Kainate receptor-mediated synaptic transmissions in the adult rodent insular cortex
| Autor: | Tao Chen, Long Jun Wu, Min Zhuo, Kohei Koga, Su Eon Sim, Bong-Kiun Kaang |
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| Rok vydání: | 2012 |
| Předmět: |
Rodent
Physiology Central nervous system Kainate receptor Neurotransmission Insular cortex Inhibitory postsynaptic potential Synaptic Transmission GABA Antagonists Benzodiazepines Mice Receptors Kainic Acid biology.animal medicine Animals Picrotoxin Receptor Cerebral Cortex Mice Knockout Alanine biology Pyramidal Cells musculoskeletal neural and ocular physiology General Neuroscience Excitatory Postsynaptic Potentials Mice Inbred C57BL medicine.anatomical_structure 2-Amino-5-phosphonovalerate nervous system Excitatory postsynaptic potential Excitatory Amino Acid Antagonists Neuroscience Thymine |
| Zdroj: | Journal of Neurophysiology. 108:1988-1998 |
| ISSN: | 1522-1598 0022-3077 |
| DOI: | 10.1152/jn.00453.2012 |
| Popis: | Kainate (KA) receptors are expressed widely in the central nervous system and regulate both excitatory and inhibitory synaptic transmission. KA receptors play important roles in fear memory, anxiety, and pain. However, little is known about their function in synaptic transmission in the insular cortex (IC), a critical region for taste, memory, and pain. Using whole cell patch-clamp recordings, we have shown that KA receptors contribute to fast synaptic transmission in neurons in all layers of the IC. In the presence of the GABAA receptor antagonist picrotoxin, the NMDA receptor antagonist AP-5, and the selective AMPA receptor antagonist GYKI 53655, KA receptor-mediated excitatory postsynaptic currents (KA EPSCs) were revealed. We found that KA EPSCs are ∼5–10% of AMPA/KA EPSCs in all layers of the adult mouse IC. Similar results were found in adult rat IC. KA EPSCs had a significantly slower rise time course and decay time constant compared with AMPA receptor-mediated EPSCs. High-frequency repetitive stimulations at 200 Hz significantly facilitated the summation of KA EPSCs. In addition, genetic deletion of GluK1 or GluK2 subunit partially reduced postsynaptic KA EPSCs, and exposure of GluK2 knockout mice to the selective GluK1 antagonist UBP 302 could significantly reduce the KA EPSCs. These data suggest that both GluK1 and GluK2 play functional roles in the IC. Our study may provide the synaptic basis for the physiology and pathology of KA receptors in the IC-related functions. |
| Databáze: | OpenAIRE |
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