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PubMed2001

Serotonin modulates expression of VIP and GRP mRNA via the 5-HT(1B) receptor in the suprachiasmatic nucleus of the rat.

The expression of vasoactive intestinal peptide (VIP) and gastrin-releasing peptide (GRP) in the suprachiasmatic nucleus (SCN) changes depending on light. VIP mRNA increases and GRP mRNA decreases in the light phase, while they do not show change without light. In the present study we investigated the involvement of serotonin (5-HT) in the expression of VIP and GRP messenger RNA in the SCN of the rat. The decrease in VIP mRNA and the increase in GRP mRNA in the light phase were amplified by 5-HT depletion using 5,6-dihydroxytryptamine injected into the lateral ventricle. These enhancements due to 5-HT depletion were reversed to control levels by applying 5-HT(1B) agonists TFMPP and CGS12066A, but not a 5-HT(1A)/5-HT(7) agonist, 8-OH-DPAT. The 5-HT(1B) receptor is known to exist on the terminals of the retinohypothalamic tract (RHT). Therefore, next we investigated the morphological relationship of RHT and 5-HT terminals by double-labeling immunocytochemistry and demonstrated that 5-HT-immunoreactive fibers and cholera toxin B subunit-labeled RHT terminals were intermingled in the ventrolateral SCN, and 5-HT axon processes had close contact with RHT terminals. Collectively, these pharmacological and morphological results suggest that 5-HT afferents from raphe nuclei modulate VIP and GRP expression in neurons of the ventrolateral SCN by activating the 5-HT(1B) receptor in the RHT.

5,6-Dihydroxytryptamine↗

PubMed1987

Relation between yawning behavior and central serotonergic neuronal system in rats.

Subcutaneously (s.c.) administered apomorphine (0.0125-0.4 mg/kg) or physostigmine (0.025-0.4 mg/kg) to rats elicited yawning. The dose-response curves were bell-shaped. The peak effects of apomorphine and physostigmine were observed with a dose of 0.1 mg/kg of each drug. Yawning elicited by apomorphine (0.1 mg/kg) or physostigmine (0.1 mg/kg) was reduced by intraperitoneally (i.p.) administered 5-hydroxytryptophan (5-HTP, 50-200 mg/kg, given 30 min before). Yawning elicited by apomorphine but not by physostigmine was enhanced by p-chlorophenylalanine (p-CPA, 25-400 mg/kg i.p., given 24 h before). Apomorphine elicited but not physostigmine-elicited yawning was enhanced by pretreatment with 5,7-dihydroxytryptamine (5,7-DHT, 8 micrograms/rat, given 14 days before into the dorsal raphe). This treatment led to a 35% depletion of serotonin (5-HT) in the striatum. 5-HTP, p-CPA or 5,7-DHT given alone did not elicit yawning. Bilateral, intrastriatal microinjection of apomorphine (1.5-50 micrograms/site) but not physostigmine (5-50 micrograms/site) elicited yawning. The dose-response curve was also bell-shaped. These results indicate that central serotonergic pathways play an important role in modulating drug-elicited yawning in rats.

5,7-Dihydroxytryptamine↗

PubMed1987

Changes in central serotoninergic transmission affect clonidine analgesia in monkeys.

The effects of changes in central serotoninergic transmission on clonidine analgesia were assessed in monkeys. The minimum electrical current required for producing jaw opening is referred to as the pain threshold. Pain was induced by electrical stimulation of tooth pulp afferents. In the first series of studies, intracerebroventricular administration of clonidine (5-30 micrograms) produced dose-dependent analgesia in monkeys. The clonidine-induced analgesia was abolished or attenuated by prior injection of the animals with p-chlorophenylalanine or 5,7-dihydroxytryptamine into the third cerebral ventricle. On the other hand, pretreatment of the animals by injecting 5-HT or its precursor 5-hydroxytryptophan into the cerebral ventricle potentiated the clonidine-induced analgesia in monkeys. In the second series of experiments, administration of clonidine (1-10 micrograms) into the diencephalic periventricular gray (of the anterior hypothalamic portion), the periaqueductal gray, or the dorsal raphe nuclei also produced dose-dependent analgesia in monkeys. The analgesia induced by clonidine injection into the diencephalic periventricular gray or the periaqueductal gray was effectively antagonized by pretreatment of the animals by injecting two 5-HT receptor antagonists (such as ketanserine and methysergide) into the diencephalic periventricular gray or the periaqueductal gray. The clonidine-induced analgesia in monkeys was not affected by pretreatment of the animals with injections of either ketanserine or methysergide into the dorsal raphe nuclei. The results suggest that the functional activity of central 5-HT neurons correlate well with the analgesic sensitivity of clonidine microinjected centrally. In addition, the analgesia induced by clonidine microinjected into the diencephalic periventricular gray or the periaqueductal gray was mediated by the 5-HT receptors at the site of injection.

