Synaptically released zinc gates long-term potentiation in fear conditioning pathways. Export

@article{citeulike:1610665, abstract = {The functional role of releasable Zn2+ in the central nervous system remains unknown. Here we show that zinc transporter 3 (ZnT-3), which maintains a high concentration of Zn2+ in synaptic vesicles and serves as a marker for zinc-containing neurons, is enriched in the lateral nucleus of the amygdala and in the temporal area 3 of the auditory cortex, an area that conveys information about the auditory conditioned stimulus to the lateral nucleus of the amygdala, but not in other conditioned stimulus areas located in the auditory thalamus. Using whole-cell recordings from amygdala slices, we demonstrated that activity-dependent release of chelatable Zn2+ is required for the induction of spike timing-dependent long-term potentiation in cortical input to the amygdala implicated in fear learning. Our data indicate that synaptically released Zn2+ enables long-term potentiation at the cortico-amygdala synapses by depressing feed-forward GABAergic inhibition of principal neurons. This regulatory mechanism, implicating pathway-dependent release of Zn2+, may serve an essential control function in assuring spatial specificity of long-lasting synaptic modifications in the neural circuit of a learned behavior.}, address = {*Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA 02478, USA.}, author = {Kodirov, S. A. and Takizawa, S. and Joseph, J. and Kandel, E. R. and Shumyatsky, G. P. and Bolshakov, V. Y.}, citeulike-article-id = {1610665}, citeulike-linkout-0 = {http://dx.doi.org/10.1073/pnas.0607131103}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/17005717}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=17005717}, day = {10}, doi = {10.1073/pnas.0607131103}, issn = {0027-8424}, journal = {Proc Natl Acad Sci U S A}, keywords = {interneuron, la, ltp}, month = {October}, number = {41}, pages = {15218--15223}, posted-at = {2007-08-31 13:06:37}, priority = {0}, title = {Synaptically released zinc gates long-term potentiation in fear conditioning pathways.}, url = {http://dx.doi.org/10.1073/pnas.0607131103}, volume = {103}, year = {2006} }

TY - JOUR ID - citeulike:1610665 L3 - citeulike-article-id:1610665 N2 - The functional role of releasable Zn2+ in the central nervous system remains unknown. Here we show that zinc transporter 3 (ZnT-3), which maintains a high concentration of Zn2+ in synaptic vesicles and serves as a marker for zinc-containing neurons, is enriched in the lateral nucleus of the amygdala and in the temporal area 3 of the auditory cortex, an area that conveys information about the auditory conditioned stimulus to the lateral nucleus of the amygdala, but not in other conditioned stimulus areas located in the auditory thalamus. Using whole-cell recordings from amygdala slices, we demonstrated that activity-dependent release of chelatable Zn2+ is required for the induction of spike timing-dependent long-term potentiation in cortical input to the amygdala implicated in fear learning. Our data indicate that synaptically released Zn2+ enables long-term potentiation at the cortico-amygdala synapses by depressing feed-forward GABAergic inhibition of principal neurons. This regulatory mechanism, implicating pathway-dependent release of Zn2+, may serve an essential control function in assuring spatial specificity of long-lasting synaptic modifications in the neural circuit of a learned behavior. IS - 41 JF - Proc Natl Acad Sci U S A SN - 0027-8424 AD - *Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA 02478, USA. EP - 15223 TI - Synaptically released zinc gates long-term potentiation in fear conditioning pathways. VL - 103 SP - 15218 KW - interneuron KW - la KW - ltp AU - Kodirov, SA AU - Takizawa, S AU - Joseph, J AU - Kandel, ER AU - Shumyatsky, GP AU - Bolshakov, VY PY - 2006/10/10/ UR - http://dx.doi.org/10.1073/pnas.0607131103 ER -