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PubMed1984

Reserpine induction of tyrosine hydroxylase in paraplegia.

Reserpine induction of tyrosine hydroxylase (TH) activity reflects the biochemical adaptability of sympathetic neurons. Midthoracic spinal cord transection in adult animals precludes TH induction in the sixth lumbar (L6) ganglion, a ganglion innervated by spinal segments caudal to the lesion. However, in animals receiving lesions as neonates, an elevation in L6 ganglion TH activity occurred after reserpine. This retained biochemical adaptability indicates an increased recuperative capacity of developing neurons.

Animals↗
PubMed1989

Depletion of serotonin using p-chlorophenylalanine (PCPA) and reserpine protects against the neurotoxic effects of p-chloroamphetamine (PCA) in the brain.

The present study attempts to determine whether the neurotoxicity of p-chloroamphetamine (PCA) is dependent on a releasable pool of serotonin (5-HT). Rats treated with PCA alone or with reserpine and PCA exhibit a profound loss of 5-HT innervation in cerebral cortex after a 2-week survival period. However, depletion of 5-HT by combined treatment with p-chlorophenylalanine (PCPA) and reserpine provides substantial protection against the neurotoxic effects of PCA. These results indicate that release of 5-HT is a necessary step in the neurotoxicity of PCA and that a peripheral source of 5-HT is involved. We suggest that 5-HT release from platelets into the peripheral circulation may result in the formation of a neurotoxic 5-HT metabolite.

Amphetamines↗
PubMed1987

Effects of reserpine and chlorpromazine on the serotonin, norepinephrine, and epinephrine levels in the pineal-paraphyseal complex of soft-shelled turtles (Lissemys punctata punctata).

Turtles were injected intramuscularly with reserpine (0.5 mg/100 g body wt) and chlorpromazine (10 mg/100 g body wt) at 2400, 1800, and 0600 hr and were sacrificed at 6, 12, and 24 hr, respectively after the treatments, i.e., at 0600 hr. The spectrofluorometric findings revealed that the serotonin, norepinephrine, and epinephrine contents of the pineal-paraphyseal complex decreased at 6 hr, increased at 12 hr, and declined again at 24 hr after the treatments. It is suggested that reserpine and chlorpromazine act largely by favoring release with transient resynthesis of these amines in the pineal-paraphyseal complex of soft-shelled turtles.

Animals↗
PubMed1985

Estradiol increases growth hormone secretion in rats exposed to swimming stress or reserpine treatment.

The secretory pattern of growth hormone (GH) in female rats differs from that in males with respect to e.g. the inter-peak baseline levels being higher in females. In the present study the influence of sex steroids on plasma GH levels was investigated in male rats under various conditions. Administration of estradiol, but not testosterone, was found to increase GH release in rats with suppressed levels induced by exposure to swimming stress or by treatment with the monoamine depleting agent reserpine. In line with previous studies, administration of estradiol was found to increase also inter-peak GH levels in adult male rats; i.e. to cause a feminization of the secretory pattern. In stressed and in reserpinized animals as well as in normal male rats, the effect of estradiol is similar to that earlier demonstrated for somatostatin antiserum, and hence it is suggested that estradiol may act antagonistic to the GH inhibiting factor.

Animals↗
PubMed1986

The effects of reserpine and haloperidol on tyrosine hydroxylase activity in the brains of aged rats.

Many neurotransmitter systems appear to be altered with aging. The effects of aging on the regulation of tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of catecholamines in the brain has been examined. The endogenous basal activity of tyrosine hydroxylase was lower in the hypothalamus of 24 month old Fisher 344 rats than in the hypothalamus of 3 month old or 6 month old animals. There was no difference in the basal activity of tyrosine hydroxylase in the locus ceruleus, frontal cortex, hippocampus, substantia nigra, or the striatum of rats of ages 3 months, 6 months and 24 months. Tyrosine hydroxylase activity was increased in the striatum of 3 month old (60%) and 6 month old (28%) rats after treatment with haloperidol or reserpine, whereas no change in enzyme activity followed administration of these drugs to 24 month old animals. In conclusion, increases in tyrosine hydroxylase activity in the brain that normally occur in the striatum of 3 month old rats after haloperidol or reserpine treatment are significantly decreased in 6 month old rats and not apparent in 24 month old rats.

Aging↗
PubMed1991

Reserpine-induced post-receptor reduction in muscarinic-mediated airway smooth muscle contraction.

