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PubMed1994

Role of 5-HT1A receptors in the antinociceptive action of 8-hydroxy-2-(di-n- propylamino)tetralin in the rat.

The role of 5-HT1A receptors in the antinociceptive action of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) was investigated by using the shock titration test in rats. A subcutaneous injection of 300 micrograms/kg 8-OH-DPAT significantly raised the threshold for flinching, jumping and vocalization whereas 100 micrograms/kg only inhibited the flinch response. l-Propranolol and (+)-[N-tert-butyl-3-4-(2-methoxyphenyl)piperazin-1-yl-2-phenyl propanamide dihydrochloride], (+)-WAY100135, two antagonists at 5-HT1A receptors at 10 mg/kg s.c. antagonized the effect of 300 micrograms/kg 8-OH-DPAT on all measures. The effect of 300 micrograms/kg 8-OH-DPAT on the three measures was unmodified in rats which had received 150 micrograms 5,7-dihydroxytryptamine intracerebroventricularly 10 days before testing. The results suggest that 8-OH-DPAT inhibits nociceptive responses by stimulating postsynaptic 5-HT1A receptors.

5,7-Dihydroxytryptamine↗
PubMed1994

Activation of 5-HT3 receptors enhances the electrically evoked release of [3H]noradrenaline in rat brain limbic structures.

The ability of 5-HT receptor agonists to modulate the electrically evoked release of [3H]noradrenaline was tested on preloaded slices of the rat brain. The 5-HT3 receptor agonist 2-methyl-5-hydroxytryptamine (2-methyl-5-HT) (10-100 microM) concentration-dependently enhanced the electrically evoked release of [3H]noradrenaline in the hippocampus and the hypothalamus, but only at 100 microM in the frontal cortex. The enhancing effect of 2-methyl-5-HT was blocked by the 5-HT3 receptor antagonist ondansetron. Elevated levels of endogenous 5-HT, achieved through selective reuptake blockade with paroxetine, as well as the addition of exogenous 5-HT in the medium, also enhanced [3H]noradrenaline release. Furthermore, this effect of paroxetine was blocked by nanomolar concentrations of the 5-HT3 receptor antagonists ondansetron, tropisetron and (S)-zacopride. Only high concentrations of the 5-HT3 receptor agonist m-chlorophenylbiguanide increased [3H]noradrenaline release from hippocampal slices, and this effect was not blocked by ondansetron nor by (S)-zacopride. The possibility that the enhancing effect of 2-methyl-5-HT could have been due to the antagonism of alpha 2-autoreceptors of noradrenergic terminals was ruled out by the unaltered effectiveness of the alpha 2-adrenoceptor agonist UK-14,304 (1 microM) to attenuate [3H]noradrenaline release in the presence of 100 microM of 2-methyl-5-HT. Moreover, in pseudo-one-pulse experiments 100 microM of 2-methyl-5-HT increased [3H]noradrenaline release in the absence of autoinhibition through alpha 2-adrenergic autoreceptors. The 5-HT1A and 5-HT1B receptor agonists 8-hydroxy-2(di-n-propyl-amino)tetralin and CP-93,129, respectively, as well as the 5-HT1 receptor agonist 5-carboxyamidotryptamine, were devoid of effect on the release of [3H]noradrenaline. The 5-HT2A/2C receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane increased the release of [3H]noradrenaline, but this effect was not blocked with the 5-HT3 receptor antagonist ondansetron. Lesioning 5-HT fibers with the neurotoxin 5,7-dihydroxytryptamine did not alter the action of 2-methyl-5-HT on [3H]noradrenaline release, indicating that this effect is not attributable to an action of this 5-HT3 receptor agonist on 5-HT terminals.

5,7-Dihydroxytryptamine↗
PubMed1995

Antidepressant-like effect by postsynaptic 5-HT1A receptor activation in mice.

The antidepressant-like effect of 5-(3(-)[((2S)-1,4-benzodioxan-2-ylmethyl)amino]propoxy)-1,3- benzodioxole (MKC-242), a novel 5-HT1A receptor agonist, was studied in the forced swimming test in mice injected i.c.v. with 5,7-dihydroxytryptamine to destroy 5-HT neurons or treated with p-chlorophenylalanine to inhibit 5-HT synthesis. MKC-242 reduced immobility time of mice pretreated with vehicle and these drugs, although it did not affect their locomotor activity. The anti-immobility effect was antagonized by 5-HT1A receptor antagonists such as propranolol and N-tert-butyl-3-(4-(2-methoxyphenyl)piperazin-1-yl)-2-phenylpropana mide. These findings support the hypothesis that postsynaptic 5-HT1A receptors play an important role in the antidepressant-like effect of 5-HT1A receptor agonists.

