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PubMed1979

Degeneration of interneurons in the lateral geniculate nucleus after 5,6-dihydroxytryptamine treatment.

Intraventricular administration of the cytotoxic compound 5,6-dihydroxytryptamine produces extensive damage in a small population of neurons in the lateral geniculate nucleus of the cat. The observed changes are characterized by osmiophilic deposits in the cytoplasm and an overall increase in the electrodensity of the matrix. No alterations in the relay cells nor in synaptic endings were observed. The cells affected by 5,6-dihydroxytryptamine, most probably tryptaminergic in nature, belong to the class of interneurons and may correspond to local inhibitory cells described in neurophysiological studies.

5,6-Dihydroxytryptamine↗
PubMed1991

Spinal antinociception by adenosine analogs and morphine after intrathecal administration of the neurotoxins capsaicin, 6-hydroxydopamine and 5,7-dihydroxytryptamine.

The effects of intrathecal pretreatment with the neurotoxins capsaicin, 6-hydroxydopamine and 5,7-dihydroxytryptamine on spinal antinociception by adenosine analogs (NECA, 5'-N-ethylcarboxamido adenosine and CHA, N6-cyclohexyl adenosine) and morphine were examined using the rat tail flick and hot plate tests. Pretreatment with 50 micrograms capsaicin for 7 to 11 days (which reduced substance P immunoreactivity in the superficial layers of the dorsal spinal cord) produced a slight increase in the action of NECA and CHA, and reduced the action on morphine in the hot plate test but not in the tail flick test. Pretreatment with 50 to 100 micrograms 6-hydroxydopamine for 7 to 14 days (which reduced spinal cord noradrenaline levels by 54-65%) reduced spinal antinociception by NECA and CHA but not that by morphine. Pretreatment with 50 micrograms 5,7-dihydroxytryptamine (which reduced spinal cord serotonin levels by 74-89%) had no effect on any agent. Acute pretreatment with 7.5-30 micrograms phentolamine reduced the spinal antinociceptive action of noradrenaline, NECA and CHA, primarily in the hot plate test. Phentolamine (30 micrograms) also reduced the action of morphine (hot plate greater than tail flick), but did not affect the action of L-baclofen. These results suggest that spinal antinociception by adenosine analogs: 1) occurs primarily at a postsynaptic site of action (capsaicin results), and 2) is dependent on release of endogenous noradrenaline and activation of spinal adrenergic receptors (6-hydroxydopamine and phentolamine results). The reduction in the effect of morphine by capsaicin (removes a source of adenosine release) and phentolamine (antagonizes the action of endogenously released adenosine) can be explained in terms of the adenosine release hypothesis of morphine action within the spinal cord.

5,7-Dihydroxytryptamine↗
PubMed1985

[Effect of the administration of 5,6-dihydroxytryptamine to the amygdala and dorsal raphe nucleus on plasma renin activity].

The effect of injections of 5,6-dihydroxytryptamine, a potent and selective neurotoxic of serotonin neurons, into amygdala and dorsal raphe mesencephalic nucleus on the plasma renin activity has been studied in male Wistar rats. Plasma renin activity was estimated on 2nd, 4th, Tth and 14th day after injections in both areas. The administration of 5,6-dihydroxytryptamine in amigdala produced a significant decrease in plasmatic renin activity between 2nd and 4th day, but the inverse effect between 7th and 14th day. Similar effects were found after injections in dorsal raphe nucleus. The contents of cerebral 5-HT were simultaneously evaluated in the entire brain when the drug was implanted in dorsal raphe, and only in amygdaloid tissue when the injection was restricted to this area. A significant decrease in serotonin content was produced 7th day in both places, while partial recuperation was found toward 14th day. The results, especially the ones related to the chemical lesion of dorsal raphe nucleus, suggest that serotoninergic brain systems are involved, as stimulators, in the control of the dynamics of renin-angiotensin system.

5,6-Dihydroxytryptamine↗
PubMed1982

Changes in sensitivity to intrathecal norepinephrine and serotonin after 6-hydroxydopamine (6-OHDA), 5,6-dihydroxytryptamine (5,6-DHT) or repeated monoamine administration.