Radioligand binding was conducted on airways of the rat and human, surgically subdivided into trachea, lung airways, and parenchyma. 3H-QNB bound uniformly to receptors in separate sections of the rat and human airway. Receptor densities generally were ranked: lung airways greater than trachea greater than parenchyma. Receptor subtypes were identified mostly by pirenzepine displacement of bound 3H-QNB. The rat trachea, and rat and human lung airways had a uniformly low affinity for pirenzepine while rat and human parenchyma demonstrated both high and low affinity pirenzepine binding. Inhibition of methacholine-stimulated smooth muscle contraction by the M1 receptor antagonist, pirenzepine, and M2 receptor antagonist, gallamine, was studied in rat trachea and bronchus in vitro. Schild plot pA2 values were compatible with low potency antagonism, thereby favoring the presence of M3 receptors at these smooth muscle sites. Reserpine treatment of rats (0.5 mg kg-1 day-1 for 7 days) produced a decrease in peak tension in response to methacholine without changing the muscarinic receptor character (Kd 3H-QNB), population density (Bmax in fmol mg-1 protein), or function (methacholine EC50). These results indicate that muscarinic receptor heterogeneity exists in the airway of both laboratory rat and man. While the muscarinic receptor subserving airway smooth muscle contraction appears to be the M3 subtype, decreased contractile responses to methacholine by trachea and bronchus from reserpine-treated rats were receptor independent.

Animals↗
PubMed1992

Subacute reserpine treatment reveals preferential coupling between the M3 muscarinic receptor subtype and phosphatidylinositol turnover.

Muscarinic receptors in the rat cerebral cortex, cardiac atria and vas deferens were identified, quantitated, and characterized relative to phosphatidylinositol (PI) turnover as the functional response to stimulation of specific receptor subtypes. Receptor densities as determined by 3H-QNB binding were ranked: cerebral cortex greater than vas deferens greater than heart. Using displacement of 3H-QNB binding by the selective M1 and M2 muscarinic receptor antagonists pirenzepine and 11[[2-[(diethylamino)methyl]-1-piperidinyl]acetyl]-5,11-dihydro- 6H-pyrido [2,3-b] [1,4] benzodiazepine-6-one (AF-DX 116) respectively, heterogeneous populations were found in the cerebral cortex and vas deferens. The M1 receptor subtype predominated in the former and the M2 predominated in the latter. An homogeneous M2 receptor population was present in the heart. Methacholine-stimulated accumulation of 3H inositol-1-phosphate was greater in the vas deferens than in the cerebral cortex, whereas PI turnover was not enhanced in cardiac atria. Reserpine treatment of rats (0.5 mg kg-1 day-1 for 7 days) increased muscarinic receptor density in the vas deferens coincident with a shift in the low affinity pKi for AF-DX 116 to a value comparable to high affinity binding, and abolished the enhanced PI hydrolysis. In the cerebral cortex, reserpine treatment shifted only the early portion of the methacholine dose-response curve to the right. These results are judged to be supportive of preferential coupling between the M3 muscarinic receptor subtype and PI turnover.

Animals↗
PubMed1985

Effects of lithium in vitro on noradrenaline-induced cyclic AMP accumulation in rat cortical slices after reserpine-induced supersensitivity.

Lithium in vitro at concentrations of 1-2 mM and above inhibited cyclic AMP accumulation due to noradrenaline in cerebral cortical slices prepared from both control rats and rats rendered supersensitive for the noradrenaline response by intraperitoneal injection of reserpine. There was no difference in the concentration-dependence of lithium inhibition between control and reserpine-treated rats.

Animals↗
PubMed1987

Pharmacological characteristics of tremor, rigidity and hypokinesia induced by reserpine in rat.

The experiments characterized the dose- and time-dependence of parkinsonian motor signs induced by reserpine in rats and a standardized system of manipulation of animals, evaluation of symptoms and analysis of data was devised. The assay procedure yielded no more than 0.5, 4.5 and 0.0% false positives with the evaluation of tremor, rigidity and hypokinesia, respectively. A dose-dependent and often complete blockade of all three signs was obtained with L-DOPA plus carbidopa (10:1) as well as with other classes of pharmacological agents that are used in the treatment of Parkinson's disease, i.e. direct or indirect dopamine (DA) agonists (amantadine, pergolide, lisuride) and inhibitors of monoamine oxidase (MAO) (clorgyline, pargyline, deprenyl, tranylcypromine). The inhibitor of the uptake of DA, nomifensine, and anticholinergics, 5-hydroxytryptamine (5-HT) antagonists, histamine antagonists and tricyclic antidepressants exerted little or no effect. The effects of putative agonists and antagonists at alpha 1- and alpha 2-adrenoceptors were also examined. Yohimbine blocked tremor and rigidity, but not hypokinesia, at 0.66 and 0.28 mg/kg, respectively. It is suggested that alpha-adrenergic mechanisms and, in particular, alpha 2-adrenoceptors, may be involved in reserpine-induced tremor and rigidity. Noradrenergic and dopaminergic systems can conceivably interact to progressively generate these different motor signs.

