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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.

Quantitative analysis of the period-3 catastrophe is developed for the standard map and for the stochastic heating map as illustrative examples of two-dimensional area preserving mappings. Analytic expression of the diffusion coefficient is derived for the stochastic heating, and compared to results of numerical observation. Here, as for the case of the standard map, the multi-periodic accelerator modes give rise to anomalous enhancement of the diffusion rate. Stochasticity in the low dimensional Hamiltonian systems has been one of the central problems not only in the field of fundamental physics, 1 ' but also under the light of practical interests of plasma confinement in the magnetic fusion devices,2''3' of plasma heating by the radio-frequency wave4' and of the long time behaviour of particle beam in high energy accelerators. 5 ''6 ' Two-dimensional area-preserving mappings have been widely employed as a useful model of the nonlinear Hamiltonian systems. In a recent paper by Lichtenberg and Lieberman/' calling one's attention to the fact that these model mappings can be smoothly transformed into dissipative mappings by variation of a parameter, they examined chaotic behaviour of both of the nonlinear conservative and dissipative systems. In order to explore statistical prop­ erties of the low dimensional Hamiltonian systems, we have been investigating various properties of the two-dimensional area-preserving maps in a series of papers.8>-Hl Here, extending our analysis on the standard map, we want to discuss the period3 catastrophe and enhanced diffusion in two-dimensional Hamiltonian systems. Summarizing our previous results obtained for the standard map, we discuss mechanism of the period-3 catastrophe in detail in the next section. In order to illustrate the generic aspect of our analysis, we examine the stochastic heating of ions by the lower hybrid wave along the line of Karney's investigation4 ' in§§ 3 and 4. We present concluding discussion in the last section.

The effects of subchronic administration of Rokujo (Cervus nippon TEMMINCK var. mantchuricus Swinhoe) extract on protein, ribonucleic acid (RNA) and deoxyribonucleic acid (DNA) syntheses in vivo were investigated in male senescence-accelerated mice (SAM). At 20 min after intraperioneal injection of amino acid and nucleosides labeled with radioisotpes, the incorporation of [14C]leucine into the serum protein was increased in the Rokujo-treated mice, in a parallel manner to the elevation of the serum protein content. Increased incorporation of [14C]uridine into RNA as well as that of [14C]leucine into protein was found in the liver and kidney of the Rokujo-treated mice. Further experiments revealed that although a brief exposure to Rokujo extract in vitro did not directly affect the RNA polymerase activity, the activity of RNA polymerase II in solubilized liver nuclei of Rokujo-treated mice was markedly accelerated. These results suggest that enhancement of RNA polymerase II activity induced by long-term Rokujo treatment is responsible for the increase in protein synthesis in vivo in SAM.

Influence of piperidine and D, L-pipecolic acid, a hypnogenic amine and its possible precursor, on the uptake of L-[3H] noradrenaline (L-[3H] NA), [3H] dopamine ([3H] DA), [3H] 5-hydroxytryptamine ([3H] 5-HT), [14C] GABA and [14C] glycine into P2, fractions of the rat brain and the spinal cord was investigated. Neither piperidine nor D, L-pipecolic acid affected the uptake of L-[3H] NA, [3H] DA, [3H] 5-HT and [14C] glycine at a dose of 10-4M. On the other hand, D, L-pipecolic acid (10-4 M). significantly (p

The regional and developmental change in specific activity of 2', 3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) and carbonic anhydrase (CAase) and influence of the neonatal treatment with 6-hydroxydopa (6-OHDOPA) were investigated in the rat. CNPase activity rapidly increased between days 5 and 20, slightly between days 20 and 70. CAase activity gradually increased during postnatal development. The activities of both enzymes were higher in the brain stem and diencephalon than in the cerebral cortex and the cerebellum of the developing and adult animal. The systemic injection of 6-OHDOPA at birth induced a significant decrease in CNPase activity in the neocortex of the adult but in all regions of the 5-day-old rat. On the other hand, the treatment produced a significant increase in CAase activity in the neocortex and paleocarotex of the developing and adult rat. The neonatal treatment with 6-OHDOPA appears to impair normal growth of the brain by interfering the interaction between neurons and glial cells in the rat brain.

