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PubMed1992

Effects of the serotonin releasers 3,4-methylenedioxymethamphetamine (MDMA), 4-chloroamphetamine (PCA) and fenfluramine on acoustic and tactile startle reflexes in rats.

The substituted amphetamines 4-chloroamphetamine (PCA), 3,4-methylenedioxymethamphetamine (MDMA) and fenfluramine (FEN) share the common neurochemical action of acutely releasing central serotonin (5-HT), and yet their behavioral effects are quite different. The present study evaluated the effects of these compounds on acoustic and tactile startle reflexes. PCA and MDMA were qualitatively similar in producing dose-related increases in acoustic and tactile startle reflexes that were slow in onset, but sustained throughout the 3.5-hr test session. Changes in motor activity did not account for the observed excitation of startle. In marked contrast to MDMA and PCA, FEN did not alter tactile startle and tended to depress acoustic startle. The excitatory effect of 20 mg/kg of MDMA was prevented by the 5-HT uptake blockers MDL 27,777A and fluoxetine. MDMA excitation was not affected by a dose of the dopamine antagonist haloperidol that attenuated the startle-enhancing effect of d-amphetamine. MDMA excitation was greatly attenuated by a general depletion of central 5-HT produced by prior intraventricular injection of the 5-HT neurotoxin 5,7-dihydroxytryptamine. PCA and MDMA excitations of startle were attenuated in rats specifically depleted of spinal 5-HT or in rats with radio frequency lesions of the dorsal raphe nucleus. Thus, PCA and MDMA have similar prolonged excitatory effects on startle reflexes that are mediated by ascending (dorsal raphe) and descending (spinal) pathways, whereas FEN differs in its lack of excitation of startle. Differences in the neurochemical properties of these compounds or their patterns of 5-HT release may underlie their different behavioral profiles.

5,7-Dihydroxytryptamine↗

PubMed1976

Studies on tolerance development to single doses of morphine in mice.

Single-dose tolerance to the antinociceptive effect of morphine can be demonstrated using an adequate initial priming dose of morphine and allowing an interval of 48 to 72 hours for its development. The threshold dose necessary to produce tolerance was found to be about 3 to 4 times greater than that for producing analgesia but higher doses of morphine did not enhance further tolerance development. Evidence of tolerance was indicated by the fact that when the antinociceptive response to morphine was assessed by the hot-plate and the tail-flick procedures, a shift in the dose-response curve of morphine to the right occurred after an adequate single priming dose of morphine. Cross-tolerance was evidenced by a decrease in analgetic response to methadone 3 days after a single priming dose of morphine and a decrease in morphine response after a single dose of methadone. The development of single-dose tolerance was inhibited by cycloheximide. Single-dose tolerance was also blocked by 5,6-dihydroxytryptamine and perhaps enhanced by L-tryptophan. Cyclic 3',5'-adensine monophosphate did not affect single-dose tolerance development significantly although the direction was in favor of augmentation. Morphine uptake by the brain was not modified by the development of single-dose tolerance. Physical dependence, as measured by naloxone-precipitated withdrawal jumping, was not observed when single-dose analgetic tolerance was maximal. The results suggest that single-dose tolerance to morphine involves the synthesis of some macromolecule and support previous findings in this laboratroy involving an association with serotonin.

5,6-Dihydroxytryptamine↗

PubMed1991

A new double labelling technique of the serotonergic neurons in wholemount CNS preparations of the snail Helix pomatia.

5,6-dihydroxytryptamine-induced pigmentation of serotonergic neurons was combined with retrograde cobalt- or nickel-lysine labelling in order to identify serotonergic cell bodies among cobalt- or nickel-labelled ones. Cobalt- or nickel-labelled serotonergic cell bodies could easily be distinguished from labelled, nonserotonergic neurons. The nonserotonergic cobalt-labelled neurons have only orange, whereas the nickel-labelled neurons have only blue colorization in their somata, while the labelled serotonergic neurons have dark pigment granules in their somata besides the blue or orange colorization. By this double labelling technique the central serotonergic neurons which send processes to different body regions through CNS nerves, can be identified in wholemount preparations.

