THIS ARTICLE HAS BEEN RETRACTED: Functional nerve growth factor and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and withdrawal

Abstract

The hypothesis tested is that cortical neurotrophins communicate through an inducible autocrine/paracrine mechanism. As ethanol (Et) can induce cortical nerve growth factor (NGF) expression, adult rats were challenged with Et on three consecutive days per week for 6 weeks. The focus of the study was layer V, the chief repository of receptor-expressing neuronal cell bodies. Brains were collected immediately after the sixth Et exposure or 72 h later [i.e., following withdrawal (WD)]. Double-label in situ hybridization-immunohistochemistry studies showed that many neuronal somata coexpressed NGF mRNA with NGF, trkA, or phosphorylated trk (p-trk), essential components of an inducible autocrine system. The frequencies of co-labeling were affected by neither Et nor WD. On the contrary, Et increased the number of NGF mRNAexpressing neurons and the amount of NGF mRNA expressed per cell. Et also increased total cortical concentration of NGF protein, the number of layer V neurons expressing trkA transcript, the amount of trkA mRNA expressed per neuron, and trkA phosphorylation. Following WD, the frequency of NGFmRNA-expressing cells increased, although transcript and protein content fell. WD induced an increase in trkA mRNA and protein expression, however, p-trk expression was unaffected. Thus, Et treatment reveals that layer V has inducible autocrine/ paracrine and anterograde neurotrophin systems. WD unveils the dynamism and recruitability of these systems.

Role of NGF in Neuronal Plasticity in the Lateral Reticular Nucleus in Chronic Inflammatory Pain

“…Therefore, we hypothesize that NGF synthesis is increased in the LRt, captured and retrogradely transported by spinoreticular neurons to their cell bodies in the deep layers of the spinal cord in this model of sustained inflammatory pain. As previously described in cortical neurons [39,40], increased NGF content could enhance TrkA synthesis and might explain the increased TrkA-IR described in our previous article [16].…”

BMP9 (Bone Morphogenetic Protein 9) Induces NGF as an Autocrine/Paracrine Cholinergic Trophic Factor in Developing Basal Forebrain Neurons

“…The possibility of a NGF/TrkA mediated autocrine system was previously suggested by studies on the cell bodies of layer V pyramidal neurons of the adult rat cortex where dual fluorescent in situ hybrization and immunolabeling of histological sections revealed co-expression of Ngf mRNA and phospho-TrkA protein (Bruns and Miller, 2007). During adulthood, NGF supplied to the basal forebrain via retrograde transport from the target regions is a major source of the growth factor (Sofroniew et al, 2001).…”

Nerve Growth Factor Involves Mutual Interaction between Neurons and Satellite Glial Cells in the Rat Trigeminal Ganglion

“…The frozen sections were hybridized with digoxigenin-labeled antisense riboprobes corresponding to partial cDNA of NGF. Plasmid DNA was a gift from Dr. Michael W. Miller (State University of New York-Upstate Medical University) [3] (Table 1). Using T7 or SP6 RNA polymerase (Invitrogen, Carlsbad, CA, USA), antisense and sense riboprobes were transcribed in vitro in the presence of DIG-labeled nucleotides (Roche Applied Science, Indianapolis, IN, USA).…”