抄録
The classical theory of neurotransmission is that a neurotransmitter is released from the nerve terminal to convey either excitatory or inhibitory signal in the postsynaptic target through anatomically defined synaptic connections. During the last decade, however, it has been becoming clear that neurotransmitters diffuse out of the synaptic cleft and act on adjacent synapses to change the strength of neurotransmission within common neural pathways. Such heterosynaptic interactions underlie diverse brain functions. Our studies have provided examples of such interactions among different synaptic inputs in the cerebellar cortex, which include: (1) the excitatory neurotransmitter released from climbing fibers produces not only direct excitation of Purkinje cells but also presynaptic inhibition of GABAergic transmission to the same PC through activation of AMPA-type glutamate receptors localized on cerebellar interneuron terminals; (2) the inhibitory neurotransmitter GABA released by cerebellar interneurons acts on adjacent parallel fiber synapses to enhance slow synaptic excitation via cross-talk between perisynaptic GABAB and metabotropic glutamate receptors; and (3) GABAergic synapses are also controlled by monoamine-induced presynaptic and ATP-mediated postsynaptic modulation with short- and long-lasting time-courses. Detailed mechanisms underlying reciprocal interactions between excitatory and inhibitory inputs would provide not only basic knowledge to better understanding of the brain function but also clues to therapeutic targets for psycho-neurological disorders. [J Physiol Sci. 2008;58 Suppl:S16]
