NERVE GROWTH-FACTOR AND THE NEOSTRIATUM

1. The present review summarizes evidence describing the expression, immunoreactivity, binding, transport, development, aging, and functions of NGF in the mammalian neostriatum. 2. Neostriatal NGF binding sites and intrinsic cholinergic neurons are co-localized, increase at a similar rate during ontogeny, and are lost to an equal extent following age- or injury-induced loss of neostriatal neurons. 3. Exogenously administered NGF augments ChAT activity in the intact caudate-putamen, nucleus accumbens, and following mechanical or excitotoxin-induced cholinergic injury. NGF antibodies lower ChAT in the intact caudate-putamen. 4. Neostriatal cholinergic interneurons are lost in the aged rat but also in Alzheimer's disease, Parkinson's disease, supranuclear palsy, and Huntington's chorea. Future studies need to address the extent to which these losses result from an abberation of NGF production, binding, or transport and whether rhNGF administration may retard or reverse these cholinergic losses.