Conclusions

While the case for the presynaptic nicotinic modulation of transmitter release is very strong, knowledge of the subtypes of nAChR involved is currently limited (see Figure 2.2). There is a good case for involvement of the 02 subunit in nAChRs that facilitates the release of dopamine from striatal nerve terminals. Evidence (reviewed earlier) comes from the pharmacological analysis of nicotinic agonist-evoked dopamine release, studies in knock-out mice, lesions coupled with radioligand autoradiography, and immunocytochemistry. The pharmacological evidence supports at least two subtypes of 02-containing nAChR: a402* and a3/a602*. There is also compelling evidence (mainly from pharmacological analysis coupled with electrophysiological methods) for an association of the a7 subunit with glutamate terminals. The particular properties of a7 nAChR may favor this relationship, enabling nicotinic stimulation to participate in a presynaptic component of LTP-like phenomena. Other subtypes of nAChR are likely to promote the release of other neurotransmitters in various brain regions. There is much to learn before the significance of nAChR diversity with respect to their functional roles in modulating synaptic transmission can be fully appreciated.

acknowledgments

Work in the authors' laboratory is supported by grants from the Biological and Biotechnological Sciences Research Council and The Wellcome Trust. The localization of nAChR subunits by electron microscopy undertaken in our laboratory has been carried out in collaboration with Professor J. Paul Bolam, University of Oxford.

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