5,7-Dihydroxytryptamine↗
PubMed1984

Possible role of central serotoninergic neurons in the development of dental pain and aspirin-induced analgesia in the monkey.

The effects of aspirin or 5-hydroxytryptamine (5-HT)-related drugs on the dental pain induced by electrical stimulation of tooth pulp afferent fibers were assessed in conscious monkeys. The electrical current required for producing jaw opening is referred to as the pain threshold. Both systemic (25 to 75 mg/kg, i.p.) or central (0.5 to 1.5 mg, third cerebral ventricle) administration of aspirin produced analgesia in monkeys. In addition, activation of central 5-HT receptors with central injection of either 5-HT or its precursor, 5-hydroxytryptophan, also produced analgesia. On the other hand, inhibition of central 5-HT receptors with central administration of either cyproheptadine (a blocking agent of 5-HT receptors), p-chlorophenylalanine (PCPA, an inhibitor of 5-HT synthesis) or 5,7-dihydroxytryptamine (5,7-DHT, a depletor of central 5-HT nerve fibers) produced an enhancement in pain sensitivity (or a decrease in pain threshold). Furthermore, the analgesia induced by aspirin was antagonized by pretreatment of monkeys with either cyproheptadine, PCPA, or 5,7-DHT. The results indicate that increases in the activity of central 5-HT neurons are associated with reduced dental pain and enhanced aspirin-induced analgesia, whereas decreases in the activity of those neurons correlate with dental hyperalgesia and diminished aspirin-induced analgesia in monkeys.

5,7-Dihydroxytryptamine↗
PubMed1987

The host serotonin projection to tectal grafts in young rats: an immunohistochemical study.

It has been shown previously that embryonic tectal tissue grafted to the midbrain of newborn rats is innervated by fibers from a variety of host regions, including the raphe nuclei. The present study examined the distribution within tectal transplants of axons arising from these serotonin-containing neurons in the host brain stem. Fetal tectal tissue was transplanted to the midbrain of young host rats aged 0 to 21 days. After 7 or more weeks, the host serotonin projection to the grafts was examined immunohistochemically using a monoclonal antibody to serotonin. In most cases, visualization of serotonin axons was enhanced by treating the animals with 5, 7-dihydroxytryptamine. Tectal transplants were found lying on or embedded within the host midbrain. In the newborn hosts, serotonin innervation was densest and most frequently encountered in the nonembedded grafts. Fibers with serotonin-like immunoreactivity were also seen in the tectal tissue grafted into older hosts. The pattern of innervation of serotonin fibers varied from one graft to another and did not correlate with any obvious morphologic or histochemical features within the grafts. This is in contrast to the distribution of host retinal and cortical axons, which have been shown to consistently project to specific and recognizable regions within the graft neuropil.

5,7-Dihydroxytryptamine↗
PubMed1983

Autoreceptor-mediated inhibition of 3H-5-hydroxytryptamine release from rat brain cortex slices by analogues of 5-hydroxytryptamine.

Rat brain cortex slices preincubated with 3H-5-hydroxytryptamine (3H-5-HT) were superfused with physiological salt solution containing paroxetine, an inhibitor of 5-hydroxytryptamine (5-HT) uptake. The effects of various indolethylamines on the electrically evoked tritium overflow (containing 66.3% unmetabolized 3H-5-HT) were investigated (the percentage of unmetabolized 3H-5-HT was not altered by the indolethylamines or metitepin). 6,7-Dihydroxytryptamine (6,7-DHT) did not affect the stimulation-evoked tritium overflow, whereas the latter was inhibited by the other tryptamine derivatives investigated; when the compounds were compared to each other on the basis of their inhibitory potencies the following rank order was obtained: unlabelled 5-HT greater than 5-methoxytryptamine greater than 4-HT greater than 6-HT greater than 5,6-DHT greater than tryptamine greater than 7-HT greater than 5,7-DHT. The inhibitory effects of these compounds were antagonized by metitepin. It is concluded that the indolethylamines inhibit the stimulation-evoked 3H-5-HT release by activating the presynaptic 5-HT autoreceptors on the 5-HT neurones of the rat brain cortex. Similarities may exist between these receptors and the postsynaptic 5-HT1 binding sites of this brain area.