5,7-Dihydroxytryptamine↗

PubMed1988

Role of ascending and descending serotonergic pathways in the antinociceptive effect of baclofen.

The role of ascending and descending serotonergic pathways in the antinociceptive effect of baclofen was examined by lesioning specific pathways with the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). Antinociception in rats was assessed using the tail flick and hot plate tests 3/4 and 10/11 days after lesioning and the placement of lesions verified by analysis of serotonin (5-HT) in brain and spinal cord. Lesions to the ventromedial tegmentum depleted 5-HT selectively in brain and inhibited the antinociceptive effect of baclofen in the tail flick test 3/4 but not 10/11 days after lesioning. Lesions to the nucleus raphe medianus produced a marked depletion of 5-HT in the hippocampus and produced the same effect on baclofen. Lesions to the nucleus raphe dorsalis were less selective, depleting 5-HT in a number of brain regions and in the spinal cord, and inhibited the antinociceptive effect of baclofen at the later but not the earlier time interval. Lesions to descending pathways by microinjection of 5,7-DHT into the ventral raphe or nucleus raphe magnus did not affect the action of baclofen significantly. Lesions to both ascending and descending pathways by intracerebroventricular 5,7-DHT increased the effect of baclofen. The hot plate test generally was less sensitive to these manipulations, although changes parallel to the tail flick test were observed in a number of instances. Both the destruction of 5-HT pathways and development of supersensitivity at 5-HT receptors may contribute to the interactions observed.

5,7-Dihydroxytryptamine↗

PubMed1992

Spinal 5-HT pathways and the antinociception induced by intramedullary clonidine in rats.

The possible involvement of spinal 5-hydroxytryptamine (5-HT) pathways in antinociception induced by microinjection of clonidine into the ventrolateral surface of the medulla oblongata was investigated in rats. Microinjection of clonidine (10-20 micrograms), but not yohimbine (1 microgram) or 0.9% saline, into the lateral medulla prolonged the hot plate latency in rats. This clonidine-induced antinociception was abolished by intramedullary injection of the alpha 2-adrenoceptor antagonist, yohimbine. Selective destruction of spinal 5-HT neurons produced by intraspinal injection of 5,7-dihydroxytryptamine (5,7-DHT; 10 micrograms) or postsynaptic blockade of spinal 5-HT receptors produced by intrathecal injection of cyproheptadine (1 microgram; a mixed 5-HT1/5-HT2 antagonist) also abolished clonidine-induced antinociception. Rats given 5,7-DHT intraspinally or cyproheptadine intrathecally showed a decrease in hot plate latency as compared with the controls. In anesthetized rats, the 5-HT release from the thoracic spinal cord was enhanced by microinjection of clonidine into the lateral medulla. This enhanced spinal 5-HT release evoked by intramedullary injection of clonidine was abolished by pretreatment of rats with intraspinal injection of 5,7-DHT. These results indicate that 5-HT pathways to the spinal cord mediate the antinociceptive effect induced by microinjection of clonidine into the ventrolateral surface of the medulla oblongata in rats.

5,7-Dihydroxytryptamine↗

PubMed1986

The antinociceptive effect of intracerebroventricularly administered prostaglandin D2 in the rat.

