Abstract

The quantal hypothesis for the release of neurotransmitters at the chemical synapse has gained wide acceptance since it was first worked out at the motor endplate in frog skeletal muscle in the 1950’s. Considering the morphological identification of synaptic vesicles (SVs) at the nerve terminals that appeared to be homogeneous in size, the hypothesis proposed that signal transduction at synapses is mediated by the release of neurotransmitters packed in SVs that are individually uniform in size; the amount of transmitter in a synaptic vesicle is called a quantum. Although quantal size—the amplitude of the postsynaptic response elicited by the release of neurotransmitters from a single vesicle—clearly depends on the number and sensitivity of the postsynaptic receptors, accumulating evidence has also indicated that the amount of neurotransmitters stored in SVs can be altered by various presynaptic factors. Here, I provide an overview of the concepts and underlying presynaptic molecular underpinnings that may regulate quantal size.

Highlights

  • Synaptic transmission requires the release of neurotransmitters from presynaptic terminals

  • Emerging evidence has suggested that quantal response, which is a postsynaptic current elicited by the fusion of a single vesicle, in the mammalian central nervous system (CNS) exhibits a certain degree of variation

  • Expression of VGLUT1, VGLUT2, and vesicular GABA/glycine transporter (VGAT) in cultured hippocampal neurons is altered by manipulations that change neural activities, i.e., exposure to tetrodotoxin and antagonists for the respective neurotransmitter receptors (De Gois et al, 2005)

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Summary

Shigeo Takamori*

Laboratory of Neural Membrane Biology, Graduate School of Brain Science, Doshisha University, Kyoto, Japan. The quantal hypothesis for the release of neurotransmitters at the chemical synapse has gained wide acceptance since it was first worked out at the motor endplate in frog skeletal muscle in the 1950’s. Considering the morphological identification of synaptic vesicles (SVs) at the nerve terminals that appeared to be homogeneous in size, the hypothesis proposed that signal transduction at synapses is mediated by the release of neurotransmitters packed in SVs that are individually uniform in size; the amount of transmitter in a synaptic vesicle is called a quantum. I provide an overview of the concepts and underlying presynaptic molecular underpinnings that may regulate quantal size.

INTRODUCTION
MINIMAL MOLECULAR COMPLEXES FOR THE FORMATION OF QUANTUM IN SVs
EXPRESSION LEVEL OF THE TRANSPORTERS
Mouse hippocampal culture
REGULATION OF THE PROTON ELECTROCHEMICAL GRADIENT
Luminal Buffers
VESICULAR SYNERGY
ALLOSTERIC REGULATION OF THE TRANSPORTER ACTIVITY
Neurotransmitter Concentrations
Trimeric G Proteins
Other Factors
CONCLUDING REMARKS

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