5-Methoxytryptamine↗
PubMed1983

Evidence for serotonergic stimulation of pituitary beta-endorphin release: preferential release from the anterior lobe in vivo.

Using gel filtration chromatography (Sephadex G-50) and radio-immunoassay for beta-endorphin (beta-END) and beta-lipotropin (beta-LPH) we investigated the site [anterior lobe (AL) vs. intermediate lobe (IL)] for serotonergic control of pituitary beta-END-like immunoreactivity (beta-END-LI) in the rat. Since the secretion of beta-LPH in vitro clearly distinguishes beta-END-LI release by the AL as compared to the IL, we interpreted changes in plasma levels of immunoreactivity resembling beta-LPH to reflect beta-END-LI release from the AL. Following the administration of L-tryptophan (200 mg/kg, 30 min, ip), a serotonin precursor, nearly all of the rise in total plasma beta-END-LI was due to the form of immunoreactivity resembling beta-LPH in molecular size. Similarly, 5-hydroxytryptophan (30 mg/kg, 30 min, ip), a serotonin precursor, and fluoxetine (10 mg/kg, 15 min, ip), a serotonin reuptake blocker, predominantly increased circulating levels of beta-LPH-sized immunoreactivity with little effect on beta-END-sized immunoreactivity. Quipazine (2.5 and 5.0 mg/kg, 30 min, ip), a serotonin receptor agonist, elevated plasma levels of both forms of beta-END-LI; however, the immunoreactive peak coeluting with beta-LPH was primarily affected, being increased 9.5-fold while that resembling beta-END was increased less than 1-fold. Immobilization stress (30 min) dramatically elevated plasma levels of both forms of immunoreactivity, however, a greater relative rise in beta-LPH than beta-END was observed. Intraventricular administration of 5,7-dihydroxytryptamine (75 micrograms, free base, 10 d), a serotonin neurotoxin, lowered plasma levels of both forms of immunoreactivity about equally in stressed animals. Further, dexamethasone, a synthetic glucocorticoid which selectively inhibits AL corticotroph secretion in vitro, attenuated the beta-LPH response to serotonergic activation in vivo. Together, these findings indicate that serotonergic drugs predominantly influence the release of beta-END-LI resembling beta-LPH and further suggest that serotonin neurons preferentially regulate the release of beta-END-LI from AL corticotrophs in vivo.

5,7-Dihydroxytryptamine↗
PubMed1989

Effects of imipramine and serotonin-2 agonists and antagonists on serotonin-2 and beta-adrenergic receptors following noradrenergic or serotonergic denervation.

The effects of chronic (14 day) administration of the tricyclic antidepressant imipramine, the serotonin-2 (5-HT2) antagonist ketanserin, and the serotonin agonist quipazine on 5-HT2 receptor binding parameters and 5-HT2-mediated behavior were examined in rats with or without prior serotonergic denervation [via 5,7-dihydroxytryptamine (5,7-DHT)] or noradrenergic denervation [via N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4)]. Chronic administration of imipramine, ketanserin, or quipazine produced a marked reduction in the number of 5-HT2 binding sites which was accompanied by reductions in the 5-HT2-mediated quipazine-induced head shake response. In animals receiving DSP4 or 5,7-DHT lesions and continuous vehicle treatment, beta-adrenergic receptor binding sites were significantly up-regulated while 5-HT2 receptor binding sites did not change. Imipramine normalized the lesion-induced increases in beta-adrenergic binding observed in DSP4 and 5,7-DHT-lesioned rats but failed to down-regulate beta-adrenergic binding sites below non-lesioned control levels. Chronic imipramine, ketanserin, and quipazine reduced quipazine-induced head shakes and down-regulated 5-HT2 binding sites in rats with noradrenergic denervation. While imipramine, ketanserin, and quipazine all down-regulated 5-HT2 binding sites in animals with serotonergic denervation, only imipramine's ability to reduce quipazine-induced head shakes was attenuated in 5,7-DHT-lesioned rats. The present results suggest that imipramine-induced down-regulation of 5-HT2 receptors may not involve presynaptic 5-HT mechanisms, and imipramine-induced alterations in 5-HT2 sensitivity as reflected in the quipazine-induced head shake may, in part, be influenced by beta-adrenergic receptors.

