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J Neurophysiol (January 11, 2006). doi:10.1152/jn.01135.2005
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01135.2005v1
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Submitted on October 27, 2005
Accepted on January 4, 2006

BDNF silences GABA synapses onto hypothalamic neuroendocrine cells through a postsynaptic dynamin-mediated mechanism

Sarah A Hewitt1 and Jaideep S Bains2*

1 Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada
2 Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada; Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada

* To whom correspondence should be addressed. E-mail: jsbains{at}ucalgary.ca.

In the paraventricular nucleus of the hypothalamus (PVN), experimental stress paradigms which suppress GABA inputs to parvocellular neuroendocrine cells (PNCs) also increase the expression of brain derived neurotrophic factor (BDNF). In the adult CNS, BDNF regulates the efficacy of GABAergic transmission, but its contributions to functional changes at inhibitory synapses in the PVN have not been investigated. Analysis of quantal transmission revealed a decrease in the frequency of miniature inhibitory postsynaptic currents (mIPSCs) in response to BDNF with no accompanying changes in their amplitude. These effects were completely blocked by prior inclusion of the TrKB receptor antagonist, K252A in the patch pipette. Inclusion of a dynamin inhibitory peptide in the patch pipette also blocked the effects of BDNF, consistent with an all-or-none removal of clusters of postsynaptic GABAA receptors. Finally, to confirm a decrease in the availability of postsynaptic GABAA receptors, we tested the effects of BDNF on focal application of the GABAA agonist, muscimol. Postsynaptic responses to muscimol were reduced following BDNF. Collectively, these data indicate that BDNF re-models functional synaptic contacts putatively by reducing the surface expression of postsynaptic GABAA receptors.




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