Abstract
Abstract Neonatal rats received intraventricular injections of mouse submandibular gland nerve growth factor (NGF) on days 1, 3, 5 and 7 postpartum. After killing the animals at day 8, activities of choline acetyltransferase (ChAT), acetylcholine esterase (AChE) and tyrosine hydroxylase (TH) were measured in different brain areas. NGF treatment increased ChAT activity in the septal area by 78%, in the hippocampus by 30%, and in the cortex by 73% relative to control animals. No increase was observed in other brain areas. The elevation of ChAT activity was not accompanied by an increased activity of AChE, and the concomitant 30–40% increase of TH activity observed in the cortex and brainstem was abolished after immunosympathectomy, reflecting the ingrowth of peripheral sympathetic peripheral fibers into the central nervous system (CNS) in response to centrally administered NGF23. In adult rats, repeated injections of NGF over 4 weeks caused a small but statistically significant increase of ChAT activity (15%) in the forebrain. In contrast, repeated intraventricular or intracortical injections into neonatal rats of large amounts of purified antibodies against mouse NGF (anit-NGF) failed to reduce ChAT activity in the same forebrain areas. Moreover, the offspring of rats autoimmunized against mouse NGF showed no reduction of ChAT activity in the brain, even though the TH activity was reduced by 76% in the superior cervical ganglia (SCG) of these animals. Antibodies against mouse NGF were also without effect on ChAT activity in cultures of dissociated septal neurons, though these cells also responded to NGF with an increase in ChAT activity. Anti-NGF blocked the effect of exogenous NGF but failed to reduce basal ChAT activity in these cultures. It is concluded that exogenous NGF can affect forebrain cholinergic neurons during their development. NGF does not seem to be identical with an endogenous neurotrophic factor produced by hippocampus or neocortex acting on cholinergic neurons of the forebrain.
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