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Disruption of Akt signaling decreases dopamine sensitivity in modulation of inhibitory synaptic transmission in rat prefrontal cortex
Journal article   Open access   Peer reviewed

Disruption of Akt signaling decreases dopamine sensitivity in modulation of inhibitory synaptic transmission in rat prefrontal cortex

Yan-Chun Li, Sha-Sha Yang and Wen-Jun Gao
Neuropharmacology, v 108, pp 403-414
Sep 2016
PMID: 27163190
url
https://doi.org/10.1016/j.neuropharm.2016.05.002View
Published, Version of Record (VoR) Open

Abstract

Synaptic Transmission - physiology Proto-Oncogene Proteins c-akt - deficiency Receptors, Dopamine D2 - agonists Dopamine - pharmacology Inhibitory Postsynaptic Potentials - physiology Rats Male Receptors, Dopamine D2 - metabolism Rats, Sprague-Dawley Neural Inhibition - physiology Animals Prefrontal Cortex - drug effects Signal Transduction - drug effects Prefrontal Cortex - metabolism Female Signal Transduction - physiology Synaptic Transmission - drug effects Neural Inhibition - drug effects Inhibitory Postsynaptic Potentials - drug effects Organ Culture Techniques Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Akt is a serine/threonine kinase, which is dramatically reduced in the prefrontal cortex (PFC) of patients with schizophrenia, and a deficiency in Akt1 results in PFC function abnormalities. Although the importance of Akt in dopamine (DA) transmission is well established, how impaired Akt signaling affects the DA modulation of synaptic transmission in the PFC has not been characterized. Here we show that Akt inhibitors significantly decreased receptor sensitivity to DA by shifting DA modulation of GABAA receptor-mediated inhibitory postsynaptic currents (IPSCs) in prefrontal cortical neurons. Akt inhibition caused a significant decrease in synaptic dopamine D2 receptor (D2R) levels with high-dose DA exposure. In addition, Akt inhibition failed to affect DA modulation of IPSCs after blockade of β-arrestin 2. β-arrestin 2-mediated interaction of clathrin with D2R was enhanced by co-application of a Akt inhibitor and DA. Taken together, the reduced response in DA modulation of inhibitory transmission mainly involved β-arrestin 2-dependent D2R desensitization.

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