5,7-Dihydroxytryptamine↗
PubMed1991

Modulation of [3H]-glutamate binding by serotonin in the rat hippocampus: an autoradiographic study.

Serotonin (5-HT) added in vitro (10 microM) increased [3H]-glutamate specific binding in the rat hippocampus, reaching statistical significance in layers rich in N-Methyl-D-Aspartate sensitive glutamate receptors. This effect was explained by a significant increase in the apparent affinity of [3H]-glutamate when 5-HT is added in vitro. Two days after lesion of serotonergic afferents to the hippocampus with 5,7-Dihydroxytryptamine [3H]-glutamate binding was significantly decreased in the CA3 region and stratum lacunosum moleculare of the hippocampus, this reduction being reversed by in vitro addition of 10 microM 5-HT. The decrease observed is due to a significant reduction of quisqualate-insensitive (radiatum CA3) and kainate receptors (strata oriens, radiatum, pyramidal of CA3). Five days after lesion [3H]-glutamate binding increased significantly in the CA3 region of the hippocampus but was not different from sham animals in the other hippocampal layers. Two weeks after lesion [3H]-glutamate binding to quisqualate-insensitive receptors was increased in all the hippocampal layers, while kainate and quisqualate-sensitive receptors were not affected. These data are consistent with the possibility that 5-HT is a direct positive modulator of glutamate receptor subtypes.

5,7-Dihydroxytryptamine↗
PubMed1991

Involvement of the GABAA/benzodiazepine chloride ionophore receptor complex in the 5,7-DHT Induced anticonflict effect.

The effects of drugs interacting with the GABAA/benzodiazepine chloride ionophore receptor complex (GABAA/BDZ-RC) on the anticonflict and biochemical effects observed after intracerebroventricular (i.c.v.) administration of 5,7-dihydroxytryptamine (5,7-DHT; 450 micrograms -14 days) were investigated in the rat using a modified Vogel's drinking conflict test. The GABAergic antagonistic drugs bicuculline, picrotoxin and Ro 15-4513 all counteracted the 5,7-DHT induced anxiolytic-like action in doses that did not alter the behavior per se, whereas flumazenil was ineffective in this respect. Also i.c.v. administration of 5-HT antagonized the 5,7-DHT induced anticonflict effect. Furthermore, 5,7-DHT-lesioned animals appeared more sensitive to the anticonflict effects of diazepam than sham-lesioned controls. The 5,7-DHT treatment produced marked depletions of 5-HT in the limbic system (80-90%) and hippocampus (90-95%), and an increase in the 5-HIAA/5-HT quotient in hippocampus. The effects on the levels of noradrenaline were comparatively small. The doses of bicuculline and picrotoxin antagonizing the 5,7-DHT induced anticonflict effect did not uniformly influence 5-HT levels or 5-HIAA/5-HT quotients. It is suggested that the anxiolytic-like effect observed in 5,7-DHT-lesioned rats in Vogel's drinking conflict test involves enhanced transmission at the GABAA/BDZ-RC.

5,7-Dihydroxytryptamine↗
PubMed1993

Effect of serotonin axon injury on the somatostatinergic system in rat frontoparietal cortex.

In order to investigate the possibility that, in the rat, some cerebral cortex somatostatin (SS) receptors may be localized presynaptically on the terminals of serotonergic neurons, serotonin [5-hydroxytryptamine, (5-HT)] neurons in the central nervous system were damaged with a local intracerebral injection of the serotonergic neurotoxin, 5,7-dihydroxytryptamine(5,7-DHT). The injection of 5,7-DHT (11 micrograms free base dissolved in 10 microliters of isotonic saline containing 0.01% ascorbic acid) in rats produced an reduction by about 74% in frontoparietal cortical 5-HT content at 1 and 3 weeks after injection. These changes were associated with a significant decrease by about 30% in the total number of specific SS receptors in the frontoparietal cortex at both times studied without influencing the apparent affinity of the receptors. Together, these results suggest that a portion of the frontoparietal cortex SS receptors may be localized presynaptically on the serotonergic nerve terminals. The 5,7-DHT did not affect SS-like immunoreactivity (SSLI) levels suggesting that SS and 5-HT are not colocalized within the same neuronal elements in the rat frontoparietal cortex.