5,6-Dihydroxytryptamine↗

PubMed1990

Effects of (+)-4-propyl-9-hydroxynaphthoxazine on midbrain dopamine neurons: an electrophysiological study.

(+)-4-Propyl-9-hydroxynaphthoxazine (PHNO) is a highly potent, D2-selective dopamine (DA) receptor agonist. In the present study, we have examined the electrophysiological effects of PHNO on identified nigrostriatal DA (NSDA), mesoaccumbens DA (MADA) and Type I caudate neurons. Intravenous PHNO dose-dependently inhibited the firing rate of NSDA and MADA neurons in both chloral hydrate (CH)-anesthetized rats (ED50 values = 21.2 +/- 1.2 and 26.5 +/- 1.4 ng/kg, respectively) and locally anesthetized, paralyzed rats (ED50 values = 105.0 +/- 1.4 and 109.1 +/- 1.4 ng/kg, respectively). PHNO was significantly more potent in the CH-anesthetized rats. There was a significant, positive correlation between basal firing rate and log ED50 for NSDA neurons in both preparations and for MADA cells only in CH-anesthetized animals. Neither pretreatment with the D1 receptor agonist SKF 38393 nor hemitransection of the forebrain altered the rate-dependent nature of PHNO-induced inhibition of NSDA neurons. Likewise, depletions of serotonin with either p-chlorophenylalanine or 5,7-dihydroxytryptamine failed to alter the rate-dependent PHNO-induced inhibition of NSDA neurons. Iontophoretically applied PHNO inhibited both NSDA and MADA neurons to a similar degree as either DA or the D2 agonist quinpirole. In contrast, the similar effects of PHNO and quinpirole on Type I caudate neurons were significantly different than those of DA. These results suggest that PHNO inhibits midbrain DA neurons via stimulation of somatodendritic autoreceptors and that PHNO exhibits an electrophysiological profile characteristic of D2 agonists. In contrast to quinpirole, however, the rate-dependent nature of PHNO-induced inhibition of these cells was resistant to modulation.

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

PubMed1990

[Central presynaptic receptors].

Experiments on two different inhibitory presynaptic receptor systems are presented. 1. Superfused and electrically stimulated brain slices are a widely used experimental model to study the release of noradrenaline and its modulation by inhibitory alpha-2 adrenoceptors. By using a minisuperfusion chamber we succeeded in studying the simplest case of autoinhibition, i.e. the release of transmitter induced by a single pulse and two consecutive pulses, respectively. When electrical stimulation is performed using a single pulse, no autoinhibition is possible, whereas following stimulation with two pulses the transmitter released by the first pulse will inhibit the effect of the second pulse. By systemically varying the time interval between the two pulses the minimal time requirement for development of autoinhibition was determined to be 100 ms. Short pulse trains of high frequency such as 4 pulses within 30 ms circumvent autoinhibition and cause inhibition-free release by each applied pulse. The release of transmitter evoked in this way is not only free from autoinhibition but, in addition, easily measurable, which makes this method of stimulation very suitable for analyses at presynaptic receptors. By using this approach it became possible, for the first time, to determine dissociation constants of antagonists and agonists at the central presynaptic alpha-2 adrenoceptor without the distortion introduced by autoinhibition occurring during release. 2. There is a substantial body of evidence for a role of medullary serotonergic nerve cells in the regulation of blood pressure and heart rate. It is hypothesized that the serotonergic neurons project to the thoracic spinal cord exerting a tonic excitatory influence on presynaptic sympathetic neurons of the intermediolateral cell column. Experiments were performed in pentobarbital anaesthetized rats to reduce this excitatory tone by activating inhibitory autoreceptors which are located on the perikarya and dendrites on the serotonergic cells and which have been shown to belong to the 5-HT1A subtype. Local stereotactic injection of the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) caused a decrease in mean arterial blood pressure (MAP) and heart rate (HR). The effects were blocked by pretreatment of the animals with the 5-HT1A antagonist spiroxatrine. Moreover, neurochemical lesioning of serotonergic neurons by intracisternal injection of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) abolished the effects of 8-OH-DPAT. Bilateral intraspinal injection of 5,7-DHT, which interrupts the medullo-spinal serotonergic pathway, markedly attenuated the effects of local intramedullary injection of 8-OH-DPAT.(ABSTRACT TRUNCATED AT 400 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1990

[Ultrastructure of the parietal region of the brain after selective damage of the serotoninergic system].

