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PubMed1992

Effects of selective neurotoxic lesion of lumbosacral serotonergic and noradrenergic systems on autotomy behaviour in rats.

Male rats underwent unilateral ligation and transection of the sciatic and saphenous nerves 2, 7 or 14 days after being injected intrathecally (at the thoracolumbar junction) with 6-hydroxydopamine (6-OHDA), 5,6-dihydroxytryptamine (5,6-DHT) or vehicle, and the development of autotomy was monitored. The effects of both neurotoxins on cervicothoracic (C5-T1) and lumbosacral (L1-S1) norepinephrine (NE), dopamine (DA) and 5-hydroxytryptamine (5-HT) spinal cord levels were analysed by HPLC in separate groups of rats. 6-OHDA treatment (20 micrograms/10 microliters) produced a rapid (from day 2) and significant (90-95%) fall in NE content only at L1-S1. 5,6-DHT administration (20 micrograms/10 microliters) produced a gradual (68%, 90% and 94%, at 2, 7 and 14 days, respectively) and selective depletion of 5-HT only at L1-S1. DA levels remained essentially unchanged after both neurotoxins. No differences in monoamine levels were detected among groups injected with vehicle. The main effects of neurotoxins on autotomy were: (1) a significant delay in the onset of autotomy in the rats injected with 6-OHDA 2 days before neurectomy; (2) a trend to autotomize earlier and more severely in the rats injected with 5,6-DHT 7 days before neurectomy and (3) an almost complete suppression of autotomy in the rats injected with 5,6-DHT 14 days before neurectomy. These results revealed that the expression of autotomy in rats can be modulated by interfering with spinal cord serotonergic activity and suggest new possible avenues for the treatment of certain specific pain diseases, such a phantom limb pain, by using selective agents capable of activating or blocking spinal cord serotonergic receptor subtypes.

5,6-Dihydroxytryptamine↗

PubMed1988

The comparative pharmacology of the behavioral syndromes induced by TRH and by 5-HT in the rat.

1. The relationship of the behavioral syndromes induced by the co-transmitters thyrotropin releasing hormone (TRH) and serotonin (5-HT) has not been previously studied with drugs selective for 5-HT receptor subtypes. 2. Both the TRH analog MK-771 (in naive rats) and 5-hydroxytryptophan (in rats with 5,7-dihydroxytryptamine [DHT] lesions) evoked reciprocal forepaw tapping, Straub tail, hunching, hindlimb abduction, and shaking behavior. Sniffing and rearing were features of the MK-771 but not the 5-HT syndrome. 3. 5-HTP potentiated MK-771-induced hyperthermia. 4. MK-771 evoked two types of shaking behavior, head shakes (HS) and wet-dog shakes (WDS). Neither independently was dose-related, unlike total shaking behaviors. 5. MK-771-induced shaking behavior was pharmacologically dissociated from other MK-771-evoked behaviors. A 5-HT1A agonist (8-OH-DPAT) blocked WDS, but like putative 5-HT1B (RU 24969) and 5-HT2 (DOI) agonists and the 5-HT antagonists methysergide (non-selective), ritanserin (5-HT2 selective), and l-propranolol (5-HT1 selective), it did not block other antagonists behavioural effects of MK-771. 6. Ipsapirone, a 5-HT1A-active drug purported both as an agonist and as an antagonist, inhibited MK-771-evoked WDS, like 8-OH-DPAT, but did not induce the serotonin syndrome, unlike 8-OH-DPAT. 7. DHT-treated rats were behaviorally supersensitive to 10 mg/kg MK-771 as indicated by a significantly shortened latency of onset of WDS and greater frequency of abnormal forepaw movements. The same rats were also supersensitive to 50 mg/kg 5-HTP to a significantly greater degree. 8. These data suggest behavioral relatedness of the TRH and 5-HT syndromes, but distinctive pharmacologic features and presumed mechanisms of action.

