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Fig. 2. PCP, Ketamine and LSD alter gluatatmate neurotransmission. (A) PCP and ketamine regulate glutamate transmission. They bind to NMDA receptors of the PFC GABAergic interneuron. The NMDA receptor hypofunction on GABAerginc neurons induces hyper-glutamatergic transmission. (B) LSD affects serotonergic transmission and gluatmate transmission. LSD binds to the 5-HT2A receptor located on thalamus glutamatergic neurons where serotonergic raphe neurons send efferent projections. Glutamate release of thalamic neuron is increased due to the effect of LSD, resulting in hyper glutamatergic transmission in the PFC. The upper orange neruon indicates presynaptic glutamatergic neuron whereas lower orange neuron indicates a postsynptic neron. The yellow neuron of figure (A) denotes GABAergic interneuron in the PFC and that of figure (B) denotes thalamic glutamatergic neuron. The green neuron is a serotonergic neuron in the raphe nucleus. AMPAR, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor; NMDAR, N-methyl-D-aspartate receptor; GABAR, gamma-Aminobutyric acid receptor; 5-HT2AR, serotonin 2A receptor.
Exp Neurobiol 2017;26:11~24 https://doi.org/10.5607/en.2017.26.1.11
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