Intracerebroventricular administration of prostaglandin D2 (PGD2), the major PG in the rat brain, produced a dose-related anti-nociceptive effect in rats as assessed by the rat tail-hot wire, hot plate and phenylquinone-induced writhing techniques. The antinociceptive action of centrally-administered PGD2 was markedly attenuated after pretreatment of the rats with 5,6-dihydroxytryptamine, a selective neurotoxin for central serotonergic neurones, and p-chlorophenylalanine, a specific inhibitor of serotonin synthesis, indicating that the PGD2 action is serotonin-mediated. Naloxone, an antagonist of endogenous opioid receptors, also antagonised the antinociceptive action of PGD2. Earlier reports from this laboratory have shown that the antinociceptive action of centrally-administered PGE1 in rats is a serotonin-mediated effect and is also antagonised by naloxone. It was further shown that PGD2, like PGE1, augments serotonin turnover in the rat brain. The present findings support the view that PGD2 shares some of the central actions of PGEs and, like the latter, may function as a neuromodulator in the central nervous system.

5,6-Dihydroxytryptamine↗

PubMed1988

Rotational behavior induced by 8-hydroxy-DPAT, a putative 5HT-1A agonist, in 6-hydroxydopamine-lesioned rats.

Rats with unilateral 6-hydroxydopamine (6-OHDA)-induced lesions of the ascending nigro-striatal pathway have been shown to rotate in response to dopamine (DA) agonists that are not considered to have postsynaptic DA stimulant properties in intact animals, suggesting a relative loss of DA receptor selectivity in the denervated striatum. The present experiments assessed the possibility that this loss of selectivity may extend to serotonin (5HT) agonist drugs. The 5HT-1a agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), at doses of 0.3-3 mg/kg SC, induced robust contralateral rotational behavior (RB) in 6-OHDA-lesioned rats that had been preselected on the basis of high responsiveness to the atypical DA agonists 3-PPP and SKF 38393. Rats with unilateral dorsal raphe lesions induced by 5,7-dihydroxytryptamine (5,7-DHT) showed contralateral RB in response to similar doses of 8-OH-DPAT but with a different behavioral pattern. The putative 5HT-1b agonist RU 24969 produced contralateral RB in 5,7-DHT-lesioned rats while showing a much weaker effect in 6-OHDA-lesioned rats. Striatal DA levels were depleted by 99% in representative 6-OHDA-lesioned rats but striatal 5HT levels were unaffected. The effects of 8-OH-DPAT in 6-OHDA-lesioned rats were therefore not attributable to destruction of ascending 5HT-containing neurons. These effects may result from indirect actions, mediated by 5-HT neurons or neuronal receptors, that result from asymmetry of brain DA systems.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1987

The serotonin/noradrenaline-link in brain. I. The role of noradrenaline and serotonin in the regulation of density and function of beta adrenoceptors and its alteration by desipramine.

The present studies were undertaken to assess the role of noradrenaline (NA) and serotonin (5HT) in the regulation of the NA receptor coupled adenylate cyclase system and its alteration by desipramine (DMI) in brain structures with or without noradrenergic neuronal projections. In contrast to cortex and limbic forebrain, where chronic DMI administration caused subsensitivity of the NA sensitive adenylate cyclase linked to a down-regulation of beta adrenoceptors, the drug failed to alter the NA receptor coupled adenylate cyclase system in the striatum. Selective lesions of serotonergic axons with 5,7-dihydroxytryptamine caused a significant increase in the density of beta adrenoceptors in cortex, limbic forebrain and striatum and prevented the down-regulation by DMI of beta adrenoceptors in cortex and limbic forebrain while the responsiveness of the NA sensitive adenylate cyclase was reduced to the same extent as in sham-lesioned control animals. The discrepancy between beta adrenoceptor number and NA responsiveness following lesions of 5HT axons was particularly profound in the striatum. The analysis of high- and low-affinity components of agonist binding demonstrated that the increase in striatal beta adrenoceptors is due to a marked increase in receptors with low affinity while the number of receptors with high affinity is unchanged. The results lend further support to the view that the synaptic availability of NA is a prerequisite for the induction of subsensitivity of the NA sensitive adenylate cyclase and for the down-regulation of its beta adrenoceptor population by DMI and that 5HT plays a pivotal role in both the regulation of the number and the function of central beta adrenoceptors.

