Postnatal development of the acetylcholine system in different parts of the rat cerebellum.

The components of the cholinergic nervous system, i.e., choline acetyltransferase, acetylcholinesterase, sodium-dependent high-affinity choline uptake, acetylcholine, and the muscarinic acetylcholine receptors, in the developing archi- and paleocerebellum of the rat have been investigated by biochemical methods. A close correlation between the development of the different elements of the system has been demonstrated in the two areas. The cholinergic structure develops first in the archicerebellum, which displays high levels of choline acetyltransferase, acetylcholinesterase, acetylcholine, and sodium-dependent high-affinity choline uptake. The paleocerebellum receives a sparser cholinergic innervation during development. The differences in the values for these components in the cerebellum as a whole may reflect the development of cholinergic and noncholinergic neuronal structures. It is concluded that the development of the cholinergic system cannot be analyzed in the cerebellum as a whole; rather specific regions such as the archi-, paleo-, or neocerebellum must be examined.

The effect of 4-(1-naphthylvinyl)-pyridine on the acetylcholine system and on the number of synaptic vesicles in the central nervous system of the rat.

The in vivo effects of 4-(1-naphthylvinyl)-pyridine on the activities of choline acetyltransferase and acetylcholinesterase, the levels of acetylcholine and choline, the sodium-dependent high affinity choline uptake and the number of synaptic vesicles were investigated in the rat brain. Our results indicate that 4-(naphthylvinyl)-pyridine (200 mg/kg, i.p.) reduced the acetylcholine level by 60% (P < 0.001), and the sodium-dependent high-affinity choline uptake in the CNS of rat. The combination of in vivo 4-(1-naphthylvinyl)-pyridine with a 15-min swimming stress induced an 87% (P < 0.001) reduction of acetylcholine in brain. The number of synaptic vesicles was reduced. We suggest that in vivo 4-(1-naphthylvinyl)-pyridine does reduce the steady-state level of acetylcholine, but that the reduction is due to a general effect of the drug on the acetylcholine system and membranes, rather than to a specific inhibitory action on the choline acetyltransferase activity.

Histochemical and atomic absorption demonstration of trace metal mobilization in the central nervous system and liver of the rat.

Histochemical and atomic absorption spectrophotometric analysis of trace metal mobilization caused by the action of ethanol in the central nervous system (CNS) and liver of the rat is described. Histochemically it has been shown that in all neurons examined (motoneurons, pyramidal and Purkinje cells) the trace metals (mainly Zn2+ and Cu2+) are mobilized. Most of the stained materials disappear from the perikaryon of the Purkinje cells, while in both the motoneurons and the pyramidal cells the trace metals are displaced from the perikaryon into the axon and axon hillock. At the same time, some of the glia cells display a high metal content. Quantitative determination of the Zn2+ and Cu2+ by means of atomic absorption spectrophotometry reveals that after 2 hours ethanol treatment both the Zn2+ and the Cu2+ levels are decreased in the archicerebellar cortex, while after 4 hours the Zn2+ levels are increased in the cerebrum and the spinal cord. The present observations on the histochemical localization and the contents of zinc and copper in different parts of the CNS and liver reveal the important role of the effect of ethanol on the trace metal mobilization.