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PubMed1976

The inhibitory effect of reserpine on the active sodium transport across the frog bladder.

1. The effects of reserpine and harman derivatives on the sodium transport across the frog bladder were examined using a short-circuit current method. The effects of harman derivatives on the Na,K-ATPase activity of the frog kidney were also investigated. 2. Reserpine and harman derivatives inhibited active sodium transport of the frog bladder and their inhibitory effect decreased as reserpine greater than harmine greater than harmaline = harman greater than harmalol. 3. Harman derivatives inhibited Na,K-ATPase activity of the frog kidney. 4. These results suggest that reserpine and harman derivatives inhibit active sodium transport by suppressing the Na,K-ATPase activity of the frog bladder.

Adenosine Triphosphatases↗
PubMed1975

Electroconvulsive shock and postsynaptic catecholamine effects: increased psychomotor stimulant action of apomorphine and clonidine in reserpine pretreated mice by repeated ECS.

Male mice were administered electric convulsive shocks (ECS) once daily for one (ECS X I), three (ECS X III) or seven days (ECS X VII). One (day 1), three (day 3) or six days (day 6) later they received reserpine 10 mg/kg, followed 2 hours later by clonidine, 1.5 mg/kg, and/or apomorphine, 1.5 mg/kg. Control animals received the same drug treatments but no ECS. The motor activity was recorded for 1 hour, starting immediately after the last drug injection. The behavioral depression induced by reserpine was equally pronounced in ECS-pretreated animals as in the control animals. The psychomotor stimulant effects of clonidine and/or apomorphine, given after reserpine was, however, enhanced by pretreatment with ECS X VII, DAY 1. Pretreatment wit- ECS X VII increased the motor activity also in animals given reserpine, apomorphine and clonidine at day 3 or day 6. ECS X III was also effective in this respect at day 1, whereas ECS X I, day 1, was ineffective. Mice given ECS X VII but no drug treatment showed at day 1 an increased motor activity during the initial 10 min and a decreased activity during the last 10 of the 1 hour recording period. At day 3 and day 6 after ECS X VII the motor activity was increased in comparison to that in untreated control animals during the whole 1 hour period. Animals given repeated ECS furthermore showed increased irritability and reduced body weight. The results indicate that repeated ECS increase the sensitivity of postsynaptic catecholamine receptors in the brain or alter neuronal structures which are connected to these receptors.

Animals↗
PubMed1991

Difference in in vivo receptor binding between [3H]N-methylspiperone and [3H]raclopride in reserpine-treated mouse brain.

The in vivo binding of [3H]N-methylspiperone (NMSP) and [3H]raclopride was compared in mice treated with reserpine (5 mg/kg, 24 hr prior to the tracer injection). With both radioligands, selective accumulation of radioactivity in the striatum following intravenous injection was observed, whereas a relatively low accumulation and a rapid decline in radioactivity in the cerebellum was seen. Reserpine significantly decreased [3H]NMSP binding in vivo, however it increased [3H]raclopride binding. By compartment model analysis, it was found that the decrease in [3H]NMSP binding was primarily due to the decrease in the association rate (K3) and the increase in [3H]raclopride was due to the decrease in the dissociation rate (K4) in vivo. As both Kd and Bmax of dopamine D2 receptors have been reported to be unaltered by reserpine, these results suggested that some unknown factors except Kd and Bmax which influence on in vivo binding of receptors might be changed by reserpine. These results revealed that it is of importance to measure kinetics of ligand-receptor binding in vivo rather than static analysis. These two different types of radioligands can be combined to reveal functional roles of dopamine receptor in vivo, especially in the study of the human brain with positron emission tomography (PET).

Animals↗
PubMed1992

L-dopa infusion mode differentially affects corpus striatal dopamine efflux in the presence of reserpine.

