Topic: GABAergic plasticity

Major depressive disorder (MDD) is a highly disabling psychiatric syndrome affecting many aspects of behavior and cognitive functions, including memory. MDD is strongly associated with stress and with deficits in specific subpopulations of GABAergic interneurons. However, the underlying molecular mechanisms linking these observations are not fully understood. The activity-regulated gene Arc/Arg3.1 is rapidly up-regulated by acquiring novel experience, learning and memory, and synaptic plasticity-inducing stimuli1,2. Acute stress has also been reported to elevate the levels of Arc/Arg3.1 mRNA o

It is well known that dopamine is a significant player in regulation of various forms of glutamatergic synaptic plasticity. In particular, activation of D1/D5 dopamine receptors was shown to increase the magnitude of hippocampal excitatory long-term potentiation (LTP) (Hansen and Manahan-Vaughan, 2014). We have also demonstrated that D1/D5 dopamine receptors supports NMDA-dependent LTP selectively in st. oriens of the CA1 region (Brzdak et al., 2019). While involvement of dopamine receptors, especially D1/D5, in the excitatory plasticity is well established, their role in the GABAergic plastic

Although diverse stimulation patterns induce excitatory plasticity, they concurrently trigger long-term potentiation (iLTP) or depression (iLTD) at inhibitory synapses. Nevertheless, the precise plasticity rules and molecular mechanisms governing the interaction between excitatory and GABAergic plasticity remain unclear. Here, we aimed to elucidate these mechanisms in slices by simultaneously recording excitatory and distinct optogenetically evoked inhibitory postsynaptic currents in hippocampal CA1 pyramidal cells (CA1PCs). Long-term plasticity was induced by NMDA treatment.Our experiments re