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J Neurophysiol (October 8, 2003). doi:10.1152/jn.00547.2003
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Submitted on June 6, 2003
Accepted on September 25, 2003

Factors underlying bursting behavior in a network of cultured hippocampal neurons exposed to zero magnesium

Patrick S. Mangan1* and Jaideep Kapur1

1 Neurology, University of Virginia, Charlottesville, VA, USA

* To whom correspondence should be addressed. E-mail: psm2b{at}virginia.edu.

Factors contributing to reduced magnesium-induced neuronal action potential bursting were investigated in primary hippocampal cell culture at high and low culture density. In nominally zero external magnesium medium, pyramidal neurons from high density cultures produced recurrent spontaneous action potential bursts superimposed on prolonged depolarizations. These bursts were partially attenuated by the NMDA receptor antagonist D-APV. Pharmacological analysis of miniature excitatory postsynaptic currents revealed two components: one sensitive to D-APV and another to the AMPA receptor antagonist DNQX. The components were kinetically distinct. Participation of NMDA receptors in reduced magnesium-induced synaptic events was supported by the localization of the NR1 subunit of the NMDA receptor with the presynaptic vesicular protein synaptophysin. Presynaptically, zero magnesium induced a significant increase in EPSC frequency likely attributable to increased neuronal hyperexcitability induced by reduced membrane surface charge screening. Mean quantal content was significantly increased in zero magnesium. Cells from low density cultures did not exhibit action potential bursting in zero magnesium but did show increased EPSC frequency. Low density neurons had less synaptophysin immunofluorescence, and fewer active synapses as determined by FM1-43 analysis. These results demonstrate that multiple factors are involved in network bursting. Increased probability of transmitter release presynaptically, enhanced NMDA receptor-mediated excitability postsynaptically, and extent of neuronal interconnectivity contribute to initiation and maintenance of elevated network excitability.




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