In the present experiment we tested the effects of L-DOPA upon dopamine (DA) efflux in vitro from superfused corpus striatal tissue fragments in medium containing reserpine. The purposes of this experiment were first, to evaluate the effects of differing infusion modes of L-DOPA upon DA efflux under conditions in which DA storage capacity has been diminished, and second, to compare this L-DOPA stimulated DA efflux with that of other putative DA secretagogues such as amphetamine and potassium. No differences were obtained in stimulated DA efflux between superfusions performed in the presence or absence of reserpine (10 microM) in the medium when L-DOPA (5 microM) was infused in a continuous (70 minute) mode during the superfusion. In contrast, a continuous infusion of either amphetamine (10 microM) or high potassium (30 mM) resulted in significantly greater stimulated DA efflux in superfusions performed with reserpine in the medium. In addition, when L-DOPA (5 microM) was administered for a brief 10-minute infusion period, a significantly greater stimulated DA efflux was obtained with superfusions containing reserpine in the medium. These results suggest that the mode of L-DOPA infusion may be an important factor in regulating DA release under conditions of diminished DA storage capacity.

Amphetamine↗
PubMed1995

Does reserpine induce parkinsonian rigidity?

The aim of the study was to find out whether the reserpine-induced rigidity is similar to that seen in parkinsonism. Simultaneous measurements of the muscle resistance of the hind foot to passive bending and stretching in the ankle joint, as well as of the electromyographic (EMG) activity of the gastrocnemius and tibialis anterior muscles of rats were carried out. Reserpine was injected in a dose of 10 mg/kg alone or with alpha-methyl-p-tyrosine (250 mg/kg) 1, 4 and 27.5 h before the measurements. Reserpine increased the muscle resistance of the rat's hind leg to passive movements. That effect was the strongest at 1-2 h after the injections, and diminished markedly afterwards. The rigidity was accompanied with an increase in the resting, as well as in the stretch-induced short- and long-latency EMG activity in the gastrocnemius muscle. However, the intensity of the latter symptom did not change for a long period of time, which seems to correlate with the striatal dopamine depletion. The results suggest that the reserpine-increased EMG activity is a good model of parkinsonian rigidity.

Adrenergic Uptake Inhibitors↗
PubMed1985

An increase in putative voltage dependent calcium channel number following reserpine treatment.

Rats were treated with reserpine (0.2 mg/kg) on days 1, 3, and 5. On day 6, binding parameters for alpha-1 adrenergic receptors (3H-prazosin) and putative voltage dependent calcium channels, VDCC (3H-nitrendipine), were determined. There was an increase in both the number (2.1 fold) and affinity (1.8 fold) of alpha-1 adrenergic receptors following reserpine treatment. In addition, there was a 2.7 fold increase in the number of VDCCs, but no change in VDCC binding affinity, following reserpine treatment. These data are consistant with the development of smooth muscle supersensitivity following reserpine treatment in a variety of tissues, and suggest that VDCC number may be modulated by the cell in response to tonic levels of catecholamines. Changes in the number of VDCCs may be an important regulatory mechanism for cell function in physiologic and pathologic states.

Animals↗
PubMed1986

Comparative responses of the central adrenaline- and noradrenaline-containing neurons after reserpine injections.

The responses of the noradrenaline (NA)- and adrenaline (A)-containing neurons to a reserpine treatment have been studied in the rat brain by using biochemical indices of the neuronal activity. Three days after multiple reserpine injections, tyrosine hydroxylase activity was significantly increased in the locus coeruleus (LC), A1-C1 and C2 regions. No change in this activity was observed in the A2 region. Furthermore, the NA and A endogenous levels were markedly reduced both in NA and A cell bodies and/or terminals, suggesting a reserpine action on NA and A neurons. The NA turnover was unchanged in all the regions analyzed. Conversely, the A turnover was reduced in the LC, A2 and C2 regions and in the nucleus periventricularis of the hypothalamus. This result suggests a different degree of sensitivity and/or response of the NA and A neurons following reserpine administration.

Animals↗
PubMed1977

The effect of a single dose of reserpine administered prior to incubation on the development of tyrosine hydroxylase activity in chick sympathetic ganglia.

