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The Journal of Neuroscience, June 14, 2006, 26(24):6618-6626; doi:10.1523/JNEUROSCI.5498-05.2006

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Cellular/Molecular
Physiological Activity Depresses Synaptic Function through an Effect on Vesicle Priming

Krista L. Moulder,¹ Xiaoping Jiang,¹ Amanda A. Taylor,¹ John W. Olney,¹ and Steven Mennerick^1,2

Departments of ¹Psychiatry and ²Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110

Correspondence should be addressed to Dr. Steven Mennerick, Department of Psychiatry, Washington University School of Medicine, 660 South Euclid Avenue, Box 8134, St. Louis, MO 63110. Email: menneris{at}psychiatry.wustl.edu

Neurons engage compensatory, homeostatic synaptic changes to maintain their overall firing rate. We examined the induction and expression of a persistent presynaptic adaptation. We explored the effect of mild extracellular potassium elevation to increase hippocampal pyramidal neuron spiking over a physiological range. With several days of mild depolarization, glutamate release adapted, as revealed by an increased mismatch between the number of active, FM1-43-positive, glutamatergic synapses and the total number of synapses defined by vesicular glutamate transporter-1 antibody staining. Surprisingly, the adaptation of glutamate terminals was all-or-none; recycling vesicle pool size at remaining active synapses was not significantly altered by the adaptation. Tetrodotoxin (TTX), but not postsynaptic receptor blockade, reversed depolarization-induced adaptation, and TTX added to normal incubation medium increased the number of active synapses, suggesting that normal spiking activity sustains a steady-state percentage of inactive terminals. Chronic mild depolarization depressed EPSCs and decreased the size of the readily releasable pool of vesicles (RRP). Several hours of 10 Hz electrical stimulation also depressed the RRP size, confirming that spiking alone induces adaptation and that strong stimulation induces more rapid presynaptic adaptation. Despite the importance of RRP alteration to the adaptation, ultrastructural experiments revealed no changes in docked or total synaptic vesicle numbers. Furthermore, -latrotoxin induced vesicle release at adapted synapses, consistent with the idea that adaptation resulted from changes in vesicle priming. These results show that glutamatergic neurotransmission persistently adapts to changes in electrical activity over a wide physiological range.

Key words: homeostasis; synapse; EPSC; glutamate; presynaptic; action potential

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Received Dec. 22, 2005; revised May 9, 2006; accepted May 10, 2006.

Correspondence should be addressed to Dr. Steven Mennerick, Department of Psychiatry, Washington University School of Medicine, 660 South Euclid Avenue, Box 8134, St. Louis, MO 63110. Email: menneris{at}psychiatry.wustl.edu

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Nonglobal Homeostatic Synaptic Plasticity?

Jonathan Ting, Alexandra P. Few, and Kenneth Custer
J. Neurosci. 2006 26: 10937-10938. [Full Text]  

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