Drugs of abuse can "hijack" synaptic plasticity, a physiological basis of learning and memory, establishing maladaptations that can promote drug addiction. A wealth of data supports the existence and importance of neuroadaptations in excitatory neurotransmission upon drug exposure. Recent discoveries, however, have shown that inhibitory neurotransmission mediated by G protein-gated inwardly rectifying potassium (K+) (GIRK/Kir3) channels is also subject to adaptation triggered by exposure to drugs of abuse. GIRK channels are expressed in neuronal populations relevant to reward and reward-related behaviors, where their activation by neurotransmitters such as GABA, dopamine, and adenosine reduces neuronal excitability. Studies in animal models have implicated GIRK channels in a number of behaviors including reward. Drugs of abuse also affect the inhibitory neurotransmission mediated by GIRK channels. These changes might be important for the development, maintenance, or relapse of addiction, making GIRK channels promising targets for novel addiction therapies.
|Original language||English (US)|
|Title of host publication||International Review of Neurobiology - Structure to Function of G Protein-Gated Inwardly Rectifying (GIRK) Channels, 2015|
|Editors||R. Adron Harris, Peter Jenner|
|Publisher||Academic Press Inc.|
|Number of pages||38|
|State||Published - 2015|
|Name||International Review of Neurobiology|
Bibliographical noteFunding Information:
The authors would like to thank Dr. Patricia Alvarez-Muñoz for her assistance in the preparation of the figures and Dr. Megan Tipps for critical review of the manuscript. This work was supported by NIH Grants to N.M. (DA007234) and K.W. (MH061933 and DA034696).
- GABA receptors
- Mesocorticolimbic system