The behaviorally defined analgesia evoked by direct application of norepinephrine (NE) or serotonin (5-HT) into the rat spinal subarachnoid space was assessed 1 to 28 days after respective intrathecal injection of 6-hydroxydopamine or 5,6-dihydroxytryptamine. These pretreatments effected supersensitivity to intrathecally administered NE and 5-HT, respectively, observable as early as 24 hr after neurotoxin-induced lesion. Dose-response curves for both NE or 5-HT, determined 7 days after pretreatment with their respective neurotoxins, were shifted significantly to the left as compared to controls. The onset of supersensitivity correlated well with the depletion of neurotransmitter levels in the spinal cord in the case of NE, but much correlation was not found for 5-HT. Whereas monoamine supersensitivity was undetectable 28 days postlesion, there was no significant recovery of spinal cord monoamine content at this time. Neurotoxin pretreatment was found to effect a significantly greater potentiation of NE- or 5-HT-induced analgesia than presynaptic reuptake blockade and elicited supersensitivity to agonists not readily taken up by presynaptic terminals, suggesting the involvement of postsynaptic components. Rats pretreated 7 days before with 5,6-dihydroxytryptamine exhibited some supersensitivity to intrathecal NE. Supersensitivity to 5-HT was not observed after 6-hydroxydopamine pretreatment. Rats made tachyphylactic to the antinociceptive effect of intrathecally injected NE displayed a complete lack of analgetic response to 5-HT. Similarly, rats tachyphylactic to 5-HT exhibited a subnormal analgetic response to NE. Combination pretreatment with both neurotoxins produced significant hyperalgesia as compared to yoked controls and to nociceptive thresholds determined before neurotoxin administration.

5,6-Dihydroxytryptamine↗
PubMed1976

Effect of 6-hydroxydopamine and 5,6-dihydroxytryptamine on the response of the coaxially stimulated guinea-pig ileum to morphine.

Studies were conducted to determine the role of norepinephrine and 5-hydroxytryptamine in the action of morphine in the coaxially stimulated guinea-pig ileum. 6-hydroxydopamine produced supersensitivity to norepinephrine and decreased the levels of norepinephrine in the ileum. 6-Hydroxydopamine did not interfere with the acute effects of morphine but did interfere with the degree of tolerance developed to morphine, which is in contrast to reported results of the effect of 6-hydroxydopamine on the analgesic response to morphine. No evidence was found that 5,6-dihydroxytryptamine altered the acute or chronic response of the ileum to morphine. Again this is in contrast to results for the analgesic receptor where 5,6-dihydroxytryptamine has been reported to inhibit the development of tolerance to morphine. Thus, the role of the biogenic amines in the action of morphine in the ileum appears to differ from their reported role in the action of morphine in the central nervous system.

5,6-Dihydroxytryptamine↗
PubMed1975

Effect of intraventricular neonatal 6-OH dopamine or 5,6-dihydroxytryptamine adminisration on the circadian periodicity of plasma corticosteroid levels in the rat.

The extent of circadian variation in plasma corticosteroid levels at 30 days of age was normal in rats who received either intraventricular 6-OH dopamine or 5,6-dihydroxytryptamine on day 3 of life. A 4-h advance in the time of peaking was present in this latter group. At the time of study the depletion of 8.00 a.m. and 8.00 p.m. levels of norepinephrine was significant in the cortex (--49%), hypothalamus (--58%), hippocampus (--65%), and amygdala (--44%) of the 6-OH dopamine-treated animals, as was a similar depletion of serotonin in these areas in the 5,6-dihydroxytryptamine-treated animals. There was no difference between 8.00 a.m. and 8.00 p.m. levels of either amine in any of these areas, in contrast to the variation seen in uninjected animals in whom 8.00 a.m. levels of both amines were higher in all areas than 8.00 p.m. levels. The female 6-hydroxydopamine-treated animals had significantly increased adrenal weights. No other significant changes were noted in the adrenals or gonads of either treated group. Body weights were not significantly altered in any of the animals. These data demonstrate that the circadian variation in plasma corticosteroid levels can develop in the presence of either marked norepinephrine or serotonin depletion in CNS areas that have been implicated in the regulation of such periodicity.

Adrenal Cortex Hormones↗
PubMed1975

A developmental study of the effects of 5,7-dihydroxytryptamine on regional tryptophan hydroxylase in rat brain.