A single dose of reserpine administered into the yolk sac of chicken eggs prior to incubation produces two distinct periods of significant increase in tyrosine hydroxylase (TH) activity over controls. The first period is 21 days of incubation (55%) and the second is between day 14 and 30 after hatching (a.h.) (69%). Cholineacetyltransferase (ChAc) and dopadecarboxylase (DDC) are not modified in the two periods of increased TH activity. Reserpine had no effect on cholinergic parasympathetic synapses and neurons in the ciliary ganglion, as judged by ChAc activity. When reserpine was acutely administered in three different posthatching periods only the injection at the latest period (days 26 and 27) caused a significant (38%) increase in TH activity at day 30. Postsynaptic nicotinic receptors were blocked selectively by injecting chlorisondamine in the chick starting at hatching for one week. The administration of chlorisondamine almost completely abolished the reserpine induced increase of TH activity at day 15 a.h. The present results support the view that the development of enzyme activities specifically related to neurotransmitter biosynthesis in chick autonomic ganglia is regulated not only by transsynaptic influences but also by regulatory inputs originating in the periphery.

Animals↗
PubMed1981

The direct effect of reserpine in vitro on prolactin release from rat anterior pituitary glands.

Anterior pituitary glands from normal untreated rats synthesize and release the hormone prolactin (Prl) during incubation under in vitro conditions. Addition of dopamine (DA) greatly inhibits the release of Prl and to a lesser extent reduces Prl synthesis. When pituitary glands are incubated in the presence of reserpine, there is a similar significant dose-related inhibition of Prl release. This effect persists even in the presence of a DA antagonist (haloperidol) and after the depletion of hypothalamic amines by in vivo treatment with reserpine. Reserpine in vitro also inhibits release of newly synthesized growth hormone from the pituitary glands of male rats; however, this is not observed when female rats are studied. We conclude that the direct effect of reserpine to inhibit Prl release is apparently independent of any interaction with catecholamine systems and is mediated by other, presently undefined mechanisms.

Animals↗
PubMed1983

Alpha-methyltyrosine attenuates and reserpine increases methamphetamine-induced neuronal changes.

The repeated administration of methamphetamine to rats has been shown to cause a long-lasting depletion of dopamine in various brain regions. In the first study, the effects of pretreatment with alphamethyltyrosine (AMT) or reserpine on the long-lasting methamphetamine-induced dopamine depletion were examined. In the second study, the effects of AMT and reserpine on central dopamine levels were measured in rats previously treated with methamphetamine. Pretreatment with AMT attenuated the long-lasting dopamine depletion induced by methamphetamine, whereas, pretreatment with reserpine increased the depletion. The acute effects of AMT and reserpine on brain dopamine were not altered when administered two weeks after the last methamphetamine injection.

Animals↗
PubMed1984

Retrograde axonal transport of beta-adrenoreceptors in rat brain: effect of reserpine.

Retrograde axonal transport of beta-adrenoreceptors was assessed by measuring the accumulation of binding sites for the beta-receptor ligand [125I]iodocyanopindolol [( 125I]ICP) distal to a unilateral 6-hydroxydopamine (6-OHDA) lesion placed in the ascending noradrenergic axons of the locus coeruleus. Accumulation of binding sites was linear over a 3 day period and was blocked by intracerebroventricular 6-OHDA given 1 day prior to sacrifice. A single dose of reserpine (5 mg/kg, i.p.) caused a long lasting (6-8 week) biphasic depletion of frontal cortex norepinephrine (NE) associated with increased frontal cortex binding of another beta-receptor ligand, [3H]dihydroalprenolol [( 3H]DHA), at 7-14 days, and again at 28 days post-reserpine. Unlike the changes in cortical beta-receptors, retrograde transport of [125I]ICP in presynaptic noradrenergic neurons was decreased or blocked completely at 7-14 days and at 6 weeks, and was increased to 470% and 240% of control at 21 days and 8 weeks after reserpine. Anterograde transport of [3H]DHA binding sites was measured by accumulation proximal to a 6-OHDA lesion in this pathway. This transport varied in a pattern similar to that seen for retrograde transport of [125I]ICP binding sites. These data and others suggest that presynaptic beta-receptors are regulated independently of frontal cortex beta-receptors, which appear to be located primarily on postsynaptic cells. On the other hand, the regulation of both anterograde and retrograde transport appears to be interrelated since both types of transport were altered in a similar way in the face of long-term NE depletion by reserpine.

