Influences of isoproterenol pretreatment on cerebral cortical bindings of [3H]clonidine and [3H]dihydroalprenolol in infant and adult rats.

Specific bindings of [3H]clonidine and [3H]dihydroalprenolol [( 3H]DHA) to crude synaptic membranes were measured after cerebral cortical slices or synaptic membranes were pre-incubated with isoproterenol, 200 microM at 37 degrees C for 40 min, in 7- and 70-day-old rats. Isoproterenol caused a significant increase of the Bmax value of [3H]clonidine binding sites at both days 7 and 70, without changing the Kd. Scatchard analysis of [3H]clonidine binding to adult synaptic membranes which was examined by using a wide range of [3H]clonidine concentration (0.05-15 nM), showed that the Bmax in only high-affinity binding sites was 4-fold increased by pretreatment of synaptic membranes with isoproterenol 200 microM. In contrast, the Bmax of [3H]DHA binding sites was significantly reduced by isoproterenol at 7 and 70 days. These results suggest that the possible interrelationship between beta- and alpha 2-adrenoceptors which exists in synaptic membranes, matures by day 7 in the cerebral cortex of rats.

[Two cases of large functioning parathyroid adenoma in atomic bomb survivors].

In a study by the Radiation Effects Research Foundation, Hiroshima and Nagasaki, of parathyroid tumors in autopsy cases, 18 cases of parathyroid adenoma were detected among 6, 102 cases that were autopsied between 1961-77. Two of these were giant adenomas 5 cm in diameter, complicated with hyperthyroidism. Both were atomic bomb survivors of Hiroshima. One was exposed to 55 rad at the age of 51 and died at age 71. The other was exposed to 28 rad at age 44 and died at age 71. These two cases are reported with a review of the literature on parathyroid tumors that developed following irradiation of the head and neck.

Ontogeny of influence of clonidine on high potassium-induced release of noradrenaline and specific [3H]clonidine binding in the rat brain cortex.

A high (20 mM) K+-induced, Ca2+-dependent release of L-[3H]-noradrenaline (NA) from cerebral cortex slices was detected in rats on day 18 of gestation. Depolarization-evoked release (% of total radioactivity) increased with age between day 18 of gestation and day 70 of postnatal life. Clonidine (0.1 microM) significantly (p less than 0.05) reduced a high K+-induced L-[3H]NA release on days 7 and 70 but not on day 1. Both KD and Bmax of specific [3H]clonidine binding to cerebral cortex membranes rapidly increased between days 1 and 7, followed by a gradual increase to the adult level. Presynaptic alpha 2-adrenoceptors which regulate NA release seems to become sensitive to alpha 2-agonists and to reach functional maturity between days 1 and 7 after birth in the cerebral cortex of rats.

Ontogenetic development of high potassium- and acetylcholine-induced release of dopamine from striatal slices of the rat.

The high K+- and acetylcholine (ACh)-induced release of [3H]dopamine (DA) were investigated in whole brain slices of fetuses and striatal slices of postnatal rats. A high K+-induced, Ca2+-dependent release of [3H]DA was demonstrated in brain on day 18 of gestation and the amount of release from the striatum increased during postnatal development. ACh induced [3H]DA release in striatal slices from 3-, 7- and 70-day-old rats but not from 1-day-old animals. ACh-induced [3H]DA release on both day 7 and day 70 was dependent on Ca2+ and significantly reduced by the addition of 5 x 10(-6) M atropine or 10(-5) M hexamethonium. It is suggested that DA is taken up into functionally releasable pools at a late fetal stage and that from around 3 days after birth, ACh may begin to regulate DA release by stimulating muscarinic and/or nicotinic receptors located on DA nerve terminals in the striatum.

High potassium-induced, calcium-dependent monoamine release from brain slices of the newborn rat.

To determine the functional significance of monoamines taken up into the newborn rat brain, a high K+-induced, Ca2+-dependent release of noradrenaline (NA), dopamine (DA) or serotonin (5-HT) from brain slices of the newborn rat was investigated and compared with that of the adult animal. Depolarization by increasing the potassium concentration in the medium induced the release of L-[3H]NA,[3H]DA or [3H]5-HT from brain slices prelabelled with the radioactive monoamines in the 2-day- or 3-day-old rat as well as in the adult. The release of three [3H]amines was markedly inhibited by perfusing with Ca2+- free medium in the presence of EGTA (2.0 mM) at both newborn and adult stages, although the inhibitory potency of Ca2+- deficiency in the newborn preparation was lower than in the adult. The degree of the release against [3H]amines initially taken up in the newborn was of the same order of magnitude as those in the adult. It is suggested that NA, DA and 5-HT are stored in a functionally releasable pool of the nerve terminals of the central monoamine neurons in the rat and that these compounds act as neurotransmitters at birth and at the adult stage.