Heterogeneity of postnatal development of ACh levels in brain regions of the mouse.

Acetylcholine (ACh) was measured from birth to the 78th day in 11 mouse brain regions. Three patterns of development emerged: ACh increased rapidly, overshot and returned to the adult level in midbrain-medulla-pons and cerebellum, ACh increased linearly to adult level in neostriatum and olfactory bulb and ACh increased linearly to a plateau and then increased to the adult level in the remaining regions.

The effects of morphine, naloxone and capsaicin on C-fiber reflex and heat evoked discharge in acute spinal cats.

The electrophysiological effects of morphine, naloxone and capsaicin were studied on c fiber reflex and heat evoked discharge in adult spinal cats. C fiber reflex was recorded from the L7 Ventral root at the time of superficial peroneal nerve electric stimulation. Heat evoked discharge was recorded from the L7 ventral root at the time of hind paw heating.

The effect of capsaicin on C-fiber reflex and heat evoked discharge in the acute spinal cat.

The effects of capsaicin were studied electrophysiologically on C-fiber reflex and heat-evoked discharge in adult spinal cats. The results can be summarized as follows: 1) 125 micrograms/Kg of capsaicin, administered intravenously, induced an increase in spontaneous discharge in the L7 ventral root; 2) 250 micrograms/Kg of capsaicin, administered intravenously, induced an increase in the C-fiber reflex response; 3) 125 micrograms/Kg of capsaicin, administered intravenously, induced an increase in the heat-evoked discharge; but 4) 25 micrograms/Kg of capsaicin, administered through the femoral artery, did not show significant alteration of the heat-evoked discharge. These findings suggest that capsaicin which produced a release of substance-P from primary afferent nerves may principally act on C-fiber and A delta-fiber.

The effects of droperidol and diazepam on the neural excitation of ketamine hydrochloride.

The effects of neuroleptics (droperidol and diazepam) were studied on the neural excitation by ketamine hydrochloride by means of the c-fiber reflex, in the spinal cat and the intact cat. Results can be summarized as follows: 1) Ketamine hydrochloride 125-500 micrograms/Kg i.v.

Evidence that dynorphin-(1-13) acts as an agonist on opioid kappa-receptors.

The study concerned the opioid-receptor subtype on which dynorphin-(1-13) acts in in vitro isolated preparations. The potency of dynorphin-(1-13) relative to that of ethylketocyclazocine (Mr 2266), a representative kappa-receptor agonist, in inhibiting the electrically evoked contractions of the guinea-pig ileum was found to be similar to that found with either mouse was deferens or rabbit ileum. Moreover, Mr 2266 was found to be several-fold more effective than naloxone to antagonize the agonist actions of both kappa-receptor agonists such as ethylketocyclazocine, ketocyclazocine and bremazocine, and dynorphin-(1-13) either in the guinea-pig ileum, mouse vas deferens, or in rabbit ileum.

Calcium requirements for electrically-induced release of an endogenous opiate receptor ligand from the guinea-pig ileum.

Calcium requirements for electrically-induced release of an endogenous opiate receptor ligand in the myenteric plexus-longitudinal muscle strip of the guinea-pig ileum were studied. The naloxone-reversible depression of the electrically evoked contraction caused by stimulation at 10 Hz in normal Krebs solution was markedly reduced by decreasing the calcium concentration in the solution. The depression was greatly diminished by increasing the magnesium concentration in the solution.

Effects of narcotic analgesics on serotonin metabolism in brain of rats and mice.

The effects of narcotic analgesics on the brain 5-hydroxytryptamine (5-Ht) and 5-hydroxyindoleacetic acid (5-HIAA) levels of rats and mice were investigated in relation to our preceding data on the effect of humoral modulatorents. The results suggest that morphine accelerates the release of brain 5-HT both in rats and mice, and that neither methadone nor pethidine alters the brain 5-HT and 5-HIAA levels in rats. The morphine-induced increase in brain 5-HT turnover is likely to be involved in the morphine-induced decrease in locomotor activity and hypothermia in rats.