The selective lesion of the afferent serotoninergic system by means of intracisternal administration of 5,7-dihydroxytryptamine produces certain structural rearrangements in a part of cellular elements and in various parts of the neuropil of the neocortical parietal area. The deficiency of serotoninergic innervation influences the metabolic processes. This is evident from the change in the structure of protein synthesizing apparatus in a number of postsynaptic neurons. It is possible that the structural rearrangements observed in the serotoninergic and in the conjugated to it mediatory systems make the base of functional disorders in the neocortex and are accompanied with certain changes in the integrative activity of the brain.

5,7-Dihydroxytryptamine↗

PubMed1990

[Ultrastructure of the serotoninergic system of the motor area of the cerebral cortex].

Owing to the microscopical investigation, using selective neurotoxin 5,7-dihydroxytryptamine, it has been possible to reveal the serotoninergic system and targets of its innervation in the rat cerebral cortex motor area. The serotoninergic axonal varicosities and synaptic boutons are present in all layers of the neocortex. Their large amount is revealed in the I and II layers. The terminals form contacts with dendrites of small size, sometimes they terminate on the head of the spines, as well as on bodies of neurons in different layers. According to their position and ultrastructural organization these neurons are, perhaps, pyramidal, that is glutamatergic, and those less in their size--refer to interneurons and can be GABAergic ones. Basing on own data and those of the literature, concerning the existence of nonsynaptic link for transmission of serotoninergic effects, a conclusion is made that a coordinating functioning of the synaptic and non-synaptic intercellular integrative mechanisms ensure a wide range of functions of the serotoninergic system in the cerebral cortex.

5,7-Dihydroxytryptamine↗

PubMed1987

Role of serotonin in opiate-induced prolactin secretion and antinociception in the developing rat.

Our laboratory has demonstrated previously that the ability of opiates to stimulate prolactin (PRL) release during ontogeny precedes the appearance of a PRL response to serotonergic drugs. The present study tests the hypothesis that opiates stimulate PRL secretion through a serotonergic mechanism in adult rats, but a nonserotonergic mechanism in neonatal rats. Morphine stimulated PRL secretion in adult and neonatal (10-day-old) rats and this increase was blocked with the opiate antagonist naloxone. Ten-day-old or adult rats were pretreated with the serotonin antagonist, cyproheptadine (CYPRO), or the neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). Both CYPRO and 5,7-DHT attenuated the PRL response to morphine in adult but not neonatal rats. 5,7-DHT decreased serotonin and 5-hydroxyindoleacetic acid substantially in the hypothalamus. When rats were pretreated with 5,7-DHT several weeks before morphine challenge, serotonin depletion was more pronounced, but the PRL response to morphine was not decreased. In addition, the PRL response to 5-hydroxytryptophan was greatly potentiated, suggesting that functional supersensitivity developed in the 5,7-DHT-treated animals. The ability of CYPRO and 5,7-DHT to block the serotonergic component of a different morphine-induced behavior in the neonate was tested using the tail immersion test for analgesia. Morphine produced profound antinociception in the rat pup which was attenuated markedly by 5,7-DHT and CYPRO. These studies demonstrate that opiates mediate their stimulatory effects on PRL release, at least in part, through a serotonergic mechanism in adult rats.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1989

Immunohistochemical identification of serotonin and noradrenalin containing structures within the nerve plexuses of rat ileum.

