Muscarinic receptor binding and oxidative enzyme activities in the adult rat superior cervical ganglion: effects of 6-hydroxydopamine and nerve growth factor

Abstract

Administration of 6-hydroxydopamine to adult rats results in changes in the superior cervical ganglion similar to those noted after axotomy; namely, a decrease in muscarinic receptor binding and increases in activities of the oxidative enzymes of the pentose phosphate pathway. These changes were either prevented or attenuated markedly by the systemic administration of nerve growth factor. Administration of nerve growth factor alone did not significantly increase N-methylscopolamine binding in the ganglion or reduce the activities of the oxidative enzymes. Explants of the ganglion maintained in serum-free medium over a period of 3 days demonstrated increases in oxidative enzyme activity and a decrease in N-methylscopolamine binding. Addition of 20 nM nerve growth factor to the culture medium prevented the decline in N-methylscopolamine binding in ganglion explants. The increases in oxidative enzyme activities were unaltered. Addition of high amounts of nerve growth factor, 200 nM, resulted in a significant increase in tyrosine hydroxylase activity but no further increase in N-methylscopolamine binding in ganglion explants. Glucocorticoids added to the culture medium did not affect the muscarinic binding or enzyme activities. Thus, decreases in muscarinic binding activity which occur in the superior cervical ganglion after axotomy or 6-hydroxydopamine treatment may be explained by a loss of nerve growth factor supplied to the ganglion. Increases in the oxidative enzymes of the pentose phosphate pathway that occur in the ganglion after axonal injury appear to involve additional factors.

Non-neuronal cell-conditioned medium regulates muscarinic receptor expression in cultured sympathetic neurons

“…5). Finally, glucocorticoid treatment did not alter muscarinic binding in SCG explants, suggesting that the hormone is not involved in regulating muscarinic receptor development in sympathetic neurons (Dombrowski et al, 1983).…”

“…By contrast, postganglionic axotomy diminished muscarinic receptor binding (Sinicropi et al, 1979), suggesting that target-related factors may be important in regulating receptor number. NGF treatment of ganglion explants prevented a decrease in the muscarinic binding found in control cultures, which suggests that NGF could mediate some of the target-related effects on receptor number (Dombrowski et al, 1983). NGF treatment of PC1 2 pheochromocytoma cells increased muscarinic receptor binding (Jumblatt and Tischler, 1982).…”

Attenuated behavioural responses to acute and chronic cocaine in GASP‐1‐deficient mice

“…Muscarinic (M‐like) receptor binding sites were measured using the non‐selective ligand [ 3 H]‐ N ‐methylscopolamine ([ 3 H]‐NMS, 78 Ci/mmol; PerkinElmer, Boston, MA, USA) according to Dombrowski et al. (1983), with minor modifications.…”

Modifications in muscarinic, dopaminergic and serotonergic receptors concentrations in the hippocampus and striatum of epileptic rats

“…Receptor density values were measured by binding assays with 10% homogenates prepared (w\v) in 150 mM sodium phosphate buffer, pH 7.4, using [ 3 H]-NMS as the ligand (Dombrowski et al, 1983). This non-selective ligand binding to all subtypes of muscarinic receptors was carried out.…”