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Michael D. Miyamoto, Ph.D.

Research Interests:

My research focuses on how repetitive stimulation increases transmitter release from motor nerves during the post-stimulation period. This enhancement of synaptic transmission or “facilitation” (lasting several minutes) is a type of short-term plasticity that may shed light on phenomena such as learning and memory. Facilitation is believed to be due to the buildup of ionic calcium (required for exocytosis) in the nerve terminal that results from entry through membrane channels. The decay in facilitation is presumably due to sequestration and extrusion of the ionic calcium by various processes. The time course of decay can be separated into four distinct components, which suggests that at least four processes (organelles?) play a role in terminating facilitation. The experimental approach involves the use of electrophysiology to monitor quantized (vesicular) transmitter release at single synapses. Its primary advantage is to allow investigation of the dynamics of facilitation and its decay, in intact nerve terminals on a “real-time” basis (millisecond time scale). Statistical patterns of quantal transmitter release and a mathematical model of the release process are used to dissociate the effects of various physiologic and pharmacologic manipulations on the four components of decay. Conceivably, modification of the decay process by certain agents may be a way to selectively prolong facilitation, which may be helpful in treating disorders involving deficiencies in synaptic transmission.

This research is not currently funded.

Selected Publications:

Hubbard, J.I., Wilson, D.F., and Miyamoto, M.: Reduction of transmitter release by d-tubocurarine. Nature 223:531-533,1969

Miyamoto, M.D. and Volle, R.L.: Enhancement by carbachol of transmitter release from motor nerve terminals. Proc. Nat. Acad. Sci. (USA) 71:1489-1492, 1974.

Miyamoto, M.D. and Breckenridge, B. McL.: A cyclic adenosine monophosphate link in the catecholamine enhancement of transmitter release at the neuromuscular junction. J. Gen. Physiol. 63: 609-624, 1974.

Miyamoto, M.D.: Binomial analysis of quantal transmitter release at glycerol treated frog neuromuscular junctions. J. Physiol. (Lond.) 250:121-142, 1975.

Miyamoto, M.D.: The actions of cholinergic drugs on motor nerve terminals. Pharmacol. Rev. 29:211-247, 1977.

Miyamoto, M.D.: Probability of quantal transmitter release from nerve terminals: theoretical considerations in the determination of spatial variation. J. Theor. Biol. 123:289-304, 1986.

Cheng, H. and Miyamoto, M.D.: Effect of hypertonicity on augmentation and potentiation and on the corresponding quantal parameters of transmitter release. J. Neurophysiol. 81:1428-1431, 1999.

Brailoiu, E., Miyamoto, M.D., and Dun, N.J.: Nicotinic acid adenine dinucleotide phosphate enhances quantal neurosecretion at the frog neuromuscular junction: possible action on synaptic vesicles in the releasable pool. Mol. Pharmacol. 60:718-724, 2001.

Brailoiu, E., Miyamoto, M.D., and Dun, N.J.: Calmodulin increases transmitter release by mobilizing quanta at the frog motor nerve terminal. Br. J. Pharmacol. 137:719-727, 2002.

Miyamoto, M.D.: Agents Affecting Neuromuscular Transmission. Chapt. 28. In: Modern Pharmacology with Clinical Applications, Sixth Ed., C.R. Craig & R.E. Stitzel (eds.) Lippincott Williams Wilkins, pp. 338-347, 2004.

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