The distribution of 5-hydroxytryptamine (= serotonin = 5-HT) and noradrenalin (NA) in the enteric plexuses of the rat ileum was studied using immunocytochemical techniques. 5-HT-like immunoreactive fibers were observed only in the myenteric plexus, surrounding the ganglionic cells, which are all unreactive. NA-like immunoreactive fibers were present in all layers of the ileum: in the myenteric plexus, they were localized in the nodes, forming a network all round the neuronal perikarya; in the Meissner plexus, positive axons were arranged in a delicate network; submucosal blood vessels were often provided by NA-immunopositive nerve plexus. In the inner circular muscle layer the immunoreactive NA-positive fibers run within nerve bundles mainly parallel with the smooth muscle cells. The 5-HT immunoreactive material was depleted by treatment with reserpine; depletion of NA by 6-hydroxy-dopamine was also observed; on the contrary, no depletion of 5-HT by 5,7-dihydroxytryptamine was obtained. To confirm the validity of these results, specific antibodies to tyrosine hydroxylase (TH) and aromatic 1-aminoacid-decarboxylase (AADC), two enzymes involved in the synthesis of catecholamines, were used. In conclusion these experiments indicate that 5-HT is present, probably as a transmitter, in certain fibres of the rat myenteric plexus, distributed in a way similar to that of NA-containing fibers. However, at variance with NA fibers, 5-HT fibers are not present in other regions of the intestine wall.

5,7-Dihydroxytryptamine↗

PubMed1989

Depletion of serotonin in the nervous system of Aplysia reduces the behavioral enhancement of gill withdrawal as well as the heterosynaptic facilitation produced by tail shock.

Noxious stimuli, such as electrical shocks to the animal's tail, enhance Aplysia's gill- and siphon-withdrawal reflex. Previous experimental work has indicated that this behavioral enhancement, known as dishabituation (if the reflex has been habituated) or sensitization (if it has not been habituated), might be mediated, at least in part, by the endogenous monoaminergic transmitter serotonin (5-HT). To assess 5-HT's role in dishabituation and sensitization of Aplysia withdrawal reflex, we treated Aplysia with the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). We found that 5,7-DHT treatment significantly reduced the dishabituation of the withdrawal reflex produced by tail shock. Treatment with the neurotoxin also blocked the heterosynaptic facilitation of monosynaptic connections between siphon sensory neurons and their follower cells, which contributes to the behavioral enhancement. Analysis by high-performance liquid chromatography indicated that 5,7-DHT treatment significantly reduced 5-HT levels in the Aplysia CNS. Moreover, the neurotoxic effects of 5,7-DHT appeared to be relatively specific for serotonergic pathways. Thus, 5,7-DHT treatment did not disrupt the ability of nonserotonergic facilitatory interneurons, the L29 cells, to facilitate the connections of siphon sensory neurons. Also, 5,7-DHT reduced 5-HT-dependent, but not dopamine-dependent, histofluorescence in Aplysia central ganglia. Finally, 5,7-DHT does not reduce the levels of the facilitatory peptides SCPA and SCPB within the Aplysia CNS. Our results, together with those of Mackey et al. (1989), indicate that 5-HT plays a major role in mediating dishabituation and sensitization of Aplysia's withdrawal reflex.

5,7-Dihydroxytryptamine↗

PubMed1989

Sexual receptivity after destruction of serotonergic terminals in hypothalamus or amygdala.

In order to localize the sites in the brain where serotonergic (5-HT) input may affect the performance of lordotic responses, the serotonin neurotoxin 5-7-dihydroxytryptamine was injected in the ventromedial hypothalamic nucleus (VMN) or in the medial amygdala (AM) in ovariectomized rats. Estrogen induced receptivity as measured by the lordotic quotient was significantly greater in animals injected in AM, but it was smaller in animals injected in the VMN, as compared to controls or animals injected with the vehicle. No differences were found when the same animals were injected with progesterone. It is proposed that serotonergic afferents exert facilitatory influences in the hypothalamus and inhibitory influences in the amygdala, as concerns estrogen-induced sexual receptivity. The integrity of 5-HT terminals in VMN and AM is not necessary for progesterone to exert its potentiating effects.

Amygdala↗

PubMed1989

Presynaptic activation of the spinal serotonergic system in the rat by phencyclidine in vitro.