5,7-Dihydroxytryptamine↗

PubMed1995

Evidence for serotonergic system involvement in the effect of morphine on gastrointestinal motility in the rat.

1. Intestinal motility was measured by the transit of charcoal meal through the small intestine of the rat. 2. Morphine given subcutaneously induced a reduction in the gastrointestinal transit (GIT), and the response was dose-dependent (0.1-2.5 mg/kg). 3. The inhibitory effect of morphine was antagonized by prior subcutaneous administration of naloxone (1 mg/kg). 4. Depletion of serotonergic neurons by para-chlorophenylalanine (100 mg/kg, ip, 3 days) completely abolished the inhibitory action of morphine. 5. Methysergide (5 mg/kg, sc) and ketanserin (5 mg/kg, sc) also reduced the morphine effect. 6. Destruction of serotonergic neurones by intracerebroventricular injection of 5,7-dihydroxytryptamine (20 mu/kg) abolished the effect of morphine. 7. These observations provide some evidence for the involvement of a central serotonergic system in the effect of morphine on gastrointestinal motility.

5,7-Dihydroxytryptamine↗

PubMed1982

Localization and release of 5-hydroxytryptamine thyrotrophin releasing hormone and substance P in rat ventral spinal cord.

1. The highest spinal cord levels of 5-hydroxytryptamine (5-HT) and thyrotrophin releasing hormone (TRH) were found in the ventral lumbar cord, in contrast to substance P which was found predominantly in the dorsal cord. 2. 5,6- and 5,7-dihydroxytryptamine, administered into the lateral ventricles reduced 5-HT in the dorsal and ventral spinal cord by up to 90%. 3. There was a parallel reduction in substance P and TRH in ventral spinal cord while methionine-enkephalin and somatostatin in ventral and dorsal cord increased. 4. Reserpine and tetrabenazine depleted 5-HT and partially depleted substance P and TRH in the ventral cord, but had no effect on either methionine-enkephalin or somatostatin. 5. The rates of loss and recovery, after reserpine and tetrabenazine, of 5-HT were different from those of the two peptides. 6. Endogenous 5-HT and TRH release from slices of lumbar cord was enhanced by high potassium. 7. p-Chloroamphetamine and fenfluramine increased 5-HT release but reduced or had no effect on TRH release. The effect of p-chloroamphetamine on TRH release was not dependent on either the presence of 5-HT or 5-HT receptor activity. 8. The results are discussed in terms of the possible co-existence, co-storage and release of 5-HT, substance P and TRH in descending bulbospinal neurones.

Animals↗

PubMed1982

Demonstration of denervation supersensitivity: a pharmacological approach.

1. Although the phenomenon of denervation supersensitivity has been extensively studied in peripheral cholinergically and adrenergically innervated organs, the consequences of denervation have not been studied in as much detail in serotonergically innervated s stems. This may be due in part to the difficulties associated with producing specific lesions of serotonergic systems and with quantifying physiological responses of the CNS due to serotonin. 2. Because the lateral ciliated cells of the gill of the bivalve mollusc, Mytilus edulis, are innervated by serotonergic motor neurons which are responsible for accelerating the beating rate of the cilia we used this as a model system with which to study the effects of denervation by physical transections of the branchial nerve and by pharmacological treatments with 5,6 dihydroxytryptamine. 3. Both treatments produced a supersensitive response of the ciliated cells to the superfusion of serotonin. Two mechanisms with different time courses may be responsible. 4. The initial faster acting component may be due to changes in re-uptake mechanisms for serotonin, while the later slowly developing component may be due to other causes, including a hyperplasia of postjunctional serotonin receptors.

5,6-Dihydroxytryptamine↗

PubMed1982

Noradrenergic and non-noradrenergic nerves containing small granular vesicles in Auerbach's plexus of the guinea-pig: evidence against the presence of noradrenergic synapses.