Tryptophan hydroxylase activity rises rapidly after birth in 5 distinct regions of the rat CNS. Near-adult levels of activity are recorded by 22 days of age in the cell-body rich regions of the brainstem and by 42 days in the terminal-rich areas, hypothalamus and remaining forebrain. The intracisternal injection of 40 mug 5,7-dihydroxytryptamine on day 2 after birth results in a near-total depletion of tryptophan hydroxylase in all CNS regions analyzed 6 or 12 days after drug administration. Enzyme activity recovers (to 11-24% of age matched controls) between day 12 and 20 after 5,7-dihydroxytryptamine in hypothalamus, midbrain and pons medulla oblongata. The growth of 5,7-DHT-treated animals is retarded between 3 and 40 days after drug administration.

Age Factors↗
PubMedDate not supplied

Dihydroxytryptamines as tools to study the neurobiology of serotonin.

The neurotoxins 5,6- and 5,7-dihydroxytryptamine are accepted tools for "chemical degeneration" of serotonergic (5-HT) axons in the CNS (for reviews, see [11, 12, 15, 20] ). Optimum application of these substances requires knowledge of their chemical properties, disposition in the biophase and mechanism of action. Current knowledge and concepts on this issue are described and results of recent studies utilizing 5,7-DHT uptake as a tool for localizing 5-HT neurons neuroanatomically are reviewed.

5,6-Dihydroxytryptamine↗
PubMed1986

Oxidation of 5-hydroxytryptamine and 5,7-dihydroxytryptamine. A new oxidation pathway and formation of a novel neurotoxin.

The electrochemical oxidation of 5-hydroxytryptamine (5-HT) in acidic solution proceeds through a minor route leading first to 5,7-dihydroxytryptamine (5,7-DHT) then to 4,5,7-trihydroxytryptamine and finally to 5-hydroxytryptamine-4,7-dione. The latter compound is a major electrochemical oxidation product of 5,7-DHT at pH 2 and 7 and a major autoxidation product at pH greater than or equal to 6. Preliminary biological results indicate that 5-hydroxytryptamine-4,7-dione is a more potent central nervous system toxin than 5,7-DHT. These results show for the first time a chemical pathway from 5-HT to 5,7-DHT and suggest possible minor metabolic oxidative pathways for the neurotransmitter 5-HT to at least two powerful neurotoxins.

5,6-Dihydroxytryptamine↗
PubMed1990

Supersensitivity to intrathecal 5-hydroxytryptamine, but not noradrenaline, following depletion of spinal 5-hydroxytryptamine by 5,7-dihydroxytryptamine administered into various sites.

The present study was conducted (a) to determine if cross-supersensitivity at spinal noradrenergic receptors could be demonstrated in antinociceptive tests following depletion of spinal cord 5-hydroxytryptamine (5HT) by the intrathecal (i.t.) and intracerebroventricular (i.c.v.) administration of 5,7-dihydroxytryptamine (5,7DHT), and (b) to compare the pattern of supersensitivity at spinal 5HT receptors following these manipulations and 5,7DHT microinjected into the ventral raphe (VR) region and the nucleus raphe magnus (NRM). Both i.t. and i.c.v. administration of 5,7DHT produced a marked depletion of spinal cord 5HT (greater than 75%) and supersensitivity to the i.t. injection of 5HT in the tail flick and hot plate tests. No supersensitivity to the i.t. injection of noradrenaline (NA) was observed. Microinjection of 5,7DHT into the VR and NRM produced less depletion of spinal cord 5HT (40-57%), and supersensitivity to the i.t. injection of 5HT was observed only in the hot plate test following microinjection of 5,7DHT into the VR. An increased incidence of signs of the 5HT behavioural syndrome, particularly tremor and Straub tail, was observed in all 5,7DHT-pretreated groups. These results indicate that cross-supersensitivity to spinal NA receptors does not occur following depletion of spinal cord 5HT. In addition, responses mediated by 5HT receptors show a differential pattern of development of supersensitivity. Thus, the 5HT behavioural syndrome (presumably mediated by 5HT1A receptors) more readily reflects the development of supersensitivity than the tail flick test (presumably mediated by 5HT2 receptors), while the hot plate test (uncharacterized subtype) shows an intermediate development of supersensitivity.

5,7-Dihydroxytryptamine↗
PubMed1988

Effects of 5,7-dihydroxytryptamine and 6-hydroxydopamine on head-twitch response induced by serotonin, p-chloroamphetamine, and tryptamine in mice.

