Induction of STAT3 signaling in activated astrocytes and sprouting septal neurons following entorhinal cortex lesion in adult rats

Entorhinal cortex lesion (ECL) leads to the activation of astrocytes and reactive axonal sprouting in the denervated fascia dentata. Previous studies indicated that CNTF or related cytokines are involved in the regulation of these processes. Therefore, we studied (1) whether the cytokine-associated STAT3 signaling pathway is activated in response to ECL and (2) which CNTF/cytokine receptor components are available for signal transduction. Lesion-induced STAT3 phosphorylation was found in reactive astrocytes of the fascia dentata. Intriguingly, rapid and transient activation of STAT3 signaling was also observed in sprouting neurons of the medial septum. Messenger RNAs for the three components of the CNTF/cytokine receptor complex were expressed and differentially regulated following ECL both in septal neurons and in reactive astrocytes of the fascia dentata. These data indicate that CNTF or related gp130-associated cytokines play a dual role after brain lesion: (1) regulation of astrocytic responses to deafferentation and (2) regulation or modulation of axonal sprouting.