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The Journal of Neuroscience, July 12, 2006, 26(28):7321-7327; doi:10.1523/JNEUROSCI.4656-05.2006
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Development/Plasticity/Repair
Activity-Dependent Bidirectional Modification of Inhibitory Synaptic Transmission in Rat Subthalamic Neurons
Lie Wang,1 Stephen T. Kitai,2 andZixiu Xiang1 1Department of Neurosurgery, University of Tennessee, Health Science Center, Memphis, Tennessee 38163, and 2Methodist University Hospital, Memphis, Tennessee 38104
Correspondence should be addressed to Zixiu Xiang, Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232. Email: zixiu_xiang{at}yahoo.com
Rebound burst activity can be generated in neurons in the subthalamic nucleus (STN) by strong GABAergic inhibitory inputs from the globus pallidus externa (GPe) that is reciprocally connected with the STN. It has been proposed that the rebound burst activity in STN neurons is a key event for generating synchronized rhythmic burst activity in the GPe–STN loop, which may be relevant to the resting tremor in Parkinson’s disease. Here we report that rebound burst firing of STN neurons induces long-lasting bidirectional modifications of GABAergic synaptic transmission in STN neurons themselves. Using the gramicidin perforated-patch clamp technique in the brain slice preparation, we recorded IPSPs from STN neurons during electrical stimulation of the internal capsule. Rebound spikes triggered by hyperpolarizing current pulses were used to induce modification of inhibitory synaptic transmission. We found that long-lasting potentiation of IPSPs could be induced in the neurons exhibiting three or more rebound spikes that had interspike intervals shorter than half of those during base spontaneous activity, whereas long-lasting depression or no change of IPSP amplitude was likely to be observed in neurons that had no rebound burst or two rebound spikes within a burst. The potentiation or depression of IPSPs was associated with a negative or positive shift of reversal potential of IPSPs (EIPSP). The modifications of IPSPs were dependent on activation of postsynaptic voltage-gated calcium channels. This study is the first demonstration that activity-dependent bidirectional modifications of inhibitory synaptic transmission are attributable to bidirectional shifts of EIPSP.
Key words: inhibitory synapses; plasticity; Cl– reversal potential; Parkinson’s disease; subthalamic nucleus; calcium channels
Received Oct. 31, 2005; revised April 28, 2006; accepted May 1, 2006.
Correspondence should be addressed to Zixiu Xiang, Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232. Email: zixiu_xiang{at}yahoo.com
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