The inhibition of forskolin-stimulated adenylate cyclase activity by 5-hydroxytryptamine (5-HT) receptor agonists was measured in rat hippocampal membranes isolated from animals treated with vehicle or islet-activating protein (IAP; pertussis toxin). In vehicle-treated animals, 5-HT, 8-hydroxy-2-(di-n-propylamino)tetralin, buspirone, and gepirone were potent in inhibiting forskolin-stimulated adenylate cyclase activity with EC50 values of 60, 76, 376, and 530 nM, respectively. IAP treatment reduced by 30-55% the 5-HT1A agonist inhibition of adenylate cyclase activity via 5-HT1A receptors. The data indicate that the inhibitory guanine nucleotide-binding protein or Go (a similar GTP-binding protein of unknown function purified from brain) mediates the 5-HT1A agonist inhibition of hippocampal adenylate cyclase.

The influence of sulfhydryl reagents and cations on specific [ 3 H]GTP binding to striatal membranes was investigated in developing rats. Two components of non-cooperative [ 3 H]GTP binding sites were observed in 15, 30, 70 and 360 day old rats but only a single component in 1 and 7 day old ones. The K D for low affinity binding increased with age. B max values for both high and low affinity binding increased with age and reached a peak at 30 days, followed by a decrease at 70 and 360 days. At 7 and 70 days, NaCl 1–100 mM did not affect [ 3 H]GTP binding but CaCl 2 and MgCl 2 significantly inhibited the binding over a concentration range of 1–100 mM. TLC analysis of [ 3 H]GTP and the metabolites in the binding medium and membranes showed that [ 3 H]GTP in both membranes and in the medium was decreased by addition of 1 mM CaCl 2 into the binding medium. On days 7 and 70, p-chloromercuriphenyl sulfonate strongly inhibited [ 3 H]GTP binding, and dithiothreitol significantly increased binding but dopamine, apomorphine, spiperone and α-flupenthixol did not increase binding up to 0.1 mM. It is suggested that sulfhydryl residues, Ca 2+ and Mg 2+ are involved in the regulation of guanine nucleotide binding and that the regulatory mechanism becomes functional at 7 days. Ca 2+ and Mg 2+ seem to act by stimulating degradation of [ 3 H]GTP. In addition, the density of GTP binding sites reaches a peak at around 30 days and the affinity decreases with age.

The involvement of essential sulfhydryl groups in alpha 2-adrenoceptor function was investigated in the cerebral cortex of 7 and 70 day old rats. N-Ethylmaleimide (NEM) inhibited specific [3H]clonidine binding to cerebral cortical membranes in a concentration-dependent and biphasic manner in both infant and adult rats. The inhibitory effect of NEM was attenuated by simultaneous addition of dithiothreitol 30 microM and 1 mM, though dithiothreitol up to 1 mM did not affect the binding. p-Chloromercuriphenylsulfonic acid also caused a significant reduction in [3H]clonidine binding at both stages. Scatchard analysis of [3H]clonidine binding showed that NEM 10 and 100 microM caused a significant decrease in Bmax of high affinity binding sites without changing KD. Neither Bmax nor KD values were changed by NEM 10 and 100 microM in low affinity sites. The treatment with NEM 10 and 100 microM significantly reduced the increase of binding induced by Mn2+ 10 and 100 microM which was observed on day 70 but not on day 7. It is suggested that two distinct categories of essential sulfhydryl groups are involved in cerebral cortical alpha 2-adrenoceptors and are functionally mature by day 7. Furthermore, sulfhydryl groups are involved in the Mn2+-induced increase of alpha 2-receptors in adult rats.