Animals↗
PubMed1988

Reserpine, para-chlorophenylalanine and fenfluramine antagonise cisplatin-induced emesis in the ferret.

The involvement of 5-hydroxytryptamine (5-HT) with cisplatin-induced emesis in the ferret was investigated using reserpine, para-chlorophenylalanine and fenfluramine. Pretreatment with reserpine (5 mg/kg, 24 hr), fenfluramine (5 mg/kg, 4 days) or para-chlorophenylalanine (100 or 400 mg/kg, 4 days) antagonised cisplatin-induced emesis. All treatments reduced the levels of 5-HT in the area postrema and at other cerebral sites, but whilst this action was relatively selective for small doses of para-chlorophenylalanine [only modest effects on noradrenaline (NA) and no change in the content of dopamine (DA) in the area postrema], other treatments reduced levels of dopamine and noradrenaline. Data are discussed in terms of an involvement of 5-HT/catecholamines in the area postrema with the mediation of emesis induced by cisplatin.

Animals↗
PubMed1993

Reserpinization severs the cooperative but not the oppositional interaction between D1 and D2 receptors.

Dopamine D1 and D2 receptors in rat brain interact synergistically to produce stereotypy and antagonistically to induce atypical jerking. This study showed that repeated reserpine treatment (5 daily injections of 1 mg/kg, s.c.), which depleted dopamine stores by 98%, rendered D1 and D2 receptors independent with respect to the production of stereotypy, i.e. either D1- or D2-selective agonists given alone induced stereotypy. In contrast, the atypical jerking induced by the D2 agonist, quinpirole, was still inhibited by the D1 agonist, SKF 82958, indicating that reserpine treatment did not render these two receptors independent with respect to initiation of this behavior.

Animals↗
PubMed1976

Effect of 10 days reserpine or apomorphine administration on sleep cycles in rats.

The duration of sleep-wakefulness periods and sleep cycles was investigated by means of EEG and EMG in rats with implanted brain electrodes and myographic electrodes in neck muscles during 5 hr trials after repeated administration of 2 depressant drugs, reserpine and apomorphine. Ten days administration of reserpine at a dose of 0.05 mg/day, SC, decreased the duration of both slow-wave and paradoxical sleep, whereas apomorphine had no effect on sleep duration or occurance of sleep phases in either the low dose (0.2 mg/kg/day, SC) or in the high dose of 0.6 mg/kg/day, SC. This finding might be correlated with previously found differences in catecholamine levels in the brain in the same model experiments.

Animals↗
PubMed1978

Time-dependent effects of reserpine on retention of passive avoidance.

Reserpine produced amnesia for a one-trial passive avoidance task when given 2, 3, 4, 5 hr before but not when given 1, 8, 12, 24 hr or 30 min before, immediately, 90 min or 2, 4, 5, 6, 8, 9, 12, 24 hr following training. The results were discussed in terms of the reserpine effect on biogenic amines and their possible role in memory formation.

Animals↗
PubMed1982

Opposite effects of CRF and ACTH on reserpine-induced hypothermia.

The effects of CRF, ACTH 1-24, alpha-MSH, and an ACTH 4-49 analog, at doses of 0, 0.1, 1, and 10 mg/kg, were tested on temperature, ptosis, and sedation in mice pretreated 18 hr previously with reserpine. IP injection of CRF at doses of 1 and 10 mg/kg significantly potentiated the reserpine-induced hypothermia while ACTH 1-24 at the same two doses had the opposite effect of significantly reversing the hypothermia as compared to diluent. The highest dose of alpha-MSH exerted a similar action to that of ACTH 1-24, but none of the doses of the ACTH 4-9 analog changed body temperature. beta-endorphin also failed to cause a reliable effect even though naloxone blocked the action of CRF on body temperature. The results suggest that CRF, like other hypothalamic peptides, can exert extra-pituitary actions after peripheral administration.

Adrenocorticotropic Hormone↗
PubMed1986

Effects of amnesic doses of reserpine or syrosingopine on mouse brain acetylcholine levels.

