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PubMed1979

Effects of brain serotonin alterations on hypothermia produced by chlorpromazine in rats.

Depressing functional serotonin or depleting serotonin levels in rat brains with either p-chlorophenylalanine, 5,6-dihydroxytryptamine or raphe lesions greatly enhanced hypothermia induced by chloropromazine (CPZ). Depressing the firing of raphe units or decreasing serotonin turnover in the brain with either a serotonin precursor (tryptophan) or the inhibitors of serotonin re-uptake (Lilly 1 10140 and chlorimipramine) also greatly enhanced the CPZ-induced hypothermia. The data indicate that serotonergic activity in the brain plays a role in the elaboration or modulation of CPZ hypothermia.

5,6-Dihydroxytryptamine↗

PubMed1979

Effect of morphine on 'wet-dog' shakes caused by cerebroventricular injection of serotonin.

Intraventricular administration of serotonin to rats causes 'wet-dog' shakes, a sign of morphine withdrawal. The frequency of shakes is dose-dependent. Shaking is potentiated by pretreatment with an inhibitor of monoamine oxidase or with 5,7-dihydroxytryptamine, and is depressed by morphine or serotonin receptor blockers. Depression of serotonin-induced shaking by morphine is reversed rapidly by naloxone. However, naloxone did not reverse the inhibition of 'wet-dog' shakes caused by serotonin receptor blockers.

5,7-Dihydroxytryptamine↗

PubMed1985

Cholecystokinin-induced hypothermia: possible involvement of serotoninergic mechanisms in the rat hypothalamus.

The thermal effects of rats which were pretreated with 5,7-dihydroxytryptamine to deplete hypothalamic 5-hydroxytryptamine (5-HT) or with a 5-HT receptor blocker to intrahypothalamic administration of cholecystokinin (CCK) were compared with those of control rats. The CCK-induced hypothermic response was attenuated by pretreatment of the rats with either hypothalamic 5-HT depletion or receptor blockade. The reduction in the CCK hypothermia in the treated rats was due to the reduction of metabolic and vasomotor response. The data indicate that CCK may act on a 5-HT pathway within the hypothalamus to induce its hypothermia by promoting a reduction in metabolic heat production and an enhancement in heat loss in rats.

5,7-Dihydroxytryptamine↗

PubMed1987

Participation of a bulbospinal serotonergic pathway in the rat brain in clonidine-induced hypotension and bradycardia.

The effects of microinjection of clonidine (1-10 micrograms in 1 microliter) into a region adjacent to the ventrolateral surface of the medulla oblongata on cardiovascular function were assessed in urethane-anesthetized rats. Intramedullary administration of clonidine, but not saline vehicle, caused a dose-dependent decrease in both the mean arterial pressure and the heart rate. The clonidine-induced hypotension was antagonized by prior spinal transection, but not bilateral vagotomy. On the other hand, the clonidine-induced bradycardia was antagonized by prior bilateral vagotomy, but not spinal transection. Furthermore, selective destruction of the spinal 5-HT nerves, produced by bilateral spinal injection of 5,7-dihydroxytryptamine, reduced the magnitude of the vasodepressor or the bradycardiac responses to clonidine microinjected into the area near the ventrolateral surface of the medulla oblongata in rats. The data indicate that a bulbospinal serotonergic pathway is involved in development of clonidine-induced hypotension and bradycardia. The induced hypotension is brought about by a decrease in sympathetic efferent activity, whereas the induced bradycardia was due to an increase in vagal efferent activity.

5,7-Dihydroxytryptamine↗

PubMed1987

Possible direct effect of serotonin on pituitary prolactin secretion: in vivo and in vitro studies.

In this work we analyze the possibility of serotonin (5-HT)-releasing prolactin (PRL) through a direct action at the pituitary level. 5-HT (2 mg/kg i.v.) stimulates PRL secretion in hypophysectomized autotransplanted animals (HAG) significantly and this effect was not influenced by pretreatment with the dopaminergic antagonist domperidone. In perifused pituitaries, 5-HT administration (0.01, 0.1 and 1 microM for 90 min, or 1, 10, 100 microM for 15 min) was ineffective in stimulating PRL release. In pituitaries obtained from animals previously treated with the neurotoxic 5,7-dihydroxytryptamine (5,7-DHT) or vehicle and incubated in the presence of 5-HT (2.5, 5 and 10 microM), no response in PRL secretion was observed. These results suggested that 5-HT does not release PRL through a direct pituitary action, and that the effect observed in HAG animals could be mediated through the release of a PRL-releasing factor after 5-HT administration.