5,7-Dihydroxytryptamine↗

PubMed1987

A study of the possible influence of central 5-HT function on clonidine-induced hypoactivity responses in mice.

Administration of the alpha 2-adrenoceptor agonist clonidine (0.1 mg/kg) produces hypoactivity in mice. This sedation response was unaltered by pretreatment with either the 5-HT reuptake inhibitor zimeldine (1 or 10 mg/kg) or the 5-HT agonist quipazine (0.25 or 2.5 mg/kg). The 5-HT1B agonist RU 24969 (0.2 or 1 mg/kg) enhanced hypoactivity responses at the higher dose. The non-selective 5-HT antagonists methysergide (1 or 10 mg/kg) and metergoline (0.2 or 1 mg/kg) potentiated clonidine-induced hypoactivity. However, the marked enhancement produced by metergoline may have been due to its potent action as a alpha 1-adrenoceptor antagonist. Nevertheless, the 5-HT2 antagonists ritanserin (0.1 or 1 mg/kg) and ketanserin (0.1 or 1 mg/kg) both potentiated clonidine hypoactivity in a dose-dependent manner. beta-Adrenoceptor antagonists also inhibit 5-HT1 receptors at high dose. Pindolol (10 mg/kg) had no effect on sedation, but [-]-propranolol (20 mg/kg) caused some attenuation. This latter effect was probably not due to inhibition of 5-HT1 receptors, because this reduction also occurred at low dose (2 mg/kg). Destruction of 5-HT neurones by intracerebroventricular injection of 5,7-dihydroxytryptamine (50 micrograms) resulted in a marginal increase in hypoactivity. In conclusion, these data shown that central 5-HT function can influence alpha 2-adrenoceptor-mediated hypoactivity responses. However, since these effects were usually only apparent after severe manipulation of 5-HT function, it suggests that while these interactions may be of pharmacological interest, they are probably not of physiological importance.

5,7-Dihydroxytryptamine↗

PubMed1993

Co-localization of serotonin and GABA in neurons of the Xenopus laevis retina.

Serotonin-synthesizing neurons in the retina of Xenopus laevis have been identified using anti-phenylalanine hydroxylase (PH) antibody which recognizes tryptophan 5-hydroxylase, the rate-limiting enzyme for serotonin synthesis. Double-labelling experiments, using anti-PH antibody and anti-serotonin antibody/5,7-dihydroxytryptamine (5,7-DHT) uptake, have shown that some serotonin-like immunoreactive/5,7-DHT-labelled neurons exhibit PH-like immunoreactivity (PH-LI) (serotonin-synthesizing neurons), but the others do not (serotonin-accumulating neurons). In the present study, triple-labelling experiments were performed using 5,7-DHT uptake and antibodies raised against GABA and PH, to determine the possible co-localization of y-aminobutyric acid (GABA) in serotonin-synthesizing and/or -accumulating neurons in the Xenopus retina. All 5,7-DHT-labelled bipolar cells lacked PH-LI; all of them were immunoreactive to GABA. In contrast, all 5,7-DHT-labelled large amacrine cells exhibited PH-LI, but none of them expressed GABA-LI. Small amacrine cells labelled with 5,7-DHT but not PH-LI exhibited GABA-LI, whilst the small amacrine cells with PH-LI lacked GABA-LI. These observations indicate that GABA is co-localized in serotonin-accumulating amacrine and bipolar cells, whereas serotonin-synthesizing large and small amacrine cells do not contain GABA-LI.

5,7-Dihydroxytryptamine↗

PubMed1987

Lesions of the serotonergic system impair the facilitation of but not the tolerance to the effects of chronic clenbuterol administration.