The appearance and distribution of varicosities containing small granular vesicles in Auerbach's plexus of the guinea-pig ileum, distal colon and rectum has been studied with the electron-microscope. Two types of varicosity were recognised. The first type was located predominantly at the surface of the plexus and did not form synapses on intrinsic neurons. This type became labelled with 5-hydroxydopamine, a specific marker for noradrenergic axons, and was destroyed by 6-hydroxydopamine and extrinsic denervation, procedures which lead to degeneration of noradrenergic nerves in the gut. The second type formed axodendritic and axosomatic synapses on intrinsic neurons and the morphology of its synaptic vesicles differed subtly from that of the first type. The second type was unaffected by 5-hydroxydopamine, 6-hydroxydopamine, or extrinsic denervation. It is concluded that the two types of small granular vesicle-containing varicosities belong to different neurons and that the first type is noradrenergic. Noradrenergic varicosities do not, therefore, form synapses in Auerbach's plexus. This conclusion is in accord with the electrophysiological findings. The second type of small granular vesicle-containing varicosity is not noradrenergic although it was formerly thought to be so. It is intrinsic to the gut and is resistant to the serotoninergic neurotoxin, 5,6-dihydroxytryptamine.

5,6-Dihydroxytryptamine↗

PubMed1983

Benzodiazepine receptors in the rat hippocampal formation: action of catecholaminergic, serotoninergic and commissural denervation.

The problem of benzodiazepine receptor localization in the rat hippocampal formation has been approached using several methods of selective deafferentation, followed by [3H]flunitrazepam binding studies. The intraventricular injection of 6-hydroxydopamine reduced, after 14 days, the norepinephrine content of the hippocampal formation by 68.4%, and decreased the number of binding sites by 32%, without change in affinity. The intraventricular injection of 5,6 dihydroxytryptamine reduced the serotonin content by 61.5% but did not alter the [3H]flunitrazepam binding. The intraventricular bilateral injection of 0.5 micrograms kainic acid selectively destroyed the pyramidal neurons in area CA3 of both hippocampi and produced an increase of 28% in [3H]flunitrazepam binding, without change in affinity. These results are discussed in relation to our previous observations about benzodiazepine receptor changes after fimbria-fornix transection. The reduction in [3H]flunitrazepam binding after administration of 6-hydroxydopamine suggests the possible localization of the benzodiazepine receptors on adrenergic presynaptic terminals. The increase in binding sites after destruction of CA3 pyramidal cells, which are the site of origin of commissural fibers, is tentatively interpreted as resulting from the sprouting of mossy fibers that replace the associational-commissural projections.

5,6-Dihydroxytryptamine↗

PubMed1987

Increase in paradoxical sleep after destruction of serotoninergic innervation in the nucleus tractus solitarius of the rat.

The evolution of paradoxical sleep, slow-wave sleep and arterial pressure was studied following microinjection of 5,7-dihydroxytryptamine in the nucleus tractus solitarius in rats. The extent of the lesions was assessed using immunohistochemistry for serotonin. Global lesions of serotoninergic nerve terminals of the intermediate and commissural regions of the nucleus produced an important and long-lasting increase in paradoxical sleep (+50-70%), a decrease in slow-wave sleep (-20%) and a moderate increase of arterial pressure during all states of the sleep-wake cycle. In addition, more discrete lesions indicated that only the lesion of the area near the obex produced the longer term increase of paradoxical sleep whereas only the lesion of the commissural region of the nucleus produced the long-term decrease of slow-wave sleep. These data demonstrate that serotoninergic projections to the nucleus tractus solitarius exert a regulatory influence upon the specific mechanisms responsible for paradoxical sleep and slow-wave sleep in rats. Furthermore, they suggest that serotonin within the nucleus tractus solitarius plays an important role in the homeostatic cardiovascular and sleep-wake-cycle regulation in rats.

5,7-Dihydroxytryptamine↗

PubMed1991

The effect of selective serotonergic neurotoxin treatment on tachykinin levels in the rat ventral spinal cord.

