| First Author | Koppensteiner P | Year | 2017 |
| Journal | Cell Rep | Volume | 20 |
| Issue | 5 | Pages | 1111-1122 |
| PubMed ID | 28768196 | Mgi Jnum | J:254865 |
| Mgi Id | MGI:6104031 | Doi | 10.1016/j.celrep.2017.07.013 |
| Citation | Koppensteiner P, et al. (2017) A Cooperative Mechanism Involving Ca(2+)-Permeable AMPA Receptors and Retrograde Activation of GABAB Receptors in Interpeduncular Nucleus Plasticity. Cell Rep 20(5):1111-1122 |
| abstractText | The medial habenula-interpeduncular nucleus (MHb-IPN) pathway, which connects the limbic forebrain to the midbrain, has recently been implicated in aversive behaviors. The MHb-IPN circuit is characterized by a unique topographical organization, an excitatory role of GABA, and a prominent co-release of neurotransmitters and neuropeptides. However, little is known about synaptic plasticity in this pathway. An application of a high-frequency stimulation resulted in a long-lasting potentiation of glutamate release in IPN neurons. Our experiments reveal that a Ca(2+)-permeable AMPA receptor (CPAR)-dependent release of GABA from IPN neurons and a retrograde activation of GABAB receptors on MHb terminals result in a long-lasting enhancement of glutamate release. Strikingly, adolescent IPN neurons lacked CPARs and exhibited an inability to undergo plasticity. In addition, fear conditioning suppressed an activity-dependent potentiation of MHb-IPN synapses, whereas fear extinction reversed this plasticity deficit, suggesting a role of the MHb-IPN synaptic plasticity in the regulation of aversive behaviors. |