Animals↗
PubMed1990

The reserpine-sensitive dopamine pool mediates (+)-amphetamine-conditioned reward in the place preference paradigm.

The neural basis of amphetamine-conditioned reward was investigated in the conditioned place preference paradigm. When bilaterally injected into the nucleus accumbens before the test session, a dopamine receptor blocker, alpha-flupenthixol, blocked the expression of the amphetamine-conditioned place preference. alpha-Flupenthixol had no significant effect on spontaneous locomotor activity. Bilateral microinjections of a tyrosine hydroxylase inhibitor, alpha-methyl-p-tyrosine (alpha-MPT), decreased (+)-amphetamine locomotor stimulation in a dose-dependent fashion. Two doses of alpha-MPT that completely blocked (+)-amphetamine locomotor stimulation had no effect on the expression of the conditioned place preference when injected into the nucleus accumbens before testing. Reserpine administered subcutaneously before testing blocked the expression of the conditioned place preference. A dose of reserpine (4.0 mg/kg), which completely blocked the conditioned place preference, did not attenuate (+)-amphetamine-induced locomotor stimulation. This dose of reserpine depleted dopamine in the nucleus accumbens to 4% of its normal value. These data show that (+)-amphetamine-conditioned reward, expressed as a conditioned place preference, is mediated by dopamine release in the nucleus accumbens. Moreover, the dopamine is released from the reserpine sensitive pool, and probably not from the newly synthesized alpha-MPT-sensitive pool.

Amphetamines↗
PubMed1990

Modulation of tyrosine hydroxylase gene expression in the rat adrenal gland by age and reserpine.

Tyrosine hydroxylase (TH), TH messenger RNA (TH mRNA) and dopamine (DA) were measured simultaneously in adrenal glands of individual Fischer 344 rats aged 2, 6, 13 and 23 months. Between 2 and 23 months TH activity rose 2-fold as compared to the youngest group. TH mRNA content of the adrenal gland rose 3-fold between 2 and 23 months. A 3-fold increase in adrenal DA content, the first catecholamine product of TH, provides evidence that the increases in TH gene expression are functionally significant. To determine if mechanisms that regulate gene expression are altered by aging, the effects of reserpine on induction of TH mRNA and TH activity were compared in another group of rats aged 2, 12 and 27 months. Consistent with the results of the first experiment, there were age-related increases in both TH activity and TH mRNA in the age-matched control groups. TH activity rose 2-fold and TH mRNA rose more than 6-fold between 2 and 27 months. The discrepancy in the relative magnitudes of increases in TH mRNA and TH protein suggest an uncoupling of regulation of TH mRNA and TH protein levels. Moreover, there were significant age-related differences with respect to modulation of TH gene expression by reserpine treatment. TH activity was induced by reserpine in the youngest group, but not in the two older age-groups. In contrast, reserpine caused significant induction of TH mRNA in all age groups. These results provide evidence that aging is accompanied by alterations in transcriptional and post-transcriptional mechanisms involved in regulation of TH gene expression.

Adrenal Glands↗
PubMed1993

Altered histamine H3 binding in rat forebrain after reserpine treatment.

Groups of 6 rats were treated for 5 days with either reserpine hydrochloride (5 mg/kg i.p., per diem), or saline. Regional binding of the histamine H3 agonist N alpha-[3H]methyl-histamine ([3H]NAMH) was determined in forebrain sections by quantitative autoradiography and Scatchard analysis. Highest maximal binding was in nucleus accumbens (107 +/- 18 fmol/mg) and corpus striatum (58 +/- 9 fmol/mg), where the apparent affinity was close to 4 nM. Maximal binding of [3H]NAMH in the insular cortex (39 +/- 6 fmol/mg) was higher than in other cortical areas examined. Reserpine treatment produced a 50% decrease in both the Bmax and the apparent Kd in the corpus striatum and nucleus accumbens, but binding parameters in the cortex and septum were unaltered. Therefore, the response of H3 receptors in rat forebrain to reserpine treatment for 5 days was regionally heterogenous such that maximal [3H]NAMH binding was typically higher in insular cortex (36 +/- 6 fmol/mg) than in corpus striatum (24 +/- 3 fmol/mg) of reserpine-treated rats.

