Short-term and complete reversal of NGF effects in rats with lesions of the nucleus basalis magnocellularis

Nerve Growth Factor (NGF) Augments Cortical and Hippocampal Cholinergic Functioning after p75NGF Receptor-Mediated Deafferentation But Impairs Inhibitory Avoidance and Induces Fear-Related Behaviors

“…There was a significant NGF effect across all regions and in each region separately in PBS/ NGF animals, ranging from 24% increase of ChAT activity in the parietal cortex to 57% increase in the frontal cortex (Table 1). These data confirm previous findings that the CBF is not saturated by endogenous NGF levels, because cholinergic markers in unlesioned animals can be f urther elevated by additional trophic factor supplementation (Fusco et al, 1989;Winkler and Thal, 1995;Winkler et al, 1998). The low-192Sap/ NGF group was significantly different from the corresponding low-192Sap/C ytC in the group-by-all-regions analysis ( p Յ 0.05; Table 1).…”

“…Confirming previous findings (Williams, 1991;Winkler and Thal, 1995;Winkler et al, 1998), treatment with NGF significantly affected both the average body weight (F (5,38) ϭ 14.89; p Ͻ 0.0001) and the course of weight gain between groups (time-bygroup interaction, F (20,152) ϭ 15.06; p Ͻ 0.0001). However, hypophagia is observed after intracerebroventricular administration of various growth factors such as brain-derived neurotrophic factor, fibroblast growth factor, and ciliary neurotrophic factor (Lapchak and Hefti, 1992;Henderson et al, 1994;Emmett et al, 1995), indicating a rather nonspecific effect of growth factors on structures that abut the ventricular system.…”

“…After a 10 min centrif ugation (12,000 ϫ g, 4°C), clear supernatants were removed and stored at Ϫ80°C for later analysis of monoamines and their metabolite content. An aliquot (40 l) of the clear perchloric acid extract was analyzed for the presence of epinephrine (EPI), norepinephrine (N E), dopamine (DA), serotonin (5-HT), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (H VA), 5-hydroxyindoleacetic acid (5-HIAA), 3-methoxy-4-hydroxyphenylglycol (M HPG), and 3-methoxytyramine (3-MT) by HPLC as previously described (Winkler et al, 1998). Four groups (PBS/C ytC, PBS/ NGF, high-192Sap/C ytC, and high-192Sap/ NGF) were chosen for assay based on the large magnitude of ChAT changes of these groups.…”

“…Sections were stained with cresyl violet. Every sixth section of the forebrain was immunostained for p75NGFr (Winkler et al, 1998). Briefly, endogenous peroxidase enzyme activity was blocked with 0.6% H 2 O 2 for 30 min, after which sections were rinsed with 1% horse serum and 0.25% Triton X-100 in 0.1 M Tris-buffered saline, pH 7.4.…”

Alcohol‐Induced Brain Pathology and Behavioral Dysfunction: Using an Animal Model To Examine Sex Differences

“…Cell counts for ChAT were taken at a magnification of ϫ 200 in the medial septal nucleus [see Winkler and Thal (1995); Winkler et al (1998)]. ChAT cells were counted bilaterally by using multiple nonoverlapping fields in the medial septal nucleus; i.e., the area in which cell counts were taken was a triangular region (1.5 ϫ 1.5 ϫ 1.5 mm) that encompassed the medial septal nucleus (Fig.…”