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NEUROSCIENCE |
7-containing nicotinic receptors on the vertebrate postsynaptic neurons1 Neurobiology Section, Division of Biological Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0357, USA
Nicotinic acetylcholine receptors (nAChRs) are expressed throughout the central nervous system and influence a variety of higher order functions including learning and memory. While the effects of presynaptic nAChRs on transmitter release have been well documented, little is known about possible postsynaptic actions. A major species of neuronal nAChRs contains the 
7 gene product and has a high relative permeability to calcium. Both on rodent hippocampal interneurons and on chick ciliary ganglion neurons these 7-nAChRs are often closely juxtaposed to GABAA receptors. We show here that in both cases activation of 7-nAChRs on the postsynaptic neuron acutely down-regulates GABA-induced currents. Nicotine application to dissociated ciliary ganglion neurons diminished subsequent GABAA receptor responses to GABA. The effect was blocked by 7-nAChR antagonists, by chelation of intracellular Ca2+ with BAPTA, and by inhibition of both Ca2+–calmodulin-dependent protein kinase II and mitogen-activated protein kinase. A similar outcome was obtained in the hippocampus where electrical stimulation to activate cholinergic fibres reduced the amplitude of subsequent GABAA receptor-mediated inhibitory postsynaptic currents. The reduction showed the same calcium and kinase dependence seen in ciliary ganglion neurons and was absent in hippocampal slices from 7-nAChR knockout mice. Moreover, 7-nAChR blockade in hippocampal slices reduced rundown of GABAA receptor-mediated whole-cell responses, indicating ongoing endogenous modulation. The results demonstrate regulation of GABAA receptors by 7-nAChRs on the postsynaptic neuron and identify a new mechanism by which nicotinic cholinergic signalling influences nervous system function.
(Received 7 November 2006;
accepted after revision 3 January 2007;
first published online 4 January 2007)
Corresponding author D. K. Berg: Neurobiology Section, Division of Biological Sciences; University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA. Email: dberg{at}ucsd.edu
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