The bioelectrical properties of Purkinje cells were analysed in sagittal slices of adult rat cerebellum by the use of intracellular recordings performed at a somatic level in current or in voltage clamp. The passive electrical constants of Purkinje cells were determined by measuring the time course and the amplitude of the voltage responses induced by hyperpolarizing current pulses. The mean value of input resistance was 21 +/- 1 M omega. Mean values of the membrane time constant and of the total electrotonic length of Purkinje cells were 19.5 +/- 1.7 ms and 0.59 +/- 0.01 ms respectively. A time dependent inward rectification was present in all cells. In current-clamp experiments it appeared as a sag in hyperpolarizing voltage responses which were followed by well developed anodal breaks. In voltage-clamped cells, the inward relaxation induced by hyperpolarizing commands fitted to a single exponential. It was already present near resting potential and could reach an amplitude of up to 4 nA for jumps near to -120 mV. This relaxation was provisionally termed Ih. Tail current relaxations also fitted to a single exponential when they were recorded in the presence of tetrodotoxin (TTX) and of Co. The inward relaxation induced by hyperpolarizing commands was readily blocked by Cs, whereas it was unaffected when Ba replaced Ca in the bath, except near rest where it was strongly reduced. The Ca channel blockers Cd, Co and D600 also markedly depressed or even suppressed the inward rectification near resting potential, and up to about -85 mV, whereas this blocking effect was much less apparent or even absent at more negative potentials. Ih was clearly enhanced when the external K concentration was raised up to 20 mM. In the presence of TTX and Co in the bath, inward relaxations induced by hyperpolarizing jumps were unaffected in Na-free solution, whereas the amplitude of tail currents was reduced. Furthermore, the reversal potential of Ih which ranged between -45 and -56 mV in the Co plus TTX containing solution, shifted toward more negative values in the Na-free medium. In contrast, Ih remained unchanged in low Cl solution. From these experiments, it is likely that K and Na are the main charge carriers of Ih. Furthermore, this current seems to be contaminated near resting potential by a Ca-dependent K current. Anodal breaks following hyperpolarizing commands were slightly attenuated when Cd or TTX were added to the bath.(ABSTRACT TRUNCATED AT 400 WORDS)

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Maternal deprivation can trigger long-lasting molecular and cellular modifications in brain functions and might facilitate the appearance of pathogenic behaviors. This study focuses on the vulnerability to develop morphine dependence in adult rats that were separated from their mother and littermates for 3 h per day for 14 d after birth and examines the adaptive changes in the enkephalinergic pathways. Place-preference conditioning was observed with 2 mg/kg morphine in deprived rats, whereas 5 mg/kg morphine was necessary to induce conditioning in nondeprived animals. A prolonged morphine conditioning was shown in deprived rats. A strong increase in oral morphine self-administration behavior and preference was observed in deprived rats. Only a very slight increase in preference for sucrose solution, a more ethological reinforcer known to interact with the opioid system, was shown in deprived rats. These results indicate that this postnatal environment change leads to a hypersensitivity to the reinforcing properties of morphine and to the development of morphine dependence. A significant decrease in preproenkephalin mRNA expression was observed in the nucleus accumbens and the caudate-putamen nucleus of deprived rats. The basal extracellular levels of the Met-enkephalin-like immunoreactivity in the nucleus accumbens were significantly lower in deprived rats when compared with nondeprived animals, whereas no change in -opioid receptor binding occurred. These results strongly support that maternal deprivation leads to a basal hypoactivity of the enkephalinergic system and hypersensitivity to morphine effects.Together, our results suggest that maternal deprivation in pups likely represents a risk factor for morphine dependence in adult rats.

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