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PubMed1996

Melatonin and deprivation myopia in chickens.

Chicken eyes elongate and become myopic if they are covered with translucent diffusors which degrade the retinal image ('deprivation myopia'). Since it has been shown that dopamine D2/D4 receptors (which mediate inhibition of melatonin synthesis) are also implicated in deprivation myopia, we have studied the role of melatonin in the visual control of eye growth. We have found that (1) diurnal melatonin rhythms and melatonin content in the retina are unchanged during deprivation myopia development despite the breakdown of both diurnal growth rhythms of the eye and diurnal rhythms in retinal dopamine metabolism, (2) diurnal melatonin rhythms and melatonin content in the retina remain unchanged after application of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) and presumably also after 6-hydroxydopamine (6-OHDA) application which both have a suppressive effect on deprivation myopia and (3) deprivation myopia was slightly reduced in both eyes after unilateral intravitreal injection of melatonin, despite that deprivation myopia is based on a mechanism intrinsic to the eye. We conclude that melatonin is not involved in the retinal signaling pathway translating visual experience to deprivation myopia.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Catecholaminergic-serotonergic balance in the CNS and reproductive cycling in aging rats.

Treatment with the serotonin (5-HT) reuptake inhibitor zimelidine, 20 mg/kg/24 hr, SC, for 14 days increased the duration of vaginal cycles in 3 month-old Long Evans hooded rats. It induced persistent vaginal estrus in 12 of 16 ten-month-old animals, and blocked reinitiation of vaginal cycles by L-dopa in 10 of 10 twenty-month-old rats. A single injection of zimelidine at 1400 hr did not alter the vaginal smear pattern of young or middle-aged cycling females or old constant estrus females. Also, a single dose of zimelidine at 1400 hr on the day of vaginal proestrus had no effect on serum LH values in young females. The serotonergic neurotoxin 5,7-dihydroxytryptamine, 4 micrograms, injected into the ventral and dorsal raphe areas (after desipramine, 25 mg/kg IP) reinitiated vaginal cycling in 8 of 13 twenty-month-old rats. These results suggest that age-dependent changes in serotonin metabolism may contribute to the age-dependent changes in luteinizing hormone secretion which eventually lead to the cessation of ovarian function in the rat and that alterations in serotonin function are an important component of the mechanism by which treatments with catecholamine precursors reinstate ovarian function in the old female rat.

5,7-Dihydroxytryptamine↗

PubMed1996

Lesioning of midbrain raphe nuclei with 5,7-DHT fails to alter ethanol intake in the low alcohol drinking (LAD) rat.

1. The effect of 10 g 5,7-dihydroxytryptamine (5,7-DHT) micro-injected into both the dorsal (DRN) and the median raphe nuclei (MRN) on the intake of ethanol in the low alcohol drinking (LAD) rat was measured using a standard 3-30% ethanol preference test. 2. The combined lesion of both midbrain structures depleted the levels of serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) significantly in each of eight major regions of the brain. The levels of norepinephrine, dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) remained unchanged after the lesion. 3. The effects of the neurotoxin lesions on the intakes of ethanol, food, water and total amount of fluid consumed were not significant. 4. The results corroborate our previous findings with the Sprague-Dawley strain of rat and suggest that although brain 5-HT may play a role in the maintenance of basal patterns of ethanol drinking, this monoamine may not be able to modify further the consumption of this fluid after lesioning with 5,7-DHT.

5,7-Dihydroxytryptamine↗

PubMed1981

Indoleamine-accumulating cells and dopaminergic cells are distributed similarly in carp retina.

Carp (Cyprinus carpio) retinas were processed for simultaneous visualization of dopaminergic (DA) and indoleamine-accumulating (ID) cells in flat-mounts under fluorescence microscope. A mixture of 5 micrograms noradrenaline (NA) and 5 micrograms 5,6-dihydroxytryptamine (5,6-DHT) was injected intravitreally into the eyes 2 h before enucleation. The spatial distribution and density were compared between NA-loaded DA-cells (greenish fluorescence) and 5,6-DHT-loaded ID-cells (yellowish). The two classes of cells were found to distribute similarly in a mixed fashion. Their densities were higher in the peripheral region than in the rest and extremely high at the retinal margin. Where the densities were higher, the size of cell bodies tended to be smaller. DA-cells were generally larger than ID-cells. Those cells, located in the intermediate and peripheral regions, appeared to be arranged in radial rows originating at the optic disc.