5,7-Dihydroxytryptamine↗

PubMed1990

Alterations of the cat's electroretinogram induced by the lesioning of the indoleamine-accumulating amacrine cells.

The neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) was used to destroy the indoleamine-accumulating amacrine cells located in the cat's retina. With 100 micrograms of 5,7-DHT, the alterations in the electroretinogram (ERG) were present in all of the treated eyes and the morphological changes were confined to some of the processes in the inner plexiform layer. The ERGs recorded from treated eyes consisted of negative waves at low intensities and depressed b wave amplitude at higher intensities. The duration of the b wave was not altered but the oscillatory potentials were strongly depressed. The changes were probably permanent. The differences in the ERG changes in cats and rabbits were suggested to arise from the differences in signal processing in the inner retina of rabbits and cats.

5,6-Dihydroxytryptamine↗

PubMedDate not supplied

Bulbospinal serotonin pressor pathways and hypotensive action of methyldopa in the rat.

The administration of methyldopa (200 mg/kg i.p.) induced a green fluorescence typical of catecholamine fluorescence, in regions of the brain stem which coincided with all the major serotonin cell groups, including the B1, B2, and B3 cell groups in the medulla. Prior administration of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin relatively specific for serotonin neurons, prevented the appearance of this methyldopa-induced fluorescence. Electrical stimulation of the ventrolateral medulla in areas that coincided with the lateral elements of the B1 and B3 serotonin cell groups evoked pressor responses recorded via cannulae in the abdominal aorta. The pressor responses were frequency-dependent and could be markedly attenuated by prior administration of 5,7-DHT either intracerebroventricularly (i.c.v.) or directly into the cervical cord to ablate descending serotonin nerve fibers. Microinjection of methyldopa (4-16 micrograms) directly into the region of the B1 and B3 cells in the ventrolateral medulla evoked a dose-dependent fall in arterial pressure observed for 4 hours. Here too, prior administration of 5,7-DHT either intracerebroventricularly or directly into the cervical cord largely prevented the hypotensive action of the microinjections of methyldopa. The administration of 5,7-DHT produced a highly selective depletion of serotonin stores without reducing the concentrations of norepinephrine. These experiments suggest that the activity of serotonin nerves descending into the spinal cord from the B1 and B3 cells in the ventrolateral medulla serves to elevate or maintain arterial pressure. They also suggest that these descending serotonin neurons may contribute to the hypotensive action of methyldopa.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Central and peripheral autonomic mechanisms involved in the circulatory actions of methyldopa.

Intracisternal (i.c.) and intravenous (i.v.) administration of methyldopa in conscious rabbits produced closely similar changes in hemodynamics, heart rate, and falls in plasma norepinephrine levels. Two weeks after giving i.c. 6-hydroxydopamine (6-OHDA), when there is widespread destruction of central noradrenergic neurons, the effects of i.c. methyldopa virtually were abolished. This suggests that noradrenergic neurons are the major central site of biotransformation into active metabolites. The circulatory and norepinephrine effects of i.v. methyldopa were attenuated but not completely abolished after giving i.c. 6-OHDA. Hence, in the rabbit about 70% of the action of methyldopa was central and about 30% was peripheral in the human therapeutic range of methyldopa concentrations. Preliminary lesion experiments suggest that the A5 nucleus plays an important role in the bradycardia. Two weeks after giving 5,6-dihydroxytryptamine (5,6-DHT) to destroy serotonergic (5HT) neurons the effects of i.c. methyldopa on mean arterial pressure (MAP) and heart rate were attenuated to approximately 50% of control effects. Therefore, some of the central effects of methyldopa apparently are mediated through 5HT pathways. We also compared the effects of i.c. methyldopa with those of i.c. clonidine (an alpha 2-adrenergic receptor agonist) and with the effects of transmitter release from the endings of noradrenergic and 5HT neurons during the first few hours after either 6-OHDA or 5,6-DHT administration. Our findings suggest that after biotransformation of methyldopa its active metabolites increase the activity of the bulbospinal noradrenergic neurons that control MAP and heart rate and reduce the activity of bulbospinal 5HT neurons.

