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. Author manuscript; available in PMC: 2017 Oct 1.
Published in final edited form as: Neurobiol Dis. 2016 Jun 17;94:85–94. doi: 10.1016/j.nbd.2016.06.008

Figure 5. A hypothesized mechanism by which hyper-excitability of mPFC pyramidal neurons induced by HIV in a HIV-1 Tg rat model is alleviated by combined chronic treatments of L-channel blocker and NMDAR antagonist.

Figure 5

Over-activation of the L-channel and NMDAR contribute to HIV-induced hyper-excitation of pyramidal neurons in the mPFC, which could alter excitatory glutamatergic outputs from the mPFC. This change could consequently affect the function of other vulnerable cortical and subcortical brain regions altered in neuroAIDS. Combined chronic treatments with selective L-channel blocker and NMDAR antagonist that preferentially target over-activated Ca2+ permeable ion channels alleviate the mPFC neuronal hyper-excitability in HIV-1 Tg rats. This novel finding from the present study suggests that combined targeting of over-active L-channels and NMDARs may be necessary and could provide more effective therapeutic potential for treating HIV-induced neurocognitive and neuropsychiatric deficits. The gray box indicates the novel findings from the current study.