5,6-Dihydroxytryptamine↗

PubMed1984

Selective lesions of the bulbospinal serotonergic pathways reduce the analgesia induced by p-chloroamphetamine in the hot-plate test.

The antinociceptive effect of the serotonin releasing compound p-chloroamphetamine (PCA) was investigated in rats by means of the hot-plate method. Selective neurotoxic lesions of the descending serotonergic pathways induced by intrathecal injections of 5,6-dihydroxytryptamine (20 micrograms, 7 days before testing), produced hyperalgesia and significantly attenuated the analgesic effect of acutely administered PCA (2.5 mg/kg). The lesions reduced the spinal serotonin content by about 90% without significantly altering noradrenaline levels. It is concluded that the descending serotonergic pathways contribute to the expression of PCA-induced hot-plate analgesia.

5,6-Dihydroxytryptamine↗

PubMed1984

Loss of vision-guided adaptation of the vestibulo-ocular reflex after depletion of brain serotonin in the rabbit.

Brain serotonin in pigmented rabbits was depleted by intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT). Before depletion, an adaptive increase in the gain of the horizontal vestibulo-ocular reflex (HVOR) could be induced regularly by continuously rotating the animals in combination with optokinetic stimulus. After the depletion, such an increase in HVOR gain did not occur, even though dynamic characteristics of the HVOR and of the optokinetic eye movement were not altered. 5,7-DHT treatment also reduced brain norepinephrine, but depletion of norepinephrine to a similar extent by intraventricular injection of 6-hydroxydopamine in other rabbits did not affect the HVOR adaptation. These results suggest that brain serotonin plays an important role in maintaining adaptive modifiability of the HVOR.

5,7-Dihydroxytryptamine↗

PubMed1985

Forebrain serotonergic involvement in avoidance learning.

The one-way active avoidance deficit caused by the serotonergic (5-HT) releasing compound p-chloroamphetamine (PCA) was examined in rats after degeneration of 5-HT neurons in the forebrain. Injection of 5,7-dihydroxytryptamine (5,7-DHT) into the forebrain in desipramine (20 mg/kg)-pretreated rats resulted in a 65-70% decrease in 5-HT concentrations in the prefrontal cortex and hippocampus without any significant effect on striatal 5-HT. Slight reductions in noradrenaline (NA) (25%) and dopamine (DA) (34%) concentrations were observed in the prefrontal cortex only. The 5,7-DHT lesions markedly attenuated the impaired avoidance performance induced by PCA (2.5 mg/kg), suggesting that the avoidance deficit depends on intact 5-HT terminals in cortex and/or hippocampus. The 5,7-DHT lesion alone caused a slight but significant impairment of acquisition. The results suggest that 5-HT terminal systems in the forebrain play an important role in avoidance learning.

5,7-Dihydroxytryptamine↗

PubMed1985

Changes in brain serotonin levels affect leukocytes, lymphocytes, T-cell subpopulations and natural killer cell activity in rats.

The intraventricular injection of 5,6-dihydroxytryptamine into desipramine-treated rats caused a marked reduction in serotonin levels 5 and 10 days after treatment without significantly affecting catecholamine levels. In these animals, total leukocytes were increased and lymphocytes decreased. The number of helper T-cells (W3/25+) was significantly decreased after 5 days, whereas the numbers of total T-cells (W3/13+) and suppressor T-cells (MRC OX8) were increased after 10 days. The percentages of total T-cells, helper T-cells and suppressor T-cells were significantly reduced after 5 days. Natural killer cell (NK) activity was markedly reduced after 5 days. This finding suggests that central serotonin-containing neurons might be involved in the regulation of certain parts of the peripheral immune system.

5,6-Dihydroxytryptamine↗

PubMed1985

Serotonin turnover in raphe neurons transplanted into rat hippocampus.

Injections of the neurotoxin, 5,7-dihydroxytryptamine, into rostral raphe nuclei in rats reduced serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in hippocampus to 35-50% of normal levels but only reduced 5-HT synthesis and catabolism by 20-35%. The small reduction in 5-HT metabolism as compared to depletion of 5-HT suggests that 5-HT turnover was increased in nerve terminals that survived the neurotoxin lesion. Transplantation of rat fetal raphe cells into the 5-HT-denervated hippocampus restored 5-HT and 5-HIAA levels and 5-HT synthesis to 125-150% of normal. This demonstrates that transplantation of fetal raphe tissue can restore metabolism to normal levels in the 5-HT denervated hippocampus.