The levels of 5-hydroxytryptamine and tachykinin neuropeptides substance P, neurokinin A, neurokinin B and neuropeptide K were measured in the spinal cord of rats treated by intraventricular injection of the selective serotonergic neurotoxin 5,7-dihydroxytryptamine. The spinal cord levels of 5-hydroxytryptamine as measured by high performance liquid chromatography with electrochemical detection decreased by more than 90% in the ventral and dorsal cord compared to controls. The levels of substance P as measured by radioimmunoassay were significantly reduced (66%, P less than 0.01) in the ventral lumbar cord only. In this region, neurokinin A, neurokinin B and neuropeptide K levels were determined by combined high performance liquid chromatography and radioimmunoassay. The neurotoxin treatment also caused a significant reduction of neurokinin A (72% reduction, P less than 0.01) and a non-significant reduction of neuropeptide K, but virtually no change in the neurokinin B level. Immunohistochemical studies of the ventral lumbar cord of sham-operated animals showed immunoreactivity for 5-hydroxytryptamine as well as for substance P and neurokinin A in nerve fibres around motor neurons. In neurotoxin-treated rats this region was devoid of immunohistochemically detectable substance P- and neurokinin A-positive fibres and showed very sparse or no 5-hydroxytryptamine immunoreactivity. We conclude that among the tachykinins both neurokinin A and substance P, but probably not neurokinin B, co-exist with 5-hydroxytryptamine in nerve terminals in the rat ventral spinal cord.

5,7-Dihydroxytryptamine↗

PubMed1991

Morphological, neurochemical, and behavioral studies on serotonergic denervation and graft-induced reinnervation of the rat hippocampus.

A procedure was developed to conduct simultaneously immunocytochemical and neurochemical studies on the serotonergic system in adjacent 300-micron-thick slices of rat hippocampus. This procedure was applied to correlate morphological (innervation pattern and density), neurochemical (5-hydroxytryptamine and 5-hydroxyindolacetic acid levels and [3H]5-hydroxytryptamine uptake and release) and behavioral (spatial learning) effects of neurotoxin-induced denervation and reinnervation by grafting fetal mesencephalic raphe cells. Intracerebroventricular injections of a low dose of 5,7-dihydroxytryptamine caused a discrete serotonergic denervation of the hippocampus. Eleven months after lesioning, 5-hydroxytryptamine and 5-hydroxyindolacetic acid levels and [3H]5-hydroxytryptamine uptake capacity were decreased by 50-60%. By this time, the residual fibers displayed an enhanced vulnerability towards K(+)-induced depolarization. Grafting of a fetal raphe cell suspension resulted in a reinnervation of the host hippocampus. The pattern of reinnervation was comparable to control innervation and the density was supranormal at the level of the graft. As observed semiquantitatively, the innervation density decreased with distance from the core of the graft. Neurochemical studies showed that the fibers were capable of synthesizing, metabolizing and releasing 5-hydroxytryptamine. The turnover of 5-hydroxytryptamine in both the denervated and the reinnervated hippocampus was comparable to that in control tissue. Previous behavioral testing of the denervated and of the denervated and implanted animals did not reveal any effect on spatial learning, either in an individual or in a social test paradigm. The latter data substantiate the notion that interference with the hippocampal serotonergic innervation does not hamper adequate spatial learning.

5,7-Dihydroxytryptamine↗

PubMed1991

The source of the transient serotoninergic input to the developing visual and somatosensory cortices in rat.

