Characteristics of chick cerebral beta-adrenoceptors assessed by cyclic adenosine 3',5' monophosphate formation and [3H]-propranolol binding.
Chick cerebral beta-adrenoceptors have been characterised by measurement of cyclic AMP accumulation in brain slices and assessment of the specific binding of [3H]-propranolol to cerebral membranes. The binding of [3H]-propranolol was inhibited by beta-adrenoceptor agonists and antagonists with affinities that correlated well with their ability to stimulate cyclic AMP formation or to antagonise the cyclic nucleotide accumulation induced by isoprenaline. The relative potencies of a number of drugs in several cerebral regions suggests that the receptors may be of the beta2 subtype. Regional distribution studies revealed the highest density of binding sites in the cerebellum and lowest in the optic lobes. However, the concentration of [3H]-propranolol that produced half-maximal specific binding was similar in all regions. Subcellular fractionation of cerebral hemisphere tissue demonstrated an enrichment of [3H]-propranolol binding sites in the synaptosomal and microsomal fractions. There are discrepancies between the topographical distribution of beta-adrenoceptor binding sites and the endogenous noradrenaline level in chick brain and between the number of binding sites and the intrinsic activity of beta-adrenoceptor mediated cyclic AMP formation.
Characteristics of chick cerebral beta-adrenoceptors assessed by cyclic adenosine 3',5' monophosphate formation and [3H]-propranolol binding. Chick cerebral beta-adrenoceptors have been characterised by measurement of cyclic AMP accumulation in brain slices and assessment of the specific binding of [3H]-propranolol to cerebral membranes. The binding of [3H]-propranolol was inhibited by beta-adrenoceptor agonists and antagonists with affinities that correlated well with their ability to stimulate cyclic AMP formation or to antagonise the cyclic nucleotide accumulation induced by isoprenaline. The relative potencies of a number of drugs in several cerebral regions suggests that the receptors may be of the beta2 subtype. Regional distribution studies revealed the highest density of binding sites in the cerebellum and lowest in the optic lobes. However, the concentration of [3H]-propranolol that produced half-maximal specific binding was similar in all regions. Subcellular fractionation of cerebral hemisphere tissue demonstrated an enrichment of [3H]-propranolol binding sites in the synaptosomal and microsomal fractions. There are discrepancies between the topographical distribution of beta-adrenoceptor binding sites and the endogenous noradrenaline level in chick brain and between the number of binding sites and the intrinsic activity of beta-adrenoceptor mediated cyclic AMP formation.