5,7-Dihydroxytryptamine↗

PubMed1985

The influence of serotonergic inputs on peptide neurons in the rat suprachiasmatic nucleus: an immunocytochemical study.

The influence of serotonin (5-hydroxytryptamine; 5-HT) innervation on peptide-containing neurons in the rat suprachiasmatic nucleus (SCN) was investigated by peroxidase-anti-peroxidase (PAP) immunocytochemistry. The 5-HT neuronal system was chemically severed by 5,6-dihydroxytryptamine (5,6-DHT) injection into the medial forebrain bundle bilaterally. After this treatment, a marked decrease of vasoactive intestinal peptide (VIP)-like immunoreactivity in neuronal perikarya occurred in the SCN corresponding to a decrease in number of 5-HT immunoreactive fibers and terminals. However, no alteration of arginine-vasopressin-like immunoreactivity was detected between 5,6-DHT-treated animals and the controls. It is speculated that VIP-like immunoreactive neurons play an important role in the SCN under the influence of strong 5-HT innervation.

5,6-Dihydroxytryptamine↗

PubMed1990

Discrete localization of high-density 5-HT1A binding sites in the midline raphe and parapyramidal region of the ventral medulla oblongata of the rat.

Serotonergic agonists that interact with the 5-HT1A receptor subtype cause marked decreases in blood pressure when administered to the medulla oblongata. In the present study, specific binding of the 5-HT1A-specific ligand, [3H]8-OH-DPAT, was determined in sections of the rat medulla oblongata using autoradiographic techniques. The highest density of binding was associated with the midline raphe nuclei and the parapyramidal regions of the rostral ventral medulla, areas that contain serotonergic neurons. Administration of the serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), 2 weeks prior to sacrifice, resulted in a marked loss of binding in the medullary raphe nuclei and the parapyramidal region. These results demonstrate the presence of 5-HT1A binding sites in discrete regions of the ventral medulla and are consistent with the hypothesis that 5-HT1A agonists reduce blood pressure by directly suppressing the activity of serotonergic neurons in the ventral medulla.

5,7-Dihydroxytryptamine↗

PubMed1993

Increased expression of preproneuropeptide Y and preprosomatostatin mRNA in striatum after selective serotoninergic lesions in rats.

The levels of neuropeptide Y and somatostatin may change when serotoninergic neurotransmission is altered in different brain regions. To assess whether serotonin regulates the synthesis of these peptides, we measured the levels of preproneuropeptide Y (ppNPY) and preprosomatostatin (ppSOM) mRNA in different brain regions after intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT), a selective serotonin neurotoxin. The mRNA of these peptides significantly increased in the striatum but not in hippocampus and frontal cortex. It thus appears that serotonin has an inhibitory effect on the biosynthesis of neuropeptide Y and somatostatin in striatum whereas it probably acts by stimulating the release of these peptides in hippocampus and frontal cortex.

5,7-Dihydroxytryptamine↗

PubMed1994

Pyroglutamyl peptidase II activity is not in the processes of bulbospinal TRHergic neurons.

Pyroglutamyl peptidase II (PPII) is a neuronal ectoenzyme involved in released thyrotropin-releasing hormone (TRH) inactivation. In an attempt to define if it is present in the pre or postsynaptic membrane, we induced neuronal degeneration of serotonin-TRHergic cells that project from raphe nuclei to the spinal cord. 2-4 weeks after intracisternal injection of 5,7-dihydroxytryptamine, TRH levels decreased over 70% in the cervical, thoracic or lumbar regions of spinal cord. In contrast, no change of PPII activity was observed. Longer times after injection (6-8 weeks), a 59-66% increase in activity was detected in the lumbar region. These data suggest that PPII is not localized in these TRHergic neurons but probably in the target cells.

5,7-Dihydroxytryptamine↗

PubMed1996

A 5-hydroxytryptamine lesion markedly reduces the incidence of burst-firing dorsal raphe neurones in the rat.

Recently, we described neurones in the rat dorsal raphe nucleus (DRN) with electrophysiological characteristics typical of 5-hydroxytryptamine (5-HT) neurones except that the neurones fired brief bursts. Here we report the effect of 5-HT lesions on the incidence of these burst-firing neurones. In vivo extracellular recordings revealed that in rats pretreated with the selective 5-HT neurotoxin, 5,7-dihydroxytryptamine, the occurrence of typical 5-HT neurones was significantly decreased (80%) compared to controls. In these 5-HT lesioned animals, the number of the burst-firing DRN neurones was also significantly reduced (91%). Neurones previously characterised as not containing 5-HT, were not altered by the lesion. These data are further evidence to support our hypothesis that burst-firing neurones in the DRN contain 5-HT.