Animals↗
PubMed1976

The effect of tricyclic antidepressants and neuroleptics on the peripheral and central action of norepinephrine in reserpine-treated mice.

The effect of exogenous norepinephrine on the ptosis induced by reserpine and its modification by tricyclic antidepressants and neuroleptics were studied in reserpine-pretreated mice. S.c injection of norepinephrine (0.3-5 mg/kg) reversed dose-dependently the ptosis induced by reserpine. The maximal effect was obtained 15 min after norepinephrine administration. Tricyclic antidepressants (2.5 and 5 mg/kg i.p.) potentiated the effect of norepinephrine. In contrast neuroleptics (1 and 5 mg/kg i.p.) antagonized it. Intracerebral injection of norepinephrine (5-20 mug) also reversed dose-dependently the ptosis induced by reserpine, and the maximal effect was obtained within 5 min. Tricyclic antidepressants potentiated the effect of norepinephrine, but neuroleptics antagonized it. Among tricyclic antidepressants, the potentiating action of secondary amines was stronger than that of tertiary amines. Chlorpromazine blocked the action of norepinephrine more strongly than did the same dose of haloperidol.

Animals↗
PubMed1983

Determination of agonist affinity for cardiac beta-adrenoceptors during reserpine-induced supersensitivity.

The positive inotropic responses to orciprenaline of paced left atria and papillary muscles and the positive chronotropic responses of spontaneously beating right atria of guinea-pigs were recorded. Tissues from guinea-pigs pretreated with reserpine exhibited supersensitivity to beta-adrenoceptor stimulation as demonstrated by the significantly lower EC50 values to orciprenaline. The antagonism of these responses by Ro 03-7894 was characteristic of irreversible beta-adrenoceptor blockade--depression of maximum response and resistant to washout. The dissociation constants (KA) of orciprenaline were determined from the concentration-response curves obtained before and after Ro 03-7894, and no difference was found between tissues from untreated and reserpine-pretreated animals. KA values were also determined from the functional antagonism of the responses by carbachol. The degree of antagonism was less after reserpine pretreatment, but there was no increase in KA value. The reserpine-induced supersensitivity does not therefore appear to be due to an increase in agonist affinity for the cardiac beta-adrenoceptor.

Adrenergic beta-Agonists↗
PubMed1983

Reserpine-induced locomotor stimulation in mice chronically treated with typical and atypical antidepressants.

Previous studies have shown that chronic treatment with antidepressants (AD) leads to an increased responsiveness of NA systems to noradrenaline (NA) or its agonist. In the present paper the influence is described of a prolonged treatment with AD of different pharmacological profiles on the effect of reserpine in the first phase of its action (amine release). It has been found that in mice treated chronically (14 days, twice a day, i.p.) with imipramine, amitriptyline, maprotiline, (+)-oxaprotiline, zimelidine, citalopram, mianserin and iprindole, the injection of reserpine induces stimulation of the locomotor activity. Only (-)-oxaprotiline and fluvoxamine do not evoke this effect. AD given alone (both single and repeated doses), reserpine alone, AD in a single dose administered jointly with reserpine do not induce the locomotor stimulation. These results suggest that a prolonged treatment with AD increases the responsiveness of the dopamine (DA) mesolimbic system and/or the NA system.

Animals↗
PubMed1983

Increased tyrosine hydroxylase activity in central adrenaline neurons after reserpine treatment.

By using preferential microdissection of the adrenaline (A) and noradrenaline (NA) neurons within the A2-C2 region of the rat medulla oblongata, it was possible to study the biochemical response of these two neuronal populations to reserpine administration. Three days after reserpine injections (10 mg/kg s.c., per day for 3 days), tyrosine hydroxylase (TH) activity was increased in the adrenergic C2 region whilst no change was observed in the noradrenergic A2 region. The response of the A neurons to reserpine was of lesser magnitude than the increase in TH activity observed under the same conditions in the NA neurons of the locus coeruleus and of the A5 region, and was likely to have originated in the A cell bodies. In contrast with previous studies, this work suggests that the A-containing neurons are responsive to reserpine administration, despite the lack of change in phenylethanolamine-N-methyltransferase activity.

Animals↗