Acute clenbuterol, a beta-adrenergic stimulant, decreases motility and antagonizes reserpine-induced hypothermia in mice. After repeated treatment with clenbuterol, the hypomotility disappears (tolerance) but the antagonism of reserpine-induced hypothermia increases (facilitation). To investigate the function of serotonin in tolerance and facilitation, lesions of the serotonergic system were performed by intracerebroventricular administration of the neurotoxin 5,7 dihydroxytryptamine (5,7-DHT). After lesions of the serotonergic system, the tolerance to clenbuterol-induced hypomotility persists, but the facilitation of the antagonism by clenbuterol of reserpine-induced hypothermia disappears. Thus, the serotonergic nerve terminals must be intact for the latter but not the former response to occur. Since the reversal of reserpine-induced hypothermia in animals is predictive of antidepressant effects in man, it is suggested that the therapeutic action of clenbuterol in depressed patients may be mediated through the serotonergic system.

5,7-Dihydroxytryptamine↗

PubMed1988

Reduction of feeding behavior by the serotonin uptake inhibitor sertraline.

Administration of the selective serotonin (5-HT) uptake inhibitor sertraline produced a dose-dependent reduction of food intake in rats. Doses of sertraline of 10 mg/kg or greater reduced the intake of solid pellets significantly (P less than 0.01) during the 1st hour of a 4-h feeding test in rats deprived of food and water for 24 h. Food intake during the remaining 3 h and water intake during the feeding test was unaffected by sertraline. Sertraline (2-18 mg/kg IP) also reduced milk consumption in food-deprived rats. Pretreatment with the nonselective 5-HT antagonists metergoline (2 mg/kg IP) or methysergide (3.3 mg/kg IP) blocked sertraline's inhibition of dry food intake, whereas pretreatment with the selective 5-HT2 receptor antagonist ketanserin (3.3 mg/kg IP) or the peripheral 5-HT2 antagonist xylamidine (2.5 mg/kg IP) failed to block sertraline's anorexic effect. The feeding-suppressant effect of 10 mg/kg sertraline was prevented following the destruction of central 5-HT neurons by the 5-HT neurotoxic agent, 5,7-dihydroxytryptamine (200 micrograms ICV). This result is consistent with sertraline's anorexic effect depending on intact 5-HT neurotransmission. Therefore, sertraline appears to reduce feeding by enhancing the action of endogenous serotonin at central synapses mediated by 5-HT1 rather than 5-HT2 receptors.

1-Naphthylamine↗

PubMed1994

Synaptic connectivity of serotonin graft efferents in the suprachiasmatic and supraoptic nuclei of the hypothalamus.

We have previously reported that a cell suspension from the rostral part of the embryonic raphe grafted to the basal hypothalamus of 5,7-dihydroxytryptamine-denervated rats produced incomplete serotonin (5-HT) re-innervation of the suprachiasmatic nucleus (SCN) as opposed to hyper-innervation of the supraoptic nucleus (SON). We took advantage of this experimental model to investigate whether the graft-derived, 5-HT fibres retained normal ultrastructural features, and, particularly, a normal density of synaptic junctions, irrespective of the extent of target re-innervation. The intrinsic features of immunostained, graft-derived 5-HT axonal varicosities in both the SCN (ventral portion) and the SON were essentially similar to those exhibited by the respective endogenous innervation. Analysis of well-preserved varicosities in uninterrupted series of thin sections allowed us to evaluate directly the proportions of junctional to non-junctional 5-HT varicosities in both regions. Synaptic incidences were also remarkably conserved after grafting (45.5% in the SCN versus 38.5% in the SON; 48% and 38% in normal rats, respectively). Synapses were primarily reestablished on dendritic shafts, which also were identified as the major post-synaptic targets of the normal 5-HT innervations. We noted, however, a tendency toward increased numbers of symmetrical versus asymmetrical synapses in both the SCN and SON of grafted rats. Thus, irrespective of whether hypo- or hyper-innervation patterns developed post-grafting, the transplanted 5-HT neurons essentially retained normal ultrastructural features in their target territories, with a normal incidence of synaptic junctions. The data provide further support to the hypothesis that the innervation territory is the major determinant of the frequency with which ingrowing 5-HT fibres make synaptic junctions.

5,7-Dihydroxytryptamine↗

PubMed1979

Electron microscopy of the indoleamine-accumulating neurons in the retina of the rabbit.