For approximately the first two weeks of life, dense serotonin immunoreactivity closely matches the pattern of thalamocortical axons innervating both the granular portion of the primary somatosensory cortex and area 17 in rodents [D'Amato et al. (1987) Proc. natn. Acad. Sci. 84, 4322-4326; Fujimiya et al. (1986) J. comp. Neurol. (1986) 246, 191-201; Rhoades et al. (1990) J. comp. Neurol. 293, 190-207]. This serotonin immunoreactivity is not contained in thalamocortical axons [Rhoades et al. (1990) 293, 190-207] but its source has never been demonstrated. In the present study, a variety of approaches were used to address this issue. The combination of electron microscopy and immunocytochemistry showed that all serotonin immunoreactivity in the developing cerebral cortex was contained in axons and that the terminals of many of these fibers made synapses with the dendrites of cortical cells. Treatment with fluoxetine, a specific inhibitor of serotonin uptake, did not result in a loss of the cortical pattern of serotonin immunoreactivity, indicating that immunoreactive fibers were not labeled solely as a result of serotonin uptake. The combination of retrograde tracing from the primary somatosensory cortex and area 17 with immunocytochemistry demonstrated numerous double-labeled cells in nucleus raphe dorsalis and the median raphe nucleus. Smaller numbers of double-labeled neurons were located in the B9 cell group and the region of the lateral midbrain tegmentum. Large electrolytic lesions that included most of the nucleus raphe dorsalis and median raphe nucleus, but which left the B9 group and more caudal serotoninergic cells undamaged, caused either a substantial reduction in density or complete disappearance of the serotonin pattern in both hemispheres. Unilateral electrolytic lesions of the medial forebrain bundle resulted in a loss of the pattern only on the side of the damage. Injection of the neurotoxin 5,7-dihydroxytryptamine directly into the mesencephalon either abolished or substantially reduced the density of the cortical serotonin immunoreactivity. Injections that produced substantial cell loss in the median raphe nucleus, but only minor cell loss in the nucleus raphe dorsalis had little effect upon the cortical pattern of serotonin immunoreactivity. These results indicate that the dense serotonin immunoreactivity which appears transiently in the visual and somatosensory cortices of perinatal rodents is contained in serotoninergic axons that arise from cells in the nucleus raphe dorsalis and perhaps also the median raphe nucleus.

5,7-Dihydroxytryptamine↗

PubMed1993

Midbrain dopaminergic neurons from postnatal rat in long-term primary culture.

Midbrain dopamine neurons project extensively throughout the vertebrate forebrain and influence a wide variety of brain functions. These neurons, which are believed to form a major brain reward system, are involved in initiation and control of motor programs, addictive behaviors, and determination of mood. Given their critical role in behavioral function, relatively little is known about their fundamental cellular physiological and pharmacological properties. A long-term dissociated culture system for postnatal rat dopamine neurons was developed to permit both acute and chronic studies of these cells. Dopamine neurons were dissociated from slices of ventral midbrain from neonatal rat pups and maintained in cell culture for several months. The dopaminergic phenotype was confirmed by catecholamine fluorescence and by tyrosine hydroxylase immunocytochemistry. After four weeks in culture, dopamine neurons had cell bodies 10-40 microns in diameter, displayed either fusiform or multipolar morphology, and had processes with varicosities of 0.5-2 microns in diameter. Electrophysiological recordings were made from 71 dopamine neurons identified by 5,7-dihydroxytryptamine fluorescence after six to 67 days in culture. The neurons had resting potentials of -51 +/- 5 mV, broad action potentials with durations of 2.9 +/- 1.3 ms, and the majority of the neurons (65%) displayed anomalous rectification. Most dopamine neurons in culture fired spontaneously in a pacemaker-like manner with a frequency of 2.3 +/- 1.3 Hz, or in a bursting pattern, typically having two to seven action potentials per burst. All neurons tested had glutamate and gamma-aminobutyric acid receptors, and 90% of neurons responded to dopamine or quinpirole with inhibition of firing, suggesting the presence of dopamine autoreceptors. Some neurons were inhibited by concentrations of quinpirole as low as 10 nM. The results show that midbrain dopamine neurons can be maintained in dissociated cell culture for periods of several months. These neurons can be identified prior to electrophysiological recording, and they express many of the physiological characteristics that have been reported for midbrain dopamine neurons in vivo.