5,7-Dihydroxytryptamine↗
PubMed1982

Responses of cortical neurones to stimulation of the nucleus raphé medianus: a pharmacological analysis of the role of indoleamines.

Single shock stimulation of the nucleus raphé medianus evoked complex responses from the large majority of neurones tested. These responses consisted of a short-latency (mean 21 msec) inhibition of firing followed by a longer latency (mean 160 msec) increase in firing rate. Occasionally, cells were encountered which exhibited pure inhibitory or pure excitatory responses. Prior treatment with the tryptophan hydroxylase inhibitor rho-chlorophenylalanine reduced the excitatory effects of raphé stimulation but greatly increased the inhibitory effects. Pretreatment with 5,7-dihydroxytryptamine (5,7-DHT), on the other hand, reduced both inhibitory and excitatory effects of raphé stimulation. Methysergide was found to be an effective antagonist of excitatory responses to iontophoretically applied 5-hydroxytryptamine (5-HT) but less effective against depressant responses to either 5-HT or tryptamine. In contrast metergoline consistently antagonized 5-HT and tryptamine-induced depressions but not 5-HT elicited excitations. When tested against stimulation evoked responses of cortical neurones methysergide antagonized the excitatory effects of raphé stimulation but had much less effect on the inhibitory responses, while the reverse held true for metergoline. The present results may be compatible with a mediation of the excitatory effects of stimulation by 5-HT and the inhibitory effects by tryptamine.

5,7-Dihydroxytryptamine↗
PubMed1982

Down-regulation of beta-adrenergic receptors following repeated injections of desmethylimipramine: permissive role of serotonergic axons.

The injection of desmethylimipramine (DMI) twice daily for 3 weeks reduced the density of beta-adrenergic receptor recognition sites located in crude synaptic membranes prepared from the cortex and hippocampus and attenuated the stimulation of the membrane-bound adenylate cyclase by isoproterenol. Both actions were abolished if prior to treatment with desmethylimipramine the serotonergic axons were destroyed by an intraventricular injection of 5,7-dihydroxytryptamine. These results show that the down-regulation of beta-adrenergic receptors elicited by repeated injections of desmethylimipramine occurs only if the serotonergic axons are intact.

5,7-Dihydroxytryptamine↗
PubMed1983

Similar behavioural effects of 5-hydroxytryptamine and substance P injected intrathecally in mice.

Intrathecal injection of 5-hydroxytryptamine (5-HT) or of substance P in mice elicited a behavioural syndrome consisting of reciprocal hindlimb scratching and biting or licking, directed towards the caudal parts of the body. 5-Hydroxtryptamine elicited more scratching than did substance P, which in turn caused a greater number of biting or licking responses. The 5-HT-induced responses were mimicked by 5,6-dihydroxytryptamine and inhibited by the 5-HT receptor blocker metergoline. The present findings indicate that 5-HT, injected intrathecally, may have similar effects as substance P in stimulating sensory pathways in the spinal cord.

5,6-Dihydroxytryptamine↗
PubMed1983

Neurogenic hypertension after depletion of norepinephrine in anterior hypothalamus induced by 6-hydroxydopamine administration into the ventral pons: role of serotonin.

Destruction of the ventral noradrenergic pathway elicited by administration of 6-hydroxydopamine (6-OHDA, 5 micrograms into each side of the ventral pons) reduced the content of norepinephrine (NE) in the anterior hypothalamus (-80%) and induced an increase in arterial blood pressure (ABP) and in heart rate. These hypertensive rats, showed hypersensitivity to the hypotensive effect of NE (0.5-2 micrograms) and clonidine (0.75-1.5 micrograms) administered into the anterior hypothalamic preoptic (AH/PO) region. Methysergide (1-2 micrograms) and, to a lesser extent, ketanserin (1-2 micrograms) administered into the anterior hypothalamic preoptic region also reduced the arterial blood pressure in these rats treated with 6-OHDA. Bilateral administration of 5,7-dihydroxytryptamine (5,7-DHT, 8 micrograms) into the median forebrain bundle decreased the content of serotonin (5-HT) in the hypothalamus (-85%) without change in arterial blood pressure but largely prevented the development of hypertension after treatment with 6-OHDA in the ventral pons. These results suggest that neurogenic hypertension is produced after the removal of NE tonic depressor activity in the anterior hypothalamus and that serotonergic mechanisms play a major role in the development of the increased arterial blood pressure in this preparation.