5,6-Dihydroxytryptamine↗

PubMed1987

Vascular responsiveness to serotonin metabolites in mineralocorticoid hypertension.

This study characterizes vascular responsiveness to serotonin and its metabolites and to several monoamines that are structurally related to serotonin in deoxycorticosterone acetate (DOCA)-salt hypertension. Mesenteric arteries from normotensive and hypertensive rats were excised and cut into helical strips for isometric force recording. Dose-response curves to serotonin in arteries from hypertensive rats were shifted significantly to the left compared with those in arteries from normotensive rats (ED25: DOCA-treated = 2.4 X 10(-8) M; control = 17.1 X 10(-8) M). Contractile responses to 5-hydroxyindole acetic acid and 5-hydroxytryptophol were greater in mesenteric arteries from hypertensive rats, whereas reactivity to 5-methoxytryptamine and melatonin in arteries from hypertensive rats did not differ from that in arteries from normotensive rats. Mesenteric arteries from both rat groups were unresponsive to the serotonin metabolite N-acetylserotonin. Contractile responses to 5,6-dihydroxytryptamine and 6-hydroxytryptamine were greater in mesenteric arteries from hypertensive rats, whereas responsiveness to 3-hydroxytryptamine in hypertensive arteries did not differ from normotensive values. Contractile responses to serotonin and its metabolites and to the structurally related monoamines were inhibited by the serotonergic antagonist ketanserin. These results demonstrate that vascular sensitivity to serotonin is increased in DOCA-hypertensive rats. Based on the experiments with serotonin metabolites and with other monoamines, the increased responsiveness to these compounds appears to be related to the structural location of hydroxyl and amine moieties.

5,6-Dihydroxytryptamine↗

PubMed1979

Serotonin and the control of ventilation in awake rats.

In awake, unrestrained, intact rats, reserpine, para-chlorophenylalanine, 6-fluorotryptophan, and para-chloroamphetamine depleted whole brain serotonin and produced a substantial and sustained hyperventilation as evidenced by a 5--9 torr drop in PaCO2. Administration of 5-hydroxytryptophan to rats treated with para-chlorophenylalanine partially alleviated the hyperventilation. No change in ventilation was observed after alpha-methyltyrosine. 5,7-Dihydroxytryptamine produced contradictory results. On the basis of these pharmacological studies, we propose that some serotonin-mediated nerve transmissions might function under physiological conditions to inhibit the central nervous system output which controls normal breathing.

5,7-Dihydroxytryptamine↗

PubMed2001

Serotonergic depletion increases conditioned suppression to background stimuli in the rat.

Dark Agouti rats were lesioned by intra-ventricular injection of 5,7-dihydroxytryptamine (DHT) and, 2 weeks later, learning was tested in a conditioned suppression of drinking procedure. Lesioned and vehicle-injected control rats were conditioned with a discrete stimulus (tone or light conditioned stimulus, CS) twice paired with footshock (unconditioned stimulus), with or without a 30-s trace interval between these events to produce strong and weak learning conditions (a trace conditioning effect). During this conditioning session, the alternate stimulus (light or tone) was presented continuously in the background. Since the 5,7-DHT lesion also reduced the baseline licking response in the experimental chambers, we used drinking during the first minute, when this non-specific effect was minimal, as the dependent variable. We tested conditioning to target CS and to the alternative experimental background stimulus in exactly the same way in the same rats. We found that a level of serotonergic depletion without any intrinsic action on the trace conditioning effect nevertheless increased conditioning to the alternative background stimulus, irrespective of trace interval or stimulus modality. Thus, for both light and tone stimuli, the effect of serotonergic depletion depended only on the discrete target versus diffuse background role of the stimulus in use. These findings have implications for the modification of human cognition by serotonergic drugs.

5,7-Dihydroxytryptamine↗

PubMed1998

Local administration of serotonin agonists blocks light-induced phase advances of the circadian activity rhythm in the hamster.

