Intraventricular Injection Of 5-hydroxytryptamine Research Articles

Daily variations in the sensitivity of proestrous LH surge in the inhibitory effect of intraventricular injection of 5-HT or GABA in rats.

Intraventricular injection of 5-hydroxytryptamine (5-HT) into female rats at 11:00 h on the day of proestrus inhibited the preovulatory surge of luteinizing hormone (LH) and ovulation. A similar response was observed after the activation of the serotonergic system by stimulation of the median raphe nucleus. A diurnal rhythm of these responses was observed. In rats acclimated to a 14-h:10-h light:dark cycle the potency of 5-HT to inhibit the LH surge and ovulation was 2.06 and 2.3 times greater, respectively, when injected at 11:00 h than at 13:00 h. Also stimulation of the median raphe nucleus at 11:00 h was significantly more effective in inhibiting these parameters than stimulation at 13:00 h. Similarly, the ability of gamma-amino-butyric acid (GABA) to inhibit the preovulatory LH surge and ovulation was greater in rats injected in the morning than in the afternoon. The results of this study indicate that during proestrus the sensitivity of 5-HT and GABA to induce inhibition of preovulatory LH release and ovulation shows daily variations with maximal effect before the critical period.

Dehydration attenuates panting response to intraventricular 5-hydroxytryptamine in the rabbit

Panting response and a fall in rectal temperature following intraventricular injection of 5-hydroxytryptamine (5-HT) were significantly reduced in dehydrated rabbits as compared with normally hydrated animals. The vasomotor heat loss response to 5-HT was essentially similar in both groups. These as well as earlier findings suggest that dehydration may modify signals generated in brain thermoregulatory centers controlling evaporative but not the vasomotor heat loss.

Effects of 5-hydroxytryptamine on defecation in open-field behavior in rats

An attempt was made to elucidate the role of the serotonergic nervous system in defecation resulting from environmental stimulation in rats. The open-field (OF) test and shuttle box method were used to study the defecation. 5-Hydroxytryptophan (5-HTP) significantly decreased the number of fecal boluses excreted in both emotional situations, namely, in both OF and shuttle box. The fecal excretion was significantly reduced compared with the controls after intraventricular injection of 5-hydroxytryptamine (5-HT). Animals pretreated with p-chlorophenylalanine (pCPA) and 5,6-dihydroxytryptamine (5,6-DHT) tended to show a slight increase in the OF defecation. 5-HTP was equally effective in diminishing the OF performance of pCPA-treated rats. The inhibitory effects of 5-HTP on the defecation were also observed after depletion of biogenic amines by reserpine treatment. Home cage defecation was increased after 5-HTP administration, decreased under pretreatment with pCPA and not influenced by intraventricular injection of 5-HT. These results suggested that the defecation after environmental stimuli was due to a change in 5-HT levels in the brain.

Antinociceptive activity of morphine after injection of biogenic amines in the cerebral ventricles of the conscious rat.

1. A simple cannula and a cannula guide for making injections into the cerebral ventricles of conscious rats are described.2. Intraventricular injections of 5-hydroxytryptamine (5-HT) or of noradrenaline (NA) were without effect on the nociceptive threshold of rats.3. Intraventricular injection of 5-HT potentiated the antinociceptive effect of morphine. Reserpine pretreatment antagonized the antinociceptive effect of morphine; this effect was reversed by intraventricular injection of 5-HT.4. Intraventricular injection of NA attenuated the antinociceptive action of morphine but was without effect on the inhibition by reserpine of the antinociceptive effect of morphine.5. Subcutaneous injection or slow intravenous infusion of either 5-HT or NA (up to 300 mug/rat) were without significant effect on the antinociceptive effects of morphine.6. Intraperitoneal administration of dopa increased the nociceptive threshold above normal, but reduced the antinociceptive effect of morphine. Intraventricular injection of either dopa or dopamine had no antinociceptive effect but inhibited that of morphine.7. It is suggested that the antinociceptive effect of morphine may depend on the balance between the concentrations of 5-HT and NA in the brain.