The effects of reserpine and syrosingopine on mouse whole brain acetylcholine levels were examined. At 2 or 24 hr following injection, the brains were removed and analyzed by mass spectrometry. No differences were found between drug-treated and control mice in the acetylcholine content of the brain at either time interval. The results suggest that whole brain acetylcholine levels do not predict the amnesic effects of either reserpine or syrosingopine.

Acetylcholine↗
PubMed1994

Repeated renal and splenic sympathetic nerve stimulation in anaesthetized pigs: maintained overflow of neuropeptide Y in controls but not after reserpine.

The overflow and the arterial vascular effects of neuropeptide Y (NPY) in response to repeated sympathetic nerve stimulation of kidney and spleen were investigated in anaesthetized pigs. The responses under control conditions were compared to those evoked in pigs with tissue stores of noradrenaline (NA) selectively depleted by reserpine pretreatment combined with sympathetic nerve transection. The renal and splenic sympathetic nerves were repeatedly stimulated at 1 h intervals with one 5 Hz stimulation for 48 s and transmitter overflow determined. Between these stimulations, 5 min stimulations with bursts of 20 Hz (for 1 s every 10 s) were given in order to induce a depletion of nerve transmitter. In the control group, overflow of NPY and NA and vasoconstrictor responses were almost identical for the 5 consecutive stimulations in the kidney, whereas in the spleen the parameters showed a slight tendency to be reduced. In the reserpine-treated group, the initial evoked overflow of NPY was increased 8-fold and 3-fold in the kidney and spleen, respectively, compared to the control group. Upon each subsequent stimulation the overflow decreased gradually, in parallel with the evoked vasoconstrictor response. After a 2 h recovery period no change in evoked overflow of NPY compared to the amount released by the previous stimulation was observed. The present study illustrates, the high capacity of maintenance of not only NA but also NPY overflow and vascular responses in control conditions, whereas the enhanced release of NPY in the absence of NA cannot be maintained. It is therefore possible that the NA-mediated prejunctional feedback mechanism is important for the maintenance of a constant NPY release in situations of high sympathetic activation.

Anesthesia↗
PubMed1996

Prejunctional regulation of reserpine-resistant sympathetic vasoconstriction and release of neuropeptide Y in the pig.

The prejunctional regulation of non-adrenergic sympathetic vasoconstriction and release of neuropeptide Y (NPY) was investigated in vivo. In reserpinized pigs (with depleted noradrenaline (NA)), it was demonstrated that brief sympathetic nerve stimulation (2 pulses of 20 Hz) of the spleen, kidney and hind limb in the presence of the alpha 2-adrenoceptor agonist UK 14,304 (1 micrograms/kg per min i.v.) evoked reproducible vasoconstrictor responses which were reduced by 40-80% in comparison to that in the absence of UK 14,304. In addition, the splenic overflow of NPY-like immunoreactivity (-LI) was reduced. After cessation of the UK 14,304 infusion all these effects were reversed by addition of the alpha 2-adrenoceptor antagonist yohimbine (0.2 mg/kg i.v.). Also the Y2 receptor agonist NPY(13-36) reduced the splenic overflow of NPY-LI. Splenic vasoconstriction per se was evoked by another Y2 receptor agonist N-acetyl[Leu28Leu31]NPY(24-36), while no vascular effects in the kidney or hind limb were observed. Both Y2 agonists displaced [125I]NPY binding to splenic membranes with higher potency than the Y1-receptor agonist [Leu31Pro34]NPY(1-36). No evidence was obtained for angiotensin II mechanisms being important for the enhanced NPY release after reserpine in spite of elevated renin release. The present results show that in the absence of NA, repetition of brief sympathetic nerve stimulation evokes vascular effects and NPY-LI release which are repeatable and these effects are efficiently modulated via alpha 2-adrenoceptors. Furthermore, the Y2 receptors may mediate both prejunctional inhibition of NPY release, as well as postjunctional vasoconstrictor effects in the pig spleen.

Animals↗
PubMed1985

Immunohistochemical investigations of the influence of reserpine on the serotonin neuron system in the rat brain.

A peroxidase-antiperoxidase immunohistochemical method with serotonin antiserum was employed to investigate the influence of reserpine on serotonin neurons of rats which were sacrificed at various times after injection (10 mg/kg i.p.). The disappearance of serotonin immunoreactivity induced by reserpine was detected only in the perikarya after 15 min, and then rapidly proceeded to the terminals. Between 2 and 4 h, immunoreactivity completely disappeared throughout the brain. The immunoreactivity reappeared in the perikarya after 6 h, and progressed toward the terminals gradually. However, there was an obvious difference in the rate of recovery of immunoreactivity between areas. After 7 days, the immunoreactivity returned to control levels.

Animals↗