Refinement of odor molecule tuning by dendrodendritic synaptic inhibition in the olfactory bulb.

@article{citeulike:2722999, abstract = {Mitral/tufted cells (M/T cells) and granule cells form reciprocal dendrodendritic synapses in the main olfactory bulb; the granule cell is excited by glutamate from the M/T cell and in turn inhibits M/T cells by gamma-aminobutyrate. The trans-synaptically excited granule cell is thought to induce lateral inhibition in neighboring M/T cells and to refine olfactory information. It remains, however, elusive how significantly and specifically this synaptic regulation contributes to the discrimination of different olfactory stimuli. This investigation concerns the mechanism of olfactory discrimination by single unit recordings of responses to a series of normal aliphatic aldehydes from individual rabbit M/T cells. This analysis revealed that inhibitory responses are evoked in a M/T cell by a defined subset of odor molecules with structures closely related to the excitatory odor molecules. Furthermore, blockade of the reciprocal synaptic transmission by the glutamate receptor antagonist or the gamma-aminobutyrate receptor antagonist markedly suppressed the odor-evoked inhibition, indicating that the inhibitory responses are evoked by lateral inhibition via the reciprocal synaptic transmission. The synaptic regulation in the olfactory bulb thus greatly enhances the tuning specificity of odor responses and would contribute to discrimination of olfactory information.}, address = {Institute for Immunology, Kyoto University Faculty of Medicine, Japan.}, author = {Yokoi, M. and Mori, K. and Nakanishi, S. }, citeulike-article-id = {2722999}, issn = {0027-8424}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, keywords = {bulb, inhibition, lateral, olfaction, olfactory}, month = {April}, number = {8}, pages = {3371--3375}, posted-at = {2008-04-27 03:10:54}, priority = {0}, title = {Refinement of odor molecule tuning by dendrodendritic synaptic inhibition in the olfactory bulb.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/7724568}, volume = {92}, year = {1995} }

TY - JOUR ID - citeulike:2722999 L3 - citeulike-article-id:2722999 TI - Refinement of odor molecule tuning by dendrodendritic synaptic inhibition in the olfactory bulb. JF - Proceedings of the National Academy of Sciences of the United States of America VL - 92 IS - 8 SP - 3371 EP - 3375 AD - Institute for Immunology, Kyoto University Faculty of Medicine, Japan. SN - 0027-8424 N2 - Mitral/tufted cells (M/T cells) and granule cells form reciprocal dendrodendritic synapses in the main olfactory bulb; the granule cell is excited by glutamate from the M/T cell and in turn inhibits M/T cells by gamma-aminobutyrate. The trans-synaptically excited granule cell is thought to induce lateral inhibition in neighboring M/T cells and to refine olfactory information. It remains, however, elusive how significantly and specifically this synaptic regulation contributes to the discrimination of different olfactory stimuli. This investigation concerns the mechanism of olfactory discrimination by single unit recordings of responses to a series of normal aliphatic aldehydes from individual rabbit M/T cells. This analysis revealed that inhibitory responses are evoked in a M/T cell by a defined subset of odor molecules with structures closely related to the excitatory odor molecules. Furthermore, blockade of the reciprocal synaptic transmission by the glutamate receptor antagonist or the gamma-aminobutyrate receptor antagonist markedly suppressed the odor-evoked inhibition, indicating that the inhibitory responses are evoked by lateral inhibition via the reciprocal synaptic transmission. The synaptic regulation in the olfactory bulb thus greatly enhances the tuning specificity of odor responses and would contribute to discrimination of olfactory information. KW - bulb KW - inhibition KW - lateral KW - olfaction KW - olfactory AU - Yokoi, M AU - Mori, K AU - Nakanishi, S PY - 1995/04/11/ UR - http://view.ncbi.nlm.nih.gov/pubmed/7724568 ER -