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.     

Reserpine-induced depletion of corticoliberin (CRF)-like immunoreactivity in the zona externa of the rat median eminence

An acute reserpine treatment has the same selective and marked depleting effect on corticoliberin-like immunoreactivity as on vasopressin-like immunoreactivity in the rat zona externa of the median eminence. Somatostan and gonadoliberin immunoreactivities appear unmodified. Reserpine effect is blocked by pretreatment with monoamine oxidase inhibitors (pargyline or tranylcypromine). Present results support the notion of an inhibitory role of monoamines, particularly catecholamines, on the release of corticoliberin.     

Effect of Shashen Maidong Decoction(沙参麦冬汤) on Gastric Motility in vivo

ＥｆｆｅｃｔｏｆＳｈａｓｈｅｎＭａｉｄｏｎｇＤｅｃｏｃｔｉｏｎｏｎＧａｓｔｒｉｃＭｏｔｉｌｉｔｙｉｎｖｉｖｏ￥ＦＥＮＧＷｅｉ－ｈｏｎｇａｎｄＨＯＵＪｉａ－ｙｕ（ＤｅｐｏｒｔｍｅｎｔｏｆＰｈａｒｍａｃｏｌｏｇｙ，ＢｅｉｊｉｎｇＵｎｉｖｅｒｓｉｔｙｏｆＴ...     

Anti-immobility activity of different antidepressant drugs using the tail suspension test in normal or reserpinized mice

Summary— The tail suspension test is a screening procedure recently used in mice to detect antidepressant activity of drugs. The ability of amine re-uptake inhibitors to decrease immobility in non-reserpinized and in reserpinized mice was studied. Reserpine (4 mg/kg ip) was injected 4 h previously. Anti-depressants were administered ip, 60 min before tail suspension. Animal activity was recorded for 6 min. Preferential serotonin re-uptake blockers (fluoxetine, fluvoxamine, clomipramine) were poorly active in non-reserpinized mice and inactive in reserpine-treated mice. Noradrenergic drugs (desipramine, demexiptiline, viloxazine) were more efficient in reserpinized than in non-reserpinized mice. The mixed serotonin- noradrenaline re-uptake inhibitor (imipramine) shows an activity which should be considered between serotonin re-uptake inhibitors and noradrenaline re-uptake inhibitors. DA re-uptake inhibitors (amineptine, GBR 12909) exhibited the highest anti-immobility effect in non reserpinized animals but were of low efficacy after reserpine treatment. Amphetamine differed from dopamine re-uptake inhibitors by its better activity in reserpinized animals. Moreover, it was the only drug showing an equal anti-immobility effect in non reserpinized and reserpinized mice because the dose of 8 mg/kg of amphetamine reduced immobility in reserpinised mice with the same intensity as the dose of 4 mg/kg in non reserpinised mice whereas no other drugs tested in this study achieved the same effect. Comparison of anti-immobility activities of putative antidepressants in non-pre-treated and in reserpine-pre-treated mice, using the tail suspension test, may be useful to discriminate amphetamines from antidepressant drugs and to differentiate between categories of amine re-uptake blockers.     

Monoamine replacement after reserpine: Catecholaminergic agonists restore motor activity but phenylethylamine restores atropine-resistant neocortical low voltage fast activity

A large dose of reserpine abolishes an atropine-resistant form of neocortical low voltage fast activity (LVFA) which normally accompanies certain patterns of motor activity in rats. An attempt was made to reverse this effect by replacement of specific monoamines or by injection of suitable agonists in rats pretreated with reserpine (10 mg/kg). The following compounds, alone or in various combinations, failed to restore atropine-resistant LVFA in reserpinized rats even though spontaneous motor activity was restored in many cases: l-DOPA (150–300 mg/kg) after pretreatment with an inhibitor of peripheral l-aromatic amino acid decarboxylase; 5-hydroxytryptophan (100–200 mg/kg); d-amphetamine (1–2 mg/kg); apomorphine (0.25–2.5 mg/kg); lysergic acid diethylamide (100–300 g/kg); and clonidine (0.5–1.0 mg/kg). In contrast β-phenylethylamine was quite effective in restoring atropine-resistant LVFA and its effects were not diminished by pretreatment with α-methyl-p-tyrosine (400 mg/kg), chlorpromazine (15 mg/kg) or trifluoperazine (5–10 mg/kg). It is suggested that a trace amine plays an essential role in the production of atropine-resistant LVFA independent of catecholamines.     

