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Molecular mechanisms: MeCP2 loss ups signal strength

A study using action potentials, the electrical impulses that trigger signaling, shows that neurons lacking MeCP2, the Rett syndrome protein, have stronger neuronal signals compared with controls, according to a study published in the July Journal of Neurophysiology.

By Michele Solis

3 August 2011 | 2 min read

This article is more than five years old.

Neuroscience—and science in general—is constantly evolving, so older articles may contain information or theories that have been reevaluated since their original publication date.

A study using action potentials, the electrical impulses that trigger neuronal signaling, shows that neurons lacking MeCP2, the Rett syndrome protein, have stronger neuronal signals compared with controls, according to a study published in the July Journal of Neurophysiology¹.

The new approach finds results contrary to those from studies that look at signaling in the absence of action potentials, which have found that neurons lacking MeCP2 have weaker-than-normal signals. This suggests that how signals are measured can affect the results of studies on autism-related mutations.

Existing models propose that autism stems from an imbalance between excitatory signals that boost activity in the brain and those that inhibit it. Loss of MeCP2 has been associated with lower excitatory signaling and elevated inhibition ²^,³.

However, the new study found that, in response to action potentials, cultured neurons lacking MeCP2 generate stronger excitatory signals compared with controls, a finding that is consistent with the seizures occurring in Rett syndrome.

Previous studies looked at synapses in the absence of electrical activity: Even without action potentials, neurons sometimes spontaneously release neurotransmitters. The ensuing signals, called ‘minis,’ can give a readout of synapse function.

This suggests that minis may not be good proxies for understanding how synapses respond to action potentials.