5,7-Dihydroxytryptamine↗

PubMed1996

Nitric oxide, but not serotonin, is involved in acquisition of food-attraction conditioning in the snail Helix pomatia.

The effects of inhibition of nitric oxide (NO) or serotonin (injection of nitro-L-arginine methyl ester (L-NAME) or 5,6-dihydroxytryptamine (5,6-DHT), respectively) on food-attraction conditioning was investigated in Helix. Blocking NO synthase (NOS) prior to conditioning significantly impaired the food-finding ability of the snails. Food-conditioned snails, after inhibition of NOS, remained able to locate the conditioned food. These results indicate that the acquisition of memory depends on NO, whereas memory recall and olfactory orientation are not dependent. Ablating the serotonergic system did not influence food-attraction conditioning, suggesting that food-attraction conditioning may be at variance with conventional associative conditioning procedures.

5,6-Dihydroxytryptamine↗

PubMed1988

Apparent hyperalgesia after lesions of the descending serotonergic pathways is due to increased tail skin temperature.

It has been suggested that the descending serotonergic pathways exercise a tonic inhibition on nociception in the spinal cord. In this study 5,6-dihydroxytryptamine (5,6-DHT, 20 micrograms base) injected intrathecally in rats reduced spinal serotonin concentration to 3.5% of control levels without significantly affecting spinal noradrenaline. The lesion reduced the mean tail-flick latency by approximately 35% and increased the mean tail skin temperature by approximately 3.5 degrees C; both parameters gradually returned to normal values within 2-3 weeks. Both in controls and in lesioned animals there was a highly significant negative correlation between tail skin temperature and tail-flick latency. Multiple regression analysis showed that the effect of lesioning on tail-flick latency was non-significant when the effect of skin temperature was taken into account. Thus the reduced tail-flick latency after lesions of descending serotonergic pathways, usually interpreted as increased nociception, may be due to changes in tail skin temperature.

5,6-Dihydroxytryptamine↗

PubMed1988

The antinociceptive role of a bulbospinal serotonergic pathway in the rat brain.

The antinociceptive role of spinal serotonin (5-HT) neurons descending from 5-HT cells near the ventrolateral surface of the medulla oblongata was investigated by stimulating these cells in normal rats, in rats with generalized or selective chemical ablation of 5-HT nerves, and in rats with postsynaptic blockade of 5-HT receptors. Electrical stimulation of the lateral medulla elicited analgesia in normal rats; the increase in pain threshold was proportional to the intensity and to the frequency of stimulation. In addition, microinjection of kainic acid or L-glutamate at the same sites also produced analgesia. However, generalized destruction of CNS 5-HT nerves produced by intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) or selective destruction of spinal 5-HT nerves produced by intraspinal injection of 5,7-DHT reduced the magnitude of the antinociceptive responses to electrical stimulation. Postsynaptic blockade of CNS 5-HT receptors produced by intraventricular injection of cyproheptadine also reduced the stimulation-produced analgesia. The specificity of the lesions for 5-HT nerves is demonstrated by the lack of effect on the levels of noradrenaline in the same brain regions. The results indicate that the activity of 5-HT nerve cells adjacent to the ventrolateral surface of the medulla oblongata and projecting to the spinal cord serves to elevate pain threshold.

5,7-Dihydroxytryptamine↗

PubMed1991

The formalin test in mice: the influence of ambient temperature.

The ambient temperature had a confounding influence on the licking response in the formalin test. No effect was demonstrated in the early phase. In the late phase, the licking activity was much lower at 20 degrees C than at 25 degrees C. Both the intensity and the duration of the response were increased by increasing the ambient temperature from 20 degrees C to 28 degrees C. 5,6-Dihydroxytryptamine lesions of descending serotonergic pathways induced an increase in the nociceptive response at an ambient temperature of 20 degrees C, while the response was no different from control values at 25 degrees C. Differences in paw skin temperature may explain these temperature dependent effects. It was concluded that control of the ambient temperature is necessary to obtain reliable results in the formalin test, late phase.

5,6-Dihydroxytryptamine↗