5,7-Dihydroxytryptamine↗

PubMed1994

Tropism of serotonergic neurons towards glial targets in the rat ependyma.

During development, recognition mechanisms between neurons and their targets are necessary for the formation of the neuronal network. Neural connections are synaptic or non-junctional. Both types of communication can be found between neurons and glial elements in the periventricular walls. Serotonergic fibers form synaptic contacts on the specialized ependymocytes of the subcommissural organ, a structure which forms the roof of the third ventricle at its junction with the aqueduct. A network of non-junctional fibers containing both GABA and serotonin spread between the cilia of the classical ependymocytes in the ventricles. These anatomical, morphological and biochemical features suggest a tropism and specific recognition mechanisms between glial elements and serotonergic neurons. This hypothesis can be tested by the study of the innervation of the subcommissural organ and the classical ependyma by grafted embryonic neurons after a chemical destruction of the serotonergic endogenous innervation. Solid implants or cell suspensions prepared from embryonic metencephalon were transplanted to either the third ventricle or the periventricular gray matter in 5,7-dihydroxytryptamine denervated rats. Grafted serotonergic neurons were able to reinnervate the classical ependyma and the subcommissural organ. The fibers forming the supraependymal plexus were non-junctional and contained both serotonin and GABA while those innervating the subcommissural organ formed synaptic contacts and contained only serotonin. The signals capable of inducing the ependymal innervation were specific for serotonergic neurons since catecholaminergic neurons present in the grafts were unable to innervate either classical or specialized ependymocytes. These results demonstrate that glial cells are targets for serotonergic neurons and that the morphological and biochemical characteristics of the serotonergic innervation are closely related to the target cell phenotype.

5,7-Dihydroxytryptamine↗

PubMed1994

Olfactory disturbance induced by deafferentation of serotonergic fibers in the olfactory bulb.

The serotonergic neurons of the brain stem project widely throughout the central nervous system, and the olfactory bulb is one of the major forebrain targets of the ascending serotonin pathway. According to physiological studies, neurons of the olfactory bulb were found to reduce their spontaneous discharge rates by electrophoretically applied serotonin. However, roles of the bulbar serotonin in the sense of smell remain unanswered. In the present study, using 5,7-dihydroxytryptamine, a specific neurotoxin for serotonin, we found that the conditioned rats who learned to avoid a repellent by olfaction lost ability of discrimination by deafferentation of the bulbar serotonergic fibers. Such olfactory dysfunction did not occur in the early stage (three days after injection of the toxin) when the serotonergic fibers disappeared in the bulb, but developed a few weeks later. Interestingly, histological examination revealed marked shrinkage of the bulbar glomerulus which is a major termination site of the bulbopetal serotonergic fibers, and also a synaptic site of olfactory receptor cells and bulbar output neurons. The results indicate that depletion of the serotonergic fibers in the olfactory bulb causes glomerular atrophy and olfactory disturbance in the rat.

5,7-Dihydroxytryptamine↗

PubMed1991

Depletion of hypothalamic norepinephrine and serotonin enhances the dexamethasone negative feedback effect on adrenocortical secretion.

The role of norepinephrine (NE) and serotonin (5-HT) in the negative feedback effect of dexamethasone (DEX) on the adrenocortical response to ether stress was investigated. Injection of the catecholamine neurotoxin, 6-hydroxydopamine, into the ventral noradrenergic bundle or the paraventricular nucleus of the hypothalamus (PVN) which produced a very significant depletion in hypothalamic NE content enhanced the negative feedback effect of DEX. Injection of the 5-HT neurotoxin, 5,7-dihydroxytryptamine, into the raphé nuclei or PVN, which caused a depletion of hypothalamic 5-HT, produced a similar effect on the adrenocortical response to DEX. The degree of negative feedback may be viewed as a balance of neural stimulatory and glucocorticoid influences of the hypothalamus. Thus the removal of the stimulatory effects of NE and 5-HT on adrenocortical secretion, by the neurotoxic lesions, enhanced the inhibitory influence of DEX.

