Selective Gating of Glutamatergic Inputs to Excitatory Neurons of Amygdala by Presynaptic GABAb Receptor
Neuron, ISSN: 0896-6273, Vol: 61, Issue: 6, Page: 917-929
2009
- 63Citations
- 114Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations63
- Citation Indexes63
- 63
- CrossRef57
- Captures114
- Readers114
- 114
- Mentions1
- Blog Mentions1
- Blog1
Article Description
GABAb receptor (GABAbR)-mediated suppression of glutamate release is critical for limiting glutamatergic transmission across the central nervous system (CNS). Here we show that, upon tetanic stimulation of afferents to lateral amygdala, presynaptic GABAbR-mediated inhibition only occurs in glutamatergic inputs to principle neurons (PNs), not to interneurons (INs), despite the presence of GABAbR in terminals to both types of neurons. The selectivity is caused by differential local GABA accumulation; it requires GABA reuptake and parallels distinct spatial distributions of presynaptic GABAbR in terminals to PNs and INs. Moreover, GABAbR-mediated suppression of theta-burst-induced long-term potentiation (LTP) occurs only in the inputs to PNs, not to INs. Thus, target-cell-specific control of glutamate release by presynaptic GABAbR orchestrates the inhibitory dominance inside amygdala and might contribute to prevention of nonadaptive defensive behaviors.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0896627309000968; http://dx.doi.org/10.1016/j.neuron.2009.01.029; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=62549114873&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/19324000; https://linkinghub.elsevier.com/retrieve/pii/S0896627309000968
Elsevier BV
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