Head-twitch response (HTR) in mice was induced by intracerebroventricular injection of tryptamine (TRA) as well as serotonin (5-HT) and p-chloroamphetamine (PCA). Pretreatment with 5,7-dihydroxytryptamine enhanced both the 5-HT-induced and the TRA-induced HTR. The PCA-induced HTR, however, was attenuated by the drug. On the other hand, pretreatment with 6-hydroxydopamine did not alter the 5-HT response but enhanced both the PCA- and the TRA-induced response. These results suggest that 5-HT may directly stimulate the post-synaptic receptors, while the PCA response may be based on the release of endogenous 5-HT. The presynaptic component of the central serotonergic system does not appear to be involved in the TRA response. Both PCA and TRA may affect catecholaminergic systems which can suppress the response.

5,7-Dihydroxytryptamine↗
PubMed1981

Effect of 5,7-dihydroxytryptamine on serotonergic control of prolactin secretion and behavior in rats.

The intracisternal administration of 5,7-dihydroxytryptamine (5,7-DHT) to rats resulted in a potentiated response to 5-hydroxytryptophan (5-HTP) when the animals were tested 30 days later. The 5-HTP-induced changes include elevation of serum prolactin, decrease in operant responding, and the magnitude of the "serotonin behavioral syndrome" observed after 5-HTP administration. The serotonin concentration in brains of 5,7-DHT-treated animals reached maximum earlier and remained elevated longer than that of controls following administration of 5-HTP. Brain norepinephrine and dopamine concentration were not affected by 5-HTP in either group of animals. The increase in serum prolactin concentration elicited by administration of the serotonergic agonists quipazine or 5-methoxy-N,N-dimethyltryptamine and by the serotonin uptake inhibitor fenfluramine also was potentiated by pretreating rats with 5,7-DHT. These data suggest that both serotonergic receptor supersensitivity and the absence of presynaptic uptake sites contribute to the enhanced responses to 5-HTP occurring in rats previously treated with 5,7-DHT. The findings further demonstrate that both behavioral and hormonal measures can be used to assess the sensitivity of serotonergic receptors and indicate that 5,7-DHT may be useful in evaluating the role of serotonergic neurons in neuroendocrine function.

5,7-Dihydroxytryptamine↗
PubMed1982

Effects of neonatal administration of 5,7-dihydroxytryptamine on locomotor activity.

Neonatal rats treated on day 3 of life with 50 or 100 micrograms 5,7-dihydroxytryptamine exhibited long-lasting selective depletions of serotonin (5-HT). The 5-HT depletions produced a shift in the peak in locomotor activity from its normal occurrence at 15 days of age to later days of age. The observation that the decreases in activity after the peak were delayed, rather than eliminated, suggests that the inhibition of locomotor activity produced by 5-HT may be of transient importance in the developing rat. The transience of the inhibition may be the result of the continuing development of nonserotonergic systems during this time period that are involved in the regulation of activity.

5,7-Dihydroxytryptamine↗
PubMed1980

Effect of 5,7-dihydroxytryptamine on the development of tolerance to ethanol.

5,7-Dihydroxytryptamine (5,7-DHT) or the vehicle was administered once into both lateral ventricles of the rat. Desmethylimipramine (DMI) was administered IP prior to the intraventricular injection of 5,7-DHT to prevent the destruction of norepinephrine (NE) terminals. Following recovery from surgery, ethanol (5 g/kg, PO) or isocaloric sucrose was given daily for 25 days. Tests at 5-day intervals showed that chronic ethanol treatment produced tolerance to the motor impairment on the moving belt test and to hypothermic effects of ethanol. The 5,7-DHT treatment did not alter either the motor impairment or hypothermia produced by the initial dose of ethanol. However, 5,7-DHT treatment produced a 75% depletion of brain serotonin (5-HT) without altering NE concentration and retarded the development of tolerance to ethanol in both measurements. This study with a specific central depletor of 5-HT, without alteration in NE concentration, extends and supports our hypothesis that brain 5-HT modulates the development of tolerance to ethanol.

5,7-Dihydroxytryptamine↗
PubMed1981

Supersensitivity to L-5-hydroxytryptophan after 5,7-dihydroxytryptamine injections in desmethylimipramine- and nomifensine-pretreated rats: behavioral evidence for postsynaptic supersensitivity.