Electrophysiological studies were carried out to investigate the mechanism of action of phencyclidine [PCP; 1-(phenylcyclohexyl)piperidine] on a segmental monosynaptic reflex using isolated spinal cord preparations from neonatal rats. PCP and its related compounds produced a concentration-dependent depression of the monosynaptic reflex with a relative potency as follows: PCP = 1-[1-(2-thienyl)cyclohexyl]piperidine greater than 1-(1-m-aminophenylcyclohexyl)piperidine much greater than 1-(1-m-nitrophenylcyclo-hexyl)piperidine approximately MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate] much greater than (+)-N-allylnormetazocine. The N-methyl-D-aspartate receptor antagonists 2-amino-5-phosphonovalerate and 2-amino-7-phosphonoheptanoate had no effect on the monosynaptic reflex. The depression of the monosynaptic reflex by PCP was antagonized by serotonin (5-HT) receptor antagonists (methiothepin, spiperone and ketanserin) but unaffected by noradrenergic (phentolamine and timolol), dopaminergic (chlorpromazine and pimozide) and cholinergic antagonists (atropine and mecamylamine). Whereas 5-HT and a putative 5-HT releaser, p-chloroamphetamine, also depressed the monosynaptic reflex, the blockade of monoamine uptake by imipramine did not. Furthermore, pretreatment of rats with desipramine and 5,7-dihydroxytryptamine largely diminished the depression of the monosynaptic reflex by PCP and p-chloroamphetamine while enhancing the depressant action of 5-HT. These results suggest that PCP acts at sites located on presynaptic terminals of spinal serotonergic neurons, enhancing 5-HT release and thereby depressing the monosynaptic reflex.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

[The interaction of the serotonin and dopaminergic systems of the brain in the mechanisms of latent inhibition in rats].

Decrease of serotonin concentration in the septo-hippocampal region of Wistar male rats was obtained by introduction of 5,7-dihydroxytryptamine in the raphe median nucleus. In seven days, after 20 pre-expositions of the conditioned stimulus (presentation of the experimental chamber) conditioned reaction of passive avoidance was elaborated. In sham-operated control the pre-exposition of the conditioned stimulus caused latent inhibition, determined by several parameters: low level of conditioned reaction reproduction, its prolonged preservation at the formed level and nonsubjection to amnesia. Introduction of haloperidol in a dose of 0.5 mg/kg one hour before learning restored the state of latent inhibition disturbed by switching off of the mesolimbic serotonin system. It is supposed that in the state of pre-exposition, the decrease of attention to nonreinforced stimulus takes place because of the intensification of inhibitory influence of the serotoninergic system and reciprocal decrease of dopaminergic system activity.

5,7-Dihydroxytryptamine↗

PubMed1988

The serotonin/norepinephrine-link in brain. II. Role of serotonin in the regulation of beta adrenoceptors in the low agonist affinity conformation.

The present studies were undertaken to characterize further the role of serotonin (5-HT) in the regulation of the norepinephrine (NE) beta adrenoceptor coupled adenylate cyclase system in the rat cortex. Although 5-HT in vitro did not influence maximum binding and Kd values of [3H]dihydroalprenolol binding or the IC50 value for isoproterenol as estimated from competition binding curves in cortical tissue from control animals, 5-HT abolished the increase in beta adrenoceptor number and the marked elevation of the IC50 value for isoproterenol in cortical membrane preparations after selective lesions with 5,7-dihydroxytryptamine (5,7-DHT). Nonlinear regression analysis of competition binding curves revealed that the increase in the maximum binding of beta adrenoceptors after 5,7-DHT is due exclusively to an increase in beta adrenoceptors in the agonist low affinity conformation and that it is this receptor population that is reduced by nanomolar concentrations of 5-HT. The increase in the density of beta adrenoceptors in the low affinity conformation occurred approximately 11 days after the lesions and remained elevated throughout the experimental period of 28 days. Ritanserin in a dose that virtually abolished 5-HT2 receptor binding in cortex did not mimic the effect of 5,7-DHT.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1985

Methyldopa hypotension and ascending projections from midline serotonin (B3) cells in the medulla.

