D1+ MSNs, and reduced cocaine CPP and locomotor activity after TrkB deletion from D2+ MSNs. The likely common action of TrkB knockout and optogenetic stimulation in D2+ MSNs is their increased activity, since deletion of TrkB from these cells increases their electrical excitability. As mentioned earlier, we also found a robust reduction of pERK after TrkB deletion from D1+ MSNs. pERK is a known downstream target of BDNF signaling, therefore, the shared behavioral effects observed after TrkB deletion from D1+ MSNs and from optogenetic activation of these cells might be due to converging effects on pERK activity. However, future work is needed to determine the precise, shared molecular underpinnings that govern the behavioral effects seen after disruption of BDNF signaling and optogenetic control of these two neuronal subtypes.