The recently discovered indoleamine-accumulating retinal neurons were studied electron microscopically after destruction of the dopaminergic retinal neurons and subsequent labeling with 5,6-dihydroxytryptamine. These observations confirm earlier fluorescence microscopical studies on the distribution of the indoleamine-accumulating neurons in the rabbit retina. Their perikarya are known to be located in the inner nuclear layer (INL) among the amacrine cell bodies. Their processes are found only in the inner plexiform layer (IPL), most of them in the innermost third part of that layer. The indoleamine-accumulating terminals are pre- and postsynaptic to bipolar neurons in the innermost sublayer of the IPL. Reciprocal synapses are probably the rule. The synaptic vesicles of indoleamine-accumulating synapses onto bipolar cells are arranged in "globular" clusters around a central electron dense, round body. A number of synapses formed by unlabeled amacrine neurons with postsynaptic indoleamine-accumulating elements were also detected. These synapses were mainly found in the outermost third of the IPL. Synaptic contacts between presynaptic indoleamine-accumulating neurons and postsynaptic unlabeled processes of amacrine cells are very rare.

5,6-Dihydroxytryptamine↗

PubMed1993

Long-term sensitization and environmental conditioning in terrestrial snails.

The hypothesis that a long-term increase of behavioural responses in snails (over a period of days) might be due to environmental conditioning was examined. Training consisted of delivering electric shocks non-contingently with test stimuli twice per day for 5 days to freely moving snails on a ball floating in water. After training, a significant difference in amplitude of a withdrawal reaction to tactile test stimulation appeared between shocked and control snails. Responses were significantly facilitated in shocked animals for up to 12 days after training, but only if the animals were tested in the environment used for training. Testing of the same groups of animals crawling freely on the glass lid of a tank in which they lived between experimental sessions revealed no difference in responses to the same stimuli between shocked and control snails. Injection of the neurotoxin 5,7-dihydroxytryptamine, which selectively impairs serotonergic cells, eliminated the differences between shocked and control animals. Changing the pH of the water in which the ball floated, by addition of citric acid, led to a significant selective increase of responsiveness in snails sensitized in this environment relative to the responsiveness of the same snails with normal water in the tank. The results suggest that the long-term sensitization of withdrawal reactions observed is at least in part a manifestation of an associative process, namely environmental conditioning.

5,7-Dihydroxytryptamine↗

PubMed1975

Response of medial preoptic neurons to electrical stimulation of the mediobasal hypothalamus, amygdala and mesencephalon in normal, serotonin or catecholamine deprived female rats.

Single cell activity from preoptic neurons was extracellularly recorded in normal female rats and the effects of electrical stimulation of the mediocortical amygdala (AMY), the N. med. raphes (MES) and the mediobasal hypothalamus (MBH) was tested. 1. One type of preoptic neurons (55%) reacted with primary excitation to a single electrical stimulus of AMY, MES or MBH, which was usually followed by a period of postexcitatory inhibition. Another type of neurons (29%) were first inhibited after stimulation of AMY, MES or MBH and then showed a period of postinhibitory excitation. The discharge rate of a third type was not affected by electrical stimulation of these structures (16%). If a neuron was affected by a stimulus in a given area it predictably reacted in the same fashion to stimulation of the other areas. 2. The postexcitatory inhibition of the majority of the primarily excited neurons was strong enough to prevent the stimulus response to a second stimulus. Occasional recordings from two neighboured cells simultaneously indicate that they can be inhibitory to each other. 3. By pulse train stimulation of the AMY or MES with varying frequencies it could be demonstrated that low frequencies (10 Hz) had a facilitatory action whereas higher frequencies (100 Hz) were inhibitory to preoptic discharge rates. 4. No obvious alteration of neuronal properties we found neither in rats treated intraventricularly with 5,6-dihydroxytryptamine, which strongly reduces central nervous system serotonin content, nor in 6-hydroxydopamine treated rats, which had low central nervous system catecholamine levels.

5,6-Dihydroxytryptamine↗

PubMed1995

Electrophysiological characterization of dopaminergic and non-dopaminergic neurones in organotypic slice cultures of the rat ventral mesencephalon.

