Muscarinic receptor-activated signal transduction pathways involved in the neuritogenic effect of astrocytes in hippocampal neurons.

Astrocytes have been shown to release factors that affect various aspects of neuronal development. We have previously shown that the acetylcholine analog carbachol, by activating muscarinic M(3) receptors in rat astrocytes, increases their ability to promote neuritogenesis in hippocampal neurons. This effect was mediated by an increased expression and release by astrocytes of several permissive factors, a most relevant of which was fibronectin.

Ethanol inhibits neuritogenesis induced by astrocyte muscarinic receptors.

In utero alcohol exposure can lead to fetal alcohol spectrum disorders, characterized by cognitive and behavioral deficits. In vivo and in vitro studies have shown that ethanol alters neuronal development. We have recently shown that stimulation of M(3) muscarinic receptors in astrocytes increases the synthesis and release of fibronectin, laminin, and plasminogen activator inhibitor-1, causing neurite outgrowth in hippocampal neurons.

Ethanol inhibits muscarinic receptor-induced axonal growth in rat hippocampal neurons.

Background: In utero alcohol exposure can lead to fetal alcohol spectrum (FAS) disorders characterized by cognitive and behavioral deficits. In vivo and in vitro studies have shown that ethanol alters neuronal development. One mechanism through which ethanol has been shown to exert its effects is the perturbation of activated signaling cascades.

The activation of M1 muscarinic receptor signaling induces neuronal differentiation in pyramidal hippocampal neurons.

Muscarinic receptors have been proposed to play an important role during brain development by regulating cell survival, proliferation, and differentiation. This study investigated the effect of muscarinic receptor activation on prenatal rat hippocampal pyramidal neuron differentiation and the signal transduction pathways involved in this effect. The cholinergic agonist carbachol, after 24 h in vitro, increased the length of the axon, without affecting the length of minor neurites.