Circadian rhythms in mammals are synchronized to environmental light-dark cycles through a direct retinal projection to the suprachiasmatic nucleus (SCN), a circadian clock. This process is thought to be modulated by other afferents to the SCN, including a dense serotonergic projection from the midbrain raphe. Previous work from this laboratory demonstrated that a systemically administered 5-hydroxytryptamine1A/7 (5-HT1A/7) agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) dose dependently attenuates light-induced phase shifts of the circadian activity rhythm of the Syrian hamster. In this study, we demonstrate that local injections (1-100 microM) of the 5-HT1A/7 agonists 8-OH-DPAT or 5-carboxamidotryptamine into the region of the SCN inhibit light-induced phase advances of the circadian wheel-running rhythm. In addition, the inhibitory effects of systemically administered 8-OH-DPAT were unaffected by either radiofrequency-induced lesions of the intergeniculate leaflet or 5,7-dihydroxytryptamine-induced lesions of serotonergic projections to the SCN. These findings support a modulatory role of serotonin in photic regulation of circadian phase through an action at the level of the SCN.

5,7-Dihydroxytryptamine↗

PubMed2002

Decrease of core body temperature in mice by dehydroepiandrosterone.

Dietary dehydroepiandrosterone (DHEA) reduces food intake in mice, and this response is under genetic control. Moreover, both food restriction and DHEA can prevent or ameliorate certain diseases and mediate other biological effects. Mice fed DHEA (0.45% w/w of food) and mice pair-fed to these mice (food restricted) for 8 weeks were tested for changes in body temperature. DHEA was more efficient than food restriction alone in causing hypothermia. DHEA injected intraperitoneally also induced hypothermia that reached a nadir at 1 to 2 hr, and slowly recovered by 20 to 24 hr. This effect was dose dependent (0.5-50 mg). Each mouse strain tested (four) was susceptible to this effect, suggesting that the genetics differ for induction of hypophagia and induction of hypothermia. Because serotonin and dopamine can regulate (decrease) body temperature, we treated mice with haloperidol (dopamine receptor antagonist), 5,7-dihydroxytryptamine (serotonin production inhibitor), or ritanserin (serotonin receptor antagonist) prior to injection of DHEA. All of these agents increased rather than decreased the hypothermic effects of DHEA. DHEA metabolites that are proximate (5-androstene-3beta, 17beta-diol and androstenedione) or further downstream (estradiol-17beta) were much less effective than DHEA in inducing hypothermia. However, the DHEA analog, 16alpha-chloroepiandrosterone, was as active as DHEA. Thus, DHEA administered parentally seems to act directly on temperature-regulating sites in the body. These results suggest that DHEA induces hypothermia independent of its ability to cause food restriction, to affect serotonin or dopamine functions, or to act via its downstream steroid metabolites.

5,7-Dihydroxytryptamine↗

PubMed1980

In vitro hippocampal uptake of tritiated serotonin (3H-5HT): A morphological, biochemical, and pharmacological approach to specificity.

The in vitro uptake of tritiated serotonin (3H-5HT) into hippocampal slices was measured in Ringer's solution (37 degrees C) containing pargyline, ascorbic acid, and dextrose. The specific uptake of 3H-5HT rose asymptotically as the 3H-5HT molarity was increased from 5 x 10(-10) to 1.5 x 10(-6) M. Linear regression analysis gave a Km value for the specific uptake of 1.4 x 10(-7) M. The nonspecific binding (NSB) was the amount of 3H-5HT retained by the slices following incubation in a medium with a very large excess of unlabeled 5-HT added to dilute the specific uptake of 3H-5HT. This NSB increased with increasing molarity of 3H-5HT, and was linearly related to 3H-5HT concentrations between 5 x 10(-9) and 1.5 x 10(-6) M. The ratio of specific uptake to NSB was highest at 5 x 10(-8) M (2.75) and lowest at 1.5 x 10(-6) M of 3H-5HT (0.54). Competition studies with noradrenaline, desipramine (a noradrenergic uptake blocker), fluoxetine (a 5-HT uptake blocker), and tryptophan confirmed the specificity of the 3H-5HT uptake mechanism. Radioautographic studies of in vitro incubated hippocampal slices showed silver grain aggregates at 3H-5HT specific uptake sites. Addition of an excess of unlabeled 5-HT to the slices, or the use of hippocampi from 5,7-dihydroxytryptamine intracerebral microinjected rats (5 microgram/400 nl into the fornix-fimbria and the cingulum bundle, 6 day survival) caused a dramatic decrease in these aggregates. The distribution of hippocampal 5-HT axons and terminals, inferred from the pattern of silver grain aggregates, is more widespread than previously described. 5-HT varicosities were clearly seen in all layers of Ammon's horn, dentate gyrus, and the subicular cortex. Innervation routes were seen to the stratum radiatum and stratum lacunosum from stratum oriens in Ammon's horn, and to the polymorphic layer of the dentate gyrus from the subicular cortex and from the fimbria. Semiquantitation of the occurrence of silver grain aggregates was done in the various hippocampal regions. The highest density in Ammon's horn was 119.5 boutons/10,000 micron2, in the dentate gyrus it was 67.4 boutons/10,000 micron2, and in the subicular cortex it was 79.2 boutons/10,000 micron2. These results are consistent with previous quantitative results.

