Max Joffe , Ph.D.
Biosketch and Research Interests
Max performed his Ph.D. work in the lab of Brad Grueter, where he examined the input- and cell type-specific effects of cocaine exposure on N-methyl-D-aspartate receptor (NMDAR) signaling in the nucleus accumbens (NAc). In particular, his work focused on the dense excitatory projections from the midline thalamus (mThal) and prefrontal cortex (PFC). His graduate work demonstrated that in the NAc core, cocaine sensitization and abstinence enhances NMDAR function at mThal-D1(+), mThal-D1(-), and PFC-D1(+) synapses. At mThal-D1(+) synapses specifically, his research demonstrated that cocaine enhances GluN2C/D function and NMDAR-dependent synaptic plasticity. Moreover, the role for these NMDARs in cocaine-conditioned behaviors was evidenced by the finding that mice with a D1-specific GluN1 genetic deletion do not reinstate a place preference to cocaine. Collectively Max’s graduate work emphasizes the emerging role for D1-NMDARs in reward learning, and highlights mThal inputs and GluN2C/D subunits as novel targets for the treatment of psychostimulant use disorders.
Max joined the Conn lab for his postdoctoral training in May 2016. He is expanding on his graduate training by investigating the regulation of fast excitatory neurotransmission by G protein-coupled receptors (GPCRs) in the context of stress-related mood disorders. Max is especially interested in the function of the PFC and how modulating glutamate transmission in that region may be beneficial in ameliorating anhedonia, lethargy, and cognitive deficits. He is beginning his postdoctoral training examining the synapse-specific function of metabotropic glutamate receptor subtype 3 (mGlu3) and whether negative allosteric modulators of mGlu3 have efficacy in mouse models of stress disorders.