A series of conjugated polymers based on benzo[1,2-b:4,5-b 0 ]dithiophene and bithiazole were systematically investigated for applications of polymer field-effect transistors and thin film phototransistors. Grazing incidence X-ray diffraction and atomic force microscopy were employed to investigate the solid state molecular organization and film morphology. The solution processability, solid state molecular organization, film morphology, charge transport and phototransistor performance can be tuned by elaborately optimizing the polymer backbone and side chains synchronously. For the optimized polymer (P5), a charge-carrier mobility of 0.194 cm 2 V À1 s À1 , a threshold voltage of À6 V and an on/off current ratio of 10 6 were achieved. Phototransistors based on this polymer showed a highest photoresponsivity of 132 A W À1 and a photocurrent/dark current ratio of 2 Â 10 5 .

No abstract

Aversive memories associated with drug withdrawal may contribute to persistent drug seeking. Molecular mechanisms that are critical for aversive memory formation have yet to be elucidated. Recently, we showed in a rat conditioned place aversion (CPA) model that synaptic actin polymerization in the amygdala were required for aversive memory information. Here, we demonstrated that actin polymerization within the amygdala triggered transportation of activity-regulated cytoskeletal-associated protein (Arc/Arg3.1) into amygdalar synapses. Increased synaptic Arc/Arg3.1 expression contributed to aversive memory formation by regulating synaptic AMPA receptor (AMPAR) endocytosis, as in vivo knockdown of amygdalar Arc/Arg3.1 with Arc/Arg3.1-shRNA prevented both AMPAR endocytosis and CPA formation. We also demonstrated that conditioned morphine withdrawal led to induction of LTD in the amygdala through AMPAR endocytosis. We further demonstrated that Arc/Arg3.1-regulated AMPAR endocytosis was GluR2 dependent, as intraamygdala injection of Tat-GluR2 3Y , a GluR2-derived peptide that has been shown to specifically block regulated, but not constitutive, AMPAR endocytosis, prevented AMPAR endocytosis, LTD induction, and aversive memory formation. Therefore, this study extends previous studies on the role of actin polymerization in synaptic plasticity and memory formation by revealing the critical molecular events involved in aversive memory formation as well as LTD induction, and by showing that Arc/Arg3.1 is a crucial mediator for actin polymerization functions, and, thus, underscores the unknown details of how actin polymerization mediates synaptic plasticity and memory.