The behavioral syndrome induced by L-5-hydroxytryptophan (L-5-HTP) in rats was used to study the supersensitivity to L-5-HTP and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) which develops after unilateral intracerebroventricular (ICV) injections of 200 microgram 5,7-dihydroxytryptamine (5,7-DHT). Pretreatment of the animals with a combination of desipramine and nomifensine was found to protect dopamine neurones better than desipramine alone. Maximal behavioral supersensitivity to L-5-HTP and 5-MeODMT was found as early as 24 h after injection of the neurotoxin, even in the presence of the specific 5-HT uptake inhibitor CGP 6085 A, or the MAO-A inhibitor clorgyline. The results indicate that a quickly occurring postsynaptic event contributes to the development of behavioral supersensitivity after ICV injections of 5,7-DHT.

5,7-Dihydroxytryptamine↗
PubMed1981

Facilitation of shock-induced fighting following intraventricular 5,7-dihydroxytryptamine and 6-hydroxydopa.

Using a 15-s intershock interval, an increase in shock-induced fighting was observed following intraventricular 96 microgram 5,7-dihydroxytryptamine (5,7-DHT) and 90 microgram 6-hydroxydopa (6-OHdopa). The incidence of predatory mouse killing was enhanced by 5,7-DHT, but was not affected by 6-OHdopa. Pain sensitivity was increased by 6-OHdopa, but both neurotoxins produced hyperreactivity to footshock. Specific serotonin depletion was produced by 5,7-DHT and norepinephrine depletion by 6-OHdopa. The increase in shock-induced fighting could not be predicted on the basis of monoamine depletion alone, since a long intershock interval was necessary to observe this increase.

5,7-Dihydroxytryptamine↗
PubMed1983

Effects of neonatal treatment with 5,7-dihydroxytryptamine or 6-hydroxydopamine on the ontogenetic development of the audiogenic immobility reaction in the rat.

The ontogenetic development of the audiogenic immobility reaction (freezing) was studied in rats given intracisternal injections of the neurotoxins 5,7-dihydroxytryptamine (5,7-DHT), 25 micrograms, or 6-hydroxydopamine (6-OHDA), 100 micrograms, neonatally (Day 1). The duration of the freezing response was strongly reduced in the 5,7-DHT-treated rats between 20-30 days of age, when normal animals show very prolonged responses. During the same period increased motor activity was observed in the 6-OHDA-treated rats while only a slight reduction of the freezing response was noted. Biochemical analyses performed on brains from animals 35 days of age showed a selective reduction (about 50%) of whole brain levels of serotonin in the 5,7-DHT-treated rats, while the noradrenaline levels were selectively reduced by about 60% in the 6-OHDA rats. A longitudinal investigation on the effects of neonatal treatment with 5,7-DHT showed a persistent selective reduction of the whole brain level of serotonin up to at least 90 days of age. Since 5,7-DHT mainly affects the serotonergic pathways, the results suggest that the disturbances noted in the ontogeny of the freezing response may be due to interference with the developing serotonergic system.

5,7-Dihydroxytryptamine↗
PubMed1979

Alcohol intake, ethanol-induced narcosis and intoxication in rats following neonatal 6-hydroxydopamine or 5, 7-dihydroxytryptamine treatment.

Newborn rats were treated with 5,7-dihydroxytryptamine (5,7-HT; 2 x 100 mg/kg s.c., 24 h interval) after pretreatment with desipramine (20 mg/kg s.c.) for depletion of brain 5-hydroxytryptamine (5-HT) or with 6-hydroxydopamine (6-OHDA; 3 x 100 mg/kg s.c., 24 h interval) for selective reduction of brain noradrenaline (NA). The 5,7-HT treatment resulted in a 53% reduction in endogenous 5-HT in the cerebral cortex and a 60% increase in the pons-medulla when determined in adult rats. The 5-HT content in the midbrain was not affected. Endogenous NA in the 6-OHDA treated animals was selectively reduced by 100% in the cerebral cortex, 35% in the midbrain and increased by 117% in the pons-medulla. No difference was found between the voluntary ethanol selection of these groups and that of the controls when measured at the age of 3 months. In a tilting-plane test, ethanol (2 g/kg i.p.) impaired the performance of the 6-OHDA treated rats significantly more than that of the controls. Moreover ethanol (4 g/kg e.p.) produced significantly longer narcosis in these rats. In contrast, the 5,7-HT treated rats were not affected significantly more than the controls in these tests. These results suggest that catecholamine neuronal systems interact with the expression of alcohol intoxication.

5,7-Dihydroxytryptamine↗