Effect of triiodothyronine and reserpine on induction and growth of mammary tumors in rats by 3-methylcholanthrene

This study was designed to investigate the effects of exogenous L-triiodothyronine (LT₃) and reserpine administration on the induction and stimulation of 3-methylcholanthrene (3-MC) mammary tumors. Two hundred-fifty-eight 30-day-old virgin 100 gm Sprague Dawley rats were divided into eight groups. Groups I–IV received either reserpine, LT₃, both, or saline 22 days after tumor induction with 3-MC. Groups V–VIII were pretreated with either reserpine, LT₃, or both for 29 days prior to tumor induction, and treatment was continued after tumor induction in all except Group VII. All rats were observed for tumor growth and sacrificed at seven months. Reserpine administration resulted in a protective effect against tumor induction in all groups in which it was used, with the most striking effects observed in the pretreated groups. Early LT₃ stimulation of tumor formation was reversed by simultaneous administration of reserpine. Prolonged administration was unnecessary when both agents were administered prior to 3-methylcholanthrene.     

Effects of phencyclidine on synaptosomal dopamine continuously appearing from phenylalanine: Sensitivity to reserpine

In the present study some effects of phencyclidine on synaptosomal (P₂) synthesis and release of labelled dopamine, continuously appearing from [¹⁴C]phenylalanine, were investigated in vitro. Also examined was the sensitivity of such effects of phencyclidine to reserpine, acting either in vitro or in vivo. Synaptosomal (P₂) preparations from rat caudate nuclei were incubated with the drugs added at various concentrations in the presence of [¹⁴C]phenylalanine substrate. The particulates were quickly separated from the medium after incubation and the separated fractions were analyzed for labelled dopamine and the synaptosomal uptake of [¹⁴C]phenylalanine. Of the total labelled dopamine formed, the fraction that was present in the medium was determined and taken as a measure of the spontaneous or basal release and its enhancement by any drug addition. Phencyclidine (3.1–36.4 μM) stimulated both the total (medium plus particulates) formation and the synaptosomal release of labelled dopamine, while reserpine (0.09–1.80 μM) inhibited the formation and enhanced the release. A coaddition of reserpine (0.09–1.80 μM) and phencyclidine to the incubation medium blocked the stimulating effect of the latter drug on the labelled dopamine synthesis; the same experiments revealed furthermore, an inhibitory effect of phencyclidine (0.91–36.4 μM) on the synthesis, an effect that was additive to the inhibition due to reserpine alone. The enhancing effect of phencyclidine on labelled dopamine release was however maintained in the presence of reserpine. Phencyclidine (0.22–36.4 μM) also inhibited the formation of labelled dopamine and enhanced its release when the P₂ fraction was prepared from reserpine-pretreated rats (5.0 and 2.5 mg/kg, i.p., at 24 and 2 hr before the experiment). Reserpine (1.80 μM) itself, added in vitro to the same P₂ preparation, was without any significant effect. The phencyclidine congener Ketamine, with or without reserpine, had little effect either on the synthesis or the release. In none of the incubations did the addition of drugs affect the synaptosomal uptake of labelled phenylalanine.     

Long-term potentiation in the dentate gyrus: Effects of noradrenaline depletion in the awake rat

The chronic rat preparation was utilized to study the effects of noradrenaline (NA) depletion on field potentials recorded from the hilus of the fascia dentata. Both single pulses and high-frequency trains were applied to the perforant path (PP). The effects of NA depletion on baseline responses as well as on long-term potentiation (LTP) were examined. Reduced NA levels resulted in an increase in the population spike amplitude and a depression of the population excitatory postsynaptic potential (EPSP). Depleted animals showed significantly higher levels of LTP of the population EPSP, but reduced levels of population spike LTP (measured 13-15 min after tetanization). There were, however, no differences in LTP levels 1 week after the potentiation tests. These results demonstrate that NA levels do not affect that component of LTP which can persist for several weeks.     

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.     

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.