GABA is the most widely distributed inhibitory transmitter in the brain, and it acts commonly by augmenting chloride permeability. When resting membrane potential (Vm) is equal to chloride equilibrium potential (EC1) GABA tends to keep Vm to its resting value. In some synapses, a pump carries chloride actively out of the cell and EC1 is different from Vm. An increased permeability leads to a hyperpolarization. In presynaptic inhibition a chloride pump brings chloride ions actively inside the cell and an increased permeability leads to a depolarization. GABAA receptors are associated with chloride channels, whereas GABAB receptors cause a selective decrease of a voltage sensitive calcium channels which operates at synaptic terminals.

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PubMedDate not supplied

Magnesium deficiency affects the pentylenetetrazol-induced convulsions in magnesium-deprived rats.

A group of 11 young albino rats was fed with a Mg2+ free diet. After a few days, the animals showed typical signs of Mg2+ deficiency, consisting in skin vasodilation, red conjunctiva and hair loss. Pentylenetetrazol (50 mg/kg i.p.) injected in these rats, 6 and 12 days after the beginning of the diet, elicited a more severe convulsive activity compared with that shown by a control group of 12 rats. These results suggest that a Mg2+ deficiency, though not necessarily responsible for the convulsive activity, may contribute to facilitate an epileptic episode or may lead to more severe convulsions. The possibility of a more powerful activation of the NMDA receptors in Mg2+ deficiency is discussed.

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PubMedDate not supplied

Reciprocal trophic interactions in the adult climbing fibre-Purkinje cell system.

This article reviews a series of experiments aimed at investigating the reciprocal trophic interactions which regulate the normal morphofunctional features and the plasticity of the adult rodent climbing fibre-Purkinje cell system. Climbing fibre deprivation induces profound functional and structural changes in the Purkinje cell. Among others, proximal Purkinje cells dendrites become studded with numerous newly formed spines some of which are innervated by parallel fibres. These structural modifications are reversed if the Purkinje cell is reinnervated by another climbing fibre. These results indicate that the olivocerebellar input inhibits spinogenesis on proximal Purkinje cell dendrites and prevents other afferents from invading its own target domain. It is proposed that the normal distribution of synapses on the Purkinje cell dendritic tree is controlled by the interplay between climbing and parallel fibre influences on Purkinje cell dendrites. Following Purkinje cell death, the distal climbing fibre branches are withdrawn. This atrophy progresses according to the time and mode of Purkinje cell degeneration and it is reversed if the climbing fibre is provided with a new target Purkinje cell. In addition, sprouting from intact climbing fibres and collateral reinnervation of Purkinje cells can be obtained by both subtotal inferior olive lesions and transplantation of embryonic cerebellar tissue on the surface of the adult cerebellum. These results indicate that specific signals produced by non-innervated Purkinje cells are responsible for inducing and guiding climbing fibre sprouting. By contrast, contact cues would be necessary for the formation and the maintenance of terminal arbour branches and synapses. It is suggested that these interactions which control the structural plasticity following lesion or transplantation also operate during the fine structural remodelling underlying the functional plasticity in the intact cerebellar cortex.

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