5,7-Dihydroxytryptamine↗

PubMed1978

Hypothalamic and raphe serotonergic systems in ovulation control.

The role of hypothalamic and midbrain serotonergic systems in the control of ovulation in the rat has been investigated using 5,7-dihydroxytryptamine (5,7-DHT) lesioning in conjunction with desmethylimipramine pretreatment. Intracisternal injection of 5,7-DHT (100 or 200 microgram) produced a dose-dependent decrease in the incidence of ovulation induced by PMS gonadotrophin (PMSG; 8 IU sc on day 30). Intraventricular injection of 200 microgram 5.7-DHT via the lateral ventricles completely blocked PMSG-induced ovulation. After injection into either site, nonovulatory animals were in proestrus on day 33 and contained fluid-filled uteri. Intracerebral injection of 5,7-DHT into the dorsal or median raphe significantly decreased the numbers of animals induced to ovulate. The extent and specificity of these chemical lesions were evaluated in the suprachiasmatic (SNR) and arcuate-median eminence regions of PMSG-treated rats using an in vitro uptake model. A general feature of every case of inhibited ovulation was the significant decrease in uptake of serotonin in the SNR, indicating destruction of serotonergic inputs to this region. This suggests that serotonergic SNR input from the dorsal raphe region is essential to ovulation. Median raphe lesions appeared to be more extensive than dorsal raphe lesions, involving serotonergic projections to the arcuate-median eminence region. In addition, ascending noradrenergic projections to the SNR were significantly destroyed, also implicating these systems in ovulation control.

5,7-Dihydroxytryptamine↗

PubMed1983

Specific neurotoxin lesions of median raphe serotonergic neurons disrupt maternal behavior in the lactating rat.

Impairments in lactation after electrolytic lesions of the median raphe (MR) nucleus have been corrected by treatment with PRL. Specific serotonin neurotoxin lesions were used in the present study to determine whether decrements in litter growth after electrolytic lesions could be attributed to serotonergic neuron damage at the MR locus, and whether MR lesions (MRL) disrupted suckling-induced PRL release. Intracerebral microinjection of 5,7-dihydroxytryptamine (5,7-DHT) into the MR nucleus produced dose-related decrements in litter growth after either 4 micrograms (sham, 1.35 +/- 0.05; MRL, 1.04 +/- 0.05 g/pup X day; P less than 0.001) or 8 micrograms 5,7-DHT (sham, 1.35 +/- 0.06; MRL, 0.87 +/- 0.11 g/pup X day; P less than 0.001). Despite hypothalamic serotonin depletions of 15% and 55%, respectively, for the two doses of 5,7-DHT, there was no difference between sham and MRL animals in either basal or suckling-induced PRL release. When lesions were placed on day 1 of lactation (L) so that killing on day 7-L corresponded to the early maximal neurotoxin effect, MRL mothers still showed litter growth decrements (0.37 +/- 0.07; sham, 0.98 +/- 0.08 g/pup X day; P less than 0.001) and normal PRL values. When maternal behavior was examined, MRL animals exhibited a higher incidence of abnormal behaviors (failure to retrieve pups, cannibalism, and failure to initiate suckling during a 1-h test period; Fisher's exact P, Sham vs. MRL, less than 0.01, less than 0.05, and 0.15, respectively) than sham animals or animals with 5,7-DHT lesions in the dorsal raphe nucleus or superior colliculus. In addition, suckling behavior scores, determined from daily suckling behavior observations, were lowest in the MRL group and correlated with litter growth only in this group (r = 0.789; P less than 0.01). These data suggest that serotonergic elements in the MR nucleus play an obligatory role in maintaining normal maternal behavior during lactation, but they are not involved in suckling induced PRL release.

