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Generalized seizures induced a widespread upregulation of adenosine A1 receptors linked to G proteins in the rat brain. Changes in receptor density were more pronounced in structures mediating seizure activity and were age-dependent.

During the past years the number of biological roles proposed for adenosine and for precursor adenine nucleotides in the central nervous system has increased considerably. In addition to its role in intermediary metabolism, adenosine displays a number of receptor-mediated physiological actions which include dilatation of cerebral vesseis (Winn et al. 1981a). Adenosine also acts as a neuromodulator or neurotransmitter, inhibiting neuronal firing (Phillis et al. 1979) and synaptic transmission (Kuroda et al. 1978) as well as altering cyclic AMP concentrations in brain tissues (Sattin and Rail 1970; Daiy, 1977). In addition the relatively selective ability of methylxanthines such as caffeine and theophylline to block effects of adenosine on neuronal firing and cvciic AMP formation. suggest that pharmacological actions of these widely used substances may be mediated by blockade of central adenosine receptors (Snyder et al. 1981). Such receptors have been visualized by autoradiography on axon terminals of excitatory neurons (Goodman et al. 1983). Thus adenosine properties are those of local hormone which is released from the nerve cells. Indeed, a release of adenosine derivatives that Is accelerated by electrical stimulation has been observed from Isolated brain tissue (Pull and Mcilwain 1972a).