Front Cell Neurosci 8:301īonci A, Williams JT (1997) Increased probability of GABA release during withdrawal from morphine. Science (New York, NY) 282:298–300īeccano-Kelly DA, Kuhlmann N, Tatarnikov I, Volta M, Munsie LN, Chou P, Cao LP, Han H, Tapia L, Farrer MJ, Milnerwood AJ (2014) Synaptic function is modulated by LRRK2 and glutamate release is increased in cortical neurons of G2019S LRRK2 knock-in mice. These changes in mPFC synapses and NAc activity begin to characterize the impact of meth on the corticostriatal circuitry.Īhmed SH, Koob GF (1998) Transition from moderate to excessive drug intake: change in hedonic set point. In the NAc, meth decreased the paired-pulse ratio and increased the frequency of spontaneous excitatory postsynaptic currents with no indication of postsynaptic changes. This change was driven by an increase in NMDA receptor currents and an increase in GluN2B surface expression. In the mPFC, meth caused postsynaptic adaptations in ionotropic glutamate receptor distribution and function, expressed as a decrease in AMPA/NMDA ratio. We assessed pre- and postsynaptic changes in glutamate transmission in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) following daily 6-h meth self-administration. There is a dearth of knowledge regarding the underlying physiological changes within this circuit following meth self-administration. In rodents, 6-h access to contingent meth results in an escalation of drug intake and impaired cognitive sequelae typically associated with changes within the corticostriatal circuitry. World-wide methamphetamine (meth) use is increasing at a rapid rate therefore, it has become increasingly important to understand the synaptic changes and neural mechanisms affected by drug exposure.
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