5,7-Dihydroxytryptamine↗

PubMed1983

Acute effects of estradiol on circulating luteinizing hormone and prolactin concentrations and on serotonin turnover in individual brain nuclei.

Two experiments tested whether serotonergic neurons participate in the acute feedback effects of estradiol on LH and PRL secretion. In the first study, ovariectomized female rats received oil vehicle or estradiol benzoate and were killed 3 h later. The turnover of serotonin [5-hydroxytryptamine (5-HT)] in microdissected brain nuclei was assessed from its accumulation after monoamine oxidase inhibition. Estradiol treatment produced a gradual rise in PRL and a decline in LH, and potentiated the accumulation of 5-HT in the medial preoptic, ventromedial, and cortical amygdaloid nuclei, suggesting increased turnover. Concentrations of the metabolite, 5-hydroxyindole acetic acid, were also elevated in these areas. 5-HT turnover was unaffected by estradiol in the interstitial nucleus of the stria terminalis, periventricular, dorsomedial, or lateral amygdaloid nuclei. The second experiment tested whether localized 5-HT depletions in these estradiol-activated nuclei blocked the acute effects of the steroid on LH or PRL. Stereotaxic microinjections of the 5-HT neurotoxin, 5,7, dihydroxytryptamine were made into the preoptic area, cortical amygdala, or medial basal hypothalamus in ovariectomized rats, pretreated with desmethylimipramine. Such treatment reduced 5-HT, without affecting catecholamines, in the targeted structures. Localized 5-HT depletion in the preoptic area and amygdala blunted the elevation of PRL, but not the decline of LH, after estradiol. 5-HT depletion in the medial basal hypothalamus elevated, whereas 5-HT depletion in the medial preoptic area lowered, resting levels of LH. These results suggest that: 1) estradiol may acutely increase PRL secretion by activating serotonergic projections to the medial preoptic and cortical amygdaloid nuclei, and 2) serotonergic neurons innervating the preoptic area stimulate LH release, whereas serotonergic systems in the medial basal hypothalamus inhibit LH release.

5,7-Dihydroxytryptamine↗

PubMed1986

Role of central serotonin systems in the stimulatory effects of ovarian hormones and naloxone on luteinizing hormone release in female rats.

The present experiments tested whether serotonergic neurons that innervate discrete areas of the hypothalamus are involved in the stimulation of LH release by ovarian hormones or the opiate antagonist naloxone in female rats. Ovariectomized rats received oil vehicle, estradiol benzoate (EB) alone, or EB followed by progesterone (P) 2 days later. Serotonin (5-HT) activity was assessed from the accumulation observed after the administration of the monoamine oxidase inhibitor pargyline. Two days after EB treatment, LH concentrations were reduced in the morning and rose by later afternoon. Administration of P to EB-primed rats stimulated a LH surge. This latter treatment also enhanced pargyline-induced 5-HT accumulation, suggesting increased 5-HT activity, in the medial preoptic nucleus and interstitial nucleus of the stria terminalis, but reduced 5-HT accumulation, suggesting decreased 5-HT activity, in the ventromedial nucleus. 5-HT activity was unaffected after EB alone, either in the morning or afternoon, or by the administration of naloxone to EB-primed rats. Specific depletion of 5-HT in the medial preoptic/stria terminalis area, achieved by microinjection of the neurotoxic indoleamine 5,7-dihydroxytryptamine resulted in a blockade of the LH surge induced by EB plus P. The present results suggest that central 5-HT neurons innervating the preoptic area are involved in the LH surge induced by progesterone, but not in the increases in LH occurring after treatment with estradiol alone or after blockade of opiate receptors.

5,7-Dihydroxytryptamine↗