Micro-injection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla of spontaneously hypertensive rats, stroke-prone strain (SHRSP), caused a fall in blood pressure of 30-40 mmHg, maximally 2-3 h after administration. This hypotension was abolished by the selective serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly, but it was not affected by intraspinal injection of 5,7-DHT to produce a selective lesion of serotonin nerves descending into the spinal cord, or by injection of 5,7-DHT into the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells. It seems likely that the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa through a projection restricted to the caudal brainstem.

5,7-Dihydroxytryptamine↗

PubMed1985

Neural pathways mediating adrenocortical responses.

The effects of hypothalamic deafferentations and brain lesions on adrenocorticotropin (ACTH) and corticosterone (CS) responses after neural stimuli were studied in rats. It was found that the various modalities are mediated by different neural pathways. Photic and acoustic stimuli utilize a posterior input, whereas the sciatic and olfactory modalities are mediated by anterior afferents and forebrain limbic structures. The effects of limbic extrahypothalamic structures on the hypothalamus are transmitted by both anterior and posterior inputs. The medial forebrain bundle (MFB) was found to have a differential role in the mediation of ACTH and CS responses. To identify the neurotransmitters involved, rats were injected with 6-hydroxydopamine in the MFB and 5,7-dihydroxytryptamine in the raphe nuclei. The depletion of hypothalamic norepinephrine and serotonin caused inhibition of the adrenocortical responses only after photic stimulation, and only of responses to limbic stimuli in the former group. In view of the location of corticotropin-releasing factor in the paraventricular nucleus, responses to afferent stimuli were studied in this region in identified neurons projecting to the median eminence. Stimuli that increased or decreased CS secretion facilitated or inhibited cell firing, respectively, thus demonstrating a possible electrophysiological correlate of neuroendocrine regulation.

5,7-Dihydroxytryptamine↗

PubMed1986

Cholinergic and GABAergic regulation of dopamine beta-hydroxylase activity in the adrenal gland of the rat.

The administration of oxotremorine together with methylatropine to rats produces a dose-dependent increase of adrenal dopamine-beta-hydroxylase (DBH) activity. This effect is abolished by denervation of the gland and by cycloheximide. The Km for tyramine is not affected by the trans-synaptic induction of DBH by oxotremorine. The induction is selective, because similar treatment does not affect adrenal dopa decarboxylase or lactate dehydrogenase in the adrenal gland. The combination of 6-hydroxydopamine i.c.v. or propranolol i.p. does not alter the effect of oxotremorine on adrenal DBH. However, propranolol reduces the tremorigenic action of the muscarinic agonist. The systemic administration of p-chlorophenylalanine or the i.c.v. injection of 5,7-dihydroxytryptamine before oxotremorine treatment does not affect the increase of adrenal DBH. Progabide, gamma-aminobutyric acid, a (GABA)A and GABAB receptor agonist that effectively crosses the blood-brain barrier, reduces the effect of oxotremorine in a dose-dependent manner. Muscimol given by either of two routes, i.c.v. at a constant rate (Alzet minipump) or i.p., produces significant decreases of adrenal DBH activity and attenuates the action of oxotremorine. Denervation of the gland abolishes the effect of muscimol i.p. in decreasing adrenal DBH activity. Baclofen, a GABAB receptor agonist, has no effect by itself or does it affect the action of oxotremorine. None of these GABA agonists has any in vitro effect on adrenal DBH activity. Bicuculline, GABAA receptor antagonist, reverses the action of progabide in oxotremorine-treated rats with respect to adrenal DBH activity, partially blocks the effect of muscimol and enhances the increase obtained with oxotremorine.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1986

[Specific lesions of serotoninergic cells in the raphe. Effect on kindling of the olfactory bulb in rats].

Limbic kindling obtained by electrical stimulation of the olfactory bulb in the rat has been studied after specific lesion of serotonergic cells in mesencephalic and pontic raphe nuclei with local microinjection of 5,7-dihydroxytryptamine. The extent of the raphe lesions was verified by immunocytochemical technics with antiserotonin antibody. Lesioned rats showed an increase of kindling rate, which confirms the inhibitory function of serotonin in the development of this phenomenon.

5,7-Dihydroxytryptamine↗