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An Electrochemiluminescence-Based Assay for MeCP2 Protein Variants

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Exogenous brain-derived neurotrophic factor rescues synaptic dysfunction in Mecp2-null mice.

David D Kline¹, Michael Ogier, Diana L Kunze

¹Department of Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|April 16, 2010

Summary

Postnatal brain-derived neurotrophic factor (BDNF) deficits in Rett syndrome (RTT) alter synaptic function in the brainstem. Restoring BDNF signaling in the nucleus tractus solitarius may help normalize cardiorespiratory control in RTT.

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Area of Science:

Neuroscience
Genetics
Developmental Biology

Background:

Rett syndrome (RTT) is a neurodevelopmental disorder linked to methyl-CpG-binding protein 2 (MeCP2) gene mutations.
Postnatal deficits in brain-derived neurotrophic factor (BDNF) are implicated in RTT pathogenesis, particularly affecting autonomic and respiratory control.
The precise impact of BDNF deficits on neuronal function and RTT endophenotypes remains unclear.

Purpose of the Study:

To investigate the effects of reduced BDNF on synaptic function in the nucleus tractus solitarius (nTS) of Mecp2-null mice, a model for RTT.
To explore the link between altered synaptic function in nTS and cardiorespiratory instability observed in RTT.

Main Methods:

Analysis of synaptic function, including excitatory postsynaptic currents (EPSCs), in nTS neurons of Mecp2-null and wild-type mice.
Assessment of neuronal excitability and response to primary afferent stimulation.
Investigation of the role of BDNF in rescuing observed synaptic alterations.

Main Results:

Mecp2-null mice exhibited significantly increased spontaneous miniature and evoked EPSC amplitudes in nTS neurons.
Mutant neurons showed enhanced action potential firing in response to afferent stimulation without increased intrinsic excitability.
These synaptopathic changes correlated with decreased BDNF availability and were rescued by exogenous BDNF application.

Conclusions:

Altered sensory gating in the nTS, driven by BDNF deficits, likely contributes to cardiorespiratory instability in RTT.
The nTS represents a potential therapeutic target for restoring homeostatic controls in RTT through BDNF signaling modulation.