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Biomedical subjects

A Akaike

Publications and source records attributed to A Akaike.

At least 145 records · Page 8Linked to original sources

Microiontophoretic studies of the dopaminergic inhibition from the ventral tegmental area to the nucleus accumbens neurons.

Microiontophoretic studies using chloral hydrate-anesthetized rats were performed to determine whether excitation of a dopaminergic pathway originating in the ventral tegmental area (VTA) inhibits neurons on the nucleus accumbens (Acc). In 13 of 17 Acc neurons which failed to respond to hippocampal stimulation, the spike generation produced by stimulation of the parafascicular nucleus of thalamus was inhibited by both VTA conditioning stimulation and iontophoretically applied dopamine. The inhibition induced by the VTA conditioning stimulation was antagonized by iontophoretic application of haloperidol in 10 of 13 Acc neurons tested. In contrast, spike generation induced by stimulation of the hippocampus was not affected by VTA conditioning stimulation in 14 of 15 Acc neurons, although iontophoretically applied dopamine produced an inhibition in 4 of those 15 Acc neurons. Spikes generated by stimulation of the VTA were obtained in 23 of 102 neurons and were not affected by iontophoretically applied haloperidol. These results strongly suggest that dopamine derived from VTA inhibits Acc neurons receiving input from the parafascicular nucleus of thalamus but not from the hippocampus.

Animals↗

Effects of haloperidol and sulpiride on dopamine-induced inhibition of nucleus accumbens neurons.

Microiontophoretic study was performed to elucidate dopaminergic mechanism in the nucleus accumbens (Acc) of rats anesthetized with chloral hydrate. Iontophoretically applied dopamine produced an inhibition of glutamate-induced firing in 28 (62%) out of 45 Acc neurons tested. The dopamine-induced inhibition of 14 Acc neurons was clearly antagonized by simultaneous application of haloperidol, and a partial antagonism by sulpiride was observed in 3 out of 10 Acc neurons. These results indicate that dopamine produces an inhibition of the Acc neuron and that, compared to haloperidol, sulpiride is a less potent blocker of the postsynaptic dopamine receptor involved in the dopamine-induced inhibition.

Animals↗

Analgesia produced by microinjection of L-glutamate into the rostral ventromedial bulbar nuclei of the rat and its inhibition by intrathecal alpha-adrenergic blocking agents.

Definite and dose-dependent analgesia followed microinjection of L-glutamate into the nucleus reticularis paragigantocellularis (NRPG) of rats. This analgesic effect was inhibited by lumbar intrathecal pretreatment with phenoxybenzamine and phentolamine but not by propranolol, methysergide or naloxone. Microinjection of L-glutamate into the nucleus raphe magnus (NRM) also produced an analgesic effect which was reduced by intrathecal pretreatment with methysergide but not by phentolamine. These findings provide direct evidence that the NRPG and NRM function separately in descending pain-suppression systems of the spinal cord.

Adrenergic alpha-Antagonists↗

Inhibition from ventral tegmental area of nucleus accumbens neurons in the rat.

The role of the ventral tegmental area (VTA), which is rich in dopamine-containing cell bodies, on nucleus accumbens (Acc) neurons was examined. In Acc neurons receiving input from parafascicular nucleus (Pf) of thalamus, VTA conditioning stimulation produced an inhibition of spike generation with Pf stimulation. In contrast, VTA conditioning stimulation did not affect Acc neurons receiving input from limbic structures such as the amygdala nucleus and hippocampus.

Amygdala↗

Analgesic action of intrathecal and intracerebral beta-endorphin in rats: comparison with morphine.

beta-Endorphin and morphine were given into the nucleus reticularis gigantocellularis (NRGC), spinal subarachnoid space and third ventricle of rats, and the antinociceptive effects were assessed by the tail-pinch method. The NRGC was 4-5 times as sensitive to beta-endorphin as was the spinal subarachnoid space and third ventricle, while the NRGC was 13-19 times as sensitive to morphine as were the other regions. Thus, it would appear that beta-endorphin has more sites of action for the production of analgesia than does morphine.

Analgesics↗

Effects of tyrosyl-arginine (kyotorphin), a new opioid dipeptide, on single neurons in the spinal dorsal horn of rabbits and the nucleus reticularis paragigantocellularis of rats.

The effects of a new endogenous opioid dipeptide (Tyr-Arg), kyotorphin, on single unit activities recorded from the lamina V type neurons in the spinal dorsal horn and the neurons in nucleus reticularis paragigantocellularis (NRPG) of the medulla oblongata were investigated in the rabbit and rat, respectively. Microelectrophoretically applied kyotorphin predominantly depressed the lamina V type neurons but excited the NRPG neurons. Such predominant effects were antagonized by naloxone. These results suggest that kyotorphin has qualitatively similar actions to those of enkephalins in both central regions examined.

Animals↗