of reserpine and haloperidol to intact rats do not exceed levels obtained following administration of either drug alone. The data suggest that up-regulation of striatal D2 binding sites occurring after substantia nigra lesions is unique relative to other forms of up-regulation and may involve the loss of a presynaptic regulatory factor other than DA.

Animals↗

PubMed1996

The influence of dizocilpine (MK-801) on the reserpine-enhanced electromyographic stretch reflex in rats.

The electromyographic (EMG) stretch reflex in the gastrocnemius and tibialis anterior muscles was elicited by passive bending and stretching of the rat's hind foot in the ankle joint. The EMG stretch reflex was increased by pretreatment with reserpine (10 mg/kg ip) which is a model compound commonly used to induce parkinsonian rigidity in laboratory animals. Dizocilpine (MK-801) (0.32, 0.64 and 1.28 mg/kg sc) inhibited long-latency supraspinal components of the reserpine-increased EMG stretch reflex, whereas a short-latency spinal component was not diminished. The present results suggest that MK-801 exhibits an antiparkinsonian action against reserpine-induced rigidity.

Animals↗

PubMed1982

The influence of reserpine on nitrogen metabolizing enzymes in chick liver.

Reserpine, a Rauwolfia alkaloid, was shown to increase activity of the hepatic nitrogen metabolizing enzymes xanthine dehydrogenase, purine nucleoside phosphorylase, and tyrosine aminotransferase, when administered orally to young chicks. Using immunochemical techniques, this increase in xanthine dehydrogenase was shown to result from an enhanced de novo enzyme synthesis. The response pattern of the three enzymes to reserpine follows the same pattern to induction by high dietary protein suggesting that a common mode of action may be involved in the regulation of these enzymes. Alpha-Adrenergic blockers, phentolamine and phenoxybenzamine, effectively prevented the increased enzyme activities caused by administration of reserpine.

Adrenergic alpha-Antagonists↗