5,7-Dihydroxytryptamine↗
PubMed1985

Effects of serotonergic activity in nucleus accumbens septi on drug-induced circling.

The effects of injections of 5-hydroxytryptamine (5-HT) into the nucleus accumbens and lesions of the nucleus accumbens induced by 5,7-dihydroxytryptamine (5,7-DHT) on drug-induced circling were investigated in rats with unilateral nigrostriatal lesions induced by 6-hydroxydopamine (6-OHDA). Injections of 5-HT (60-120 micrograms in 1 microliter; 1 microliter/min) into the nucleus accumbens caused a significant decrease in the circling response to 5.0 mg/kg of d-amphetamine (s.c.). The distribution of radioactivity after intracerebral injections of [3H]5-HT using these parameters showed that although much of the injected material was retained in the nucleus accumbens there was also considerable spread to the frontal cortex. However, in further behavioural experiments, using an injection procedure (0.5 microliter; 0.11 microliter/min) which caused much greater retention of injected material in the nucleus accumbens, with minimal spread to the frontal cortex, the ability of 5-HT injected into the accumbens to block amphetamine-induced circling was not diminished. Moreover, injections of 5-HT into the frontal cortex did not have any effect on amphetamine-induced circling. Lesions of the nucleus accumbens induced by 5,7-DHT caused a significant enhancement of the contralateral circling response to 1.0 mg/kg of apomorphine and a similar but non-significant tendency to increase the circling responses to several other doses of apomorphine and amphetamine. The results provide evidence that serotonergic mechanisms in the nucleus accumbens inhibit circling behaviour generated by unilateral activation of nigrostriatal dopaminergic mechanisms.

5,7-Dihydroxytryptamine↗
PubMed1985

Drug-induced activation of the inferior olivary nucleus in young rabbits. Differential effects of harmaline and quipazine.

Ontogenic evolution of behavioural and electrophysiological responses to the serotonergic agents, quipazine and harmaline, was studied in the maturing rabbit in normal and pretreated conditions. As regards behavioural effects, tremor induced by quipazine was present from the first postnatal day and was antagonized by methysergide, but not by p-chlorophenylalanine (PCPA) or pretreatment with 5,7-dihydroxytryptamine (5,7-DHT). In contrast, tremor induced by harmaline could not be elicited before the second postnatal week and was partially antagonized by methysergide and 5,7-DHT, but not by PCPA. Electrophysiological studies of cell activity in the inferior olivary nucleus revealed a similar dependency on age since rhythmic activation of the inferior olivary nucleus could be registered from the first postnatal day with quipazine and only from the 8th postnatal day with harmaline; drug interactions with methysergide, PCPA and 5,7-DHT were the same as for the behavioural observations. It is suggested that quipazine directly activates serotonin receptors which are already present at birth, whereas harmaline requires the presence of serotonergic fibres for such activation.

5,7-Dihydroxytryptamine↗
PubMed1985

Down-regulation of beta-adrenoceptors in rat cortex by repeated administration of desipramine, electroconvulsive shock and clenbuterol requires 5-HT neurones but not 5-HT.

Repeated administration to rats of desipramine (5 mg kg-1, twice daily for 14 days), clenbuterol (5 mg kg-1, twice daily for 14 days) or electroconvulsive shocks (5 ECS over 10 days) decreased the number of beta-adrenoceptors in the cortex. Injection of 5,7-dihydroxytryptamine into the lateral ventricle produced a selective depletion of cerebral 5-HT, particularly in the cortex. In confirmation of earlier studies, this lesion prevented the decrease in the number of beta-adrenoceptors produced by desipramine. However, it was found that this lesion also prevented the down-regulation of beta-adrenoceptors produced by repeated electroconvulsive shock and administration of clenbuterol. Treatment of rats with p-chlorophenylalanine (PCPA) produced a similar depletion of cerebral content of 5-HT. However, this depletion did not prevent the decrease in density of beta-adrenoceptors induced by desipramine or electroconvulsive shock. It is concluded that the modulation of the decrease in the number of beta-adrenoceptors by diverse antidepressant treatments is not by the action of 5-HT itself, but by the action of some other factor present at 5-HT terminals, which is removed by a neurotoxic lesion.

5,7-Dihydroxytryptamine↗