5,7-Dihydroxytryptamine↗

PubMed1983

Autoradiographic localization of [3H]-imipramine binding sites: association with serotonergic neurons.

Localization of the binding sites for a radioactive form of the tricyclic antidepressant imipramine has been accomplished using receptor autoradiographic techniques. These studies demonstrated a marked overlap between regions presenting dense concentrations of imipramine binding sites and regions known to receive serotonergic projections. Lesions of the serotonergic neurons were created by intracerebroventricular injections of the potent neurotoxin 5,7-dihydroxytryptamine. The effectiveness of these lesions was ascertained by immunohistochemical localization of serotonin containing neurons in both lesioned and vehicle treated control animals. Animals lesioned in this fashion, showed a dramatic loss of imipramine binding sites in all of the areas which were previously densely labeled. The catecholamine containing neurons were lesioned in another group of animals using 6-hydroxydopamine. The effects of these lesions were ascertained using fluorescence histochemical techniques. In these animals, the imipramine binding sites were unaltered. These results suggest that imipramine binding sites are presynaptic and are located on serotonin containing terminals and not on catecholamine containing neurons.

5,7-Dihydroxytryptamine↗

PubMed1987

Nature of salivation produced by thyrotropin-releasing hormone (TRH).

In the unanesthetized cat, TRH was injected into the cerebral ventricles (ICV) through chronically implanted cannulae and the nature of the evoked salivation was investigated. TRH injected in doses from 0.1 to 1.0 mg evoked salivation which was not dose-dependent. The antimuscarinic drug atropine as well as the ganglionic blocking agent mecamylamine injected also ICV prevented the salivation induced by ICV TRH. On the other hand, virtually no effect on the TRH-salivation was induced by the following drugs injected ICV: alpha and the beta adrenergic blocking agents, yohimbine and propranolol; dopamine antagonist, chlorpromazine; 5-hydroxytryptamine antagonist, methysergide; and the antihistamine, antazoline. Further, in cats pretreated with ICV reserpine and 6-hydroxydopamine, but not with ICV 5,6-dihydroxytryptamine and hemicholinium, the salivation caused by ICV TRH was abolished. It is concluded that central cholinoceptive and catecholaminergic mechanisms are involved in the salivation induced by ICV TRH.

5,6-Dihydroxytryptamine↗

PubMed1987

3-Acetylpyridine lesions and four serotonergic behavioral syndromes in the rat.

We studied the effect of 3-acetylpyridine (3-AP) lesions on the serotonergic-myoclonic syndromes evoked by quipazine (QP), 5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT), fenfluramine (FF), and p-chloroamphetamine (PCA) in the adult rat. Eleven behaviors were scored from videotapes by an observer blind to drug status. In unlesioned rats, drugs could be differentiated by forelimb and axial myoclonus, pivoting and backing. All drugs significantly suppressed rearing. 3-AP produced a lasting action-enhanced body tremor which differed from axial myoclonus in its vertical direction and rhythmicity. 3-AP lesions modified the effect of drugs on several behaviors, increasing axial (QP, FF, PCA) and forelimb (5-MeO-DMT, FF, PCA) myoclonus and decreasing locomotor score. Prior lesions with 5,7-dihydroxytryptamine did not prevent the effect of 3-AP or any behaviors of the serotonin syndrome, but had a slight effect on the magnitude of forelimb myoclonus, head weaving, and hunching induced by some drugs. Neither lesion abolished or reduced myoclonus. These data suggest that intact 5-HT terminals are not requisite for the tremorogenic and cytotoxic effect of 3-AP. To the extent that chemical lesions with 3-AP are selective for the inferior olive (IO), the role of the IO in myoclonus in several 5-HT rodent myoclonic models appears to be regulatory rather than stimulatory.

5,7-Dihydroxytryptamine↗