Affiliations: Laboratory of Behavioral Neuroscience, Department of
Psychology, Davidson College, Davidson, North Carolina 28035, USA
Note: [] Corresponding author: Julio J. Ramirez, Ph.D., R. Stuart Dickson
Professor, Laboratory of Behavioral Neuroscience, Department of Psychology, P.
O. Box 7017, Davidson College, Davidson, North Carolina 28035-7017, USA. Tel.:
+1 704 894 2888; Fax: +1 704 894 2512; E-mail: juramirez@davidson.edu
Abstract: {\it Purpose:} Recent research on the purine derivative of
hypoxanthine Neotrofin™
(4-[[3-(1,6-dihydro-6-oxo-9-purin-9-yl)-1-oxopropyl]amino]benzoic acid;
AIT-082) has indicated that Neotrofin treatment elevates the mRNA levels of
various neurotrophic factors, including nerve growth factor (NGF), in the CNS.
Several previous studies have indicated that NGF may regulate septodentate
sprouting after entorhinal cortex lesions in rats. Thus, the objective of this
investigation was to determine whether Neotrofin treatment would enhance
lesion-induced septodentate sprouting from 4 to 15 days postlesion. {\it Methods:} Sham-operated rats or rats with EC lesions were
injected (i.p.) with either Neotrofin (30 mg/kg) or saline (0.9%) immediately
after surgery and every day thereafter until the end of the treatment regimen.
Septodentate sprouting, as indicated by intensity of acetylcholinesterase
(AChE) label in the dentate gyrus, was assessed with optical densitometry. {\it Results:} We observed that Neotrofin elevated the AChE-label in
the outer molecular layer of the ventral dentate gyrus at 4 days postlesion and
of the dorsal dentate gyrus at 15 days postlesion. {\it Conclusions:} Neotrofin appears to have exerted limited
stimulatory effects on lesion-induced sprouting by a cholinergic pathway.