The aim of the present study was to characterize electrophysiologically neurones in organotypic cultures of the rat ventral mesencephalon and to compare these results with results published for the same neurones in other types of preparation. Intracellular recordings were obtained in 3- to 8-week-old organotypic slice cultures of the ventral mesencephalon prepared from new-born rats. Dopaminergic neurones were distinguished from non-dopaminergic neurones by staining with the autofluorescent serotonin analogue 5,7-dihydroxytryptamine and briefly viewing the preparation with short exposures to ultraviolet (UV) light (365 nm). Short exposures to UV light did not affect the electrophysiological properties. There were no significant differences between dopaminergic and non-dopaminergic neurones with regard to resting membrane potential or action potential threshold and amplitude, and in both types of neurone spontaneous burst activity and glutamatergic excitatory postsynaptic potentials were seen. There were differences in the following parameters, which can be used to distinguish between the two types of neurone. Dopaminergic neurones had broad action potentials (2-9 ms), high input resistance (mean 81 M omega), were silent or fired spontaneously at a low frequency (0-9 Hz), and no spontaneous GABAA-ergic inhibitory postsynaptic potentials or inward rectification were present. In contrast, non-dopaminergic neurones had fast action potentials (0.6-3.2 ms), low input resistance (mean 32 M omega), were silent or fired spontaneously at relatively high firing frequency (0-28 Hz), and sometimes inhibitory postsynaptic potentials and inward rectification were seen. In the presence of 1 microM tetrodotoxin and 10 mM tetraethylammonium, Ca2+ spikes could be evoked in both dopaminergic and non-dopaminergic neurones. Dopaminergic neurones in 3- to 8-week-old organotypic slice cultures have a number of distinguishing electrophysiological characteristics similar to those recorded in other types of acute or cultured preparations. However, some intrinsic regulatory mechanisms, namely the slow oscillatory potentials, inward rectification and the K+ current, IA, seem to be missing in the cultured neurones.

5,7-Dihydroxytryptamine↗

PubMed1988

Transmitter expression and morphological development of embryonic medullary and mesencephalic raphé neurones after transplantation to the adult rat central nervous system. II. Grafts to the hippocampus.

Suspensions of cells taken from the mesencephalic or medullary raphé regions of the 13-14 day old embryonic rat brain were injected into the hippocampus of adult rats which had previously been denervated of its serotoninergic input by 5,7-dihydroxytryptamine. At periods of up to 14 months after implantation, the brains were taken for immunohistochemical analysis of 5-hydroxytryptamine (5HT)-, substance P (SP)- and thyrotropin releasing hormone (TRH)-like immunoreactivity. Surviving grafts were found in all animals. The implants derived from mesencephalic raphé contained neurones immunoreactive to 5HT, SP or both substances together. On average 19% of the potential number of mesencephalic 5HT neurones were found in the grafts. Outgrowth of 5HT-immunoreactive fibres was extensive, and displayed the typical pattern of 5HT innervation in the normal hippocampus-the densest plexuses were found in the dentate gyrus, with sparser networks in the CA1 and CA2 regions. SP-positive processes were principally found only in the graft itself. Transplants of medullary raphé cells contained 5HT-immunoreactive neurones, some of which also contained SP-and/or TRH-like immunoreactivity, thereby mirroring the situation found in the caudal raphé complex in situ. An average of 18% of the total available medullary serotoninergic neurones were found at each graft site. A rich outgrowth of 5HT-immunoreactive varicose processes was evident, with the same pattern as the 5HT innervation by the mesencephalic raphé grafts, and as in the normal hippocampus. SP- and TRH-positive fibres were essentially detectable only in the graft, but not in the host hippocampus. The present studies indicate that the milieu of the hippocampus does not preferentially attenuate the survival of the serotoninergic cells which do not normally project to it. Nor is the fibre outgrowth of these medullary raphé 5HT neurones significantly different from that of the mesencephalic raphé. However, the hippocampal environment may be responsible for the appearance of SP-LI in the otherwise apparently solely 5HT-containing mesencephalic raphé neurones, and for repressing the outgrowth of fibres containing TRH-, or SP-like immunoreactivity, regardless of their origin.

5,7-Dihydroxytryptamine↗