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ABSTRACT Quasar winds can shock and sweep up ambient interstellar medium (ISM) gas, contributing to galactic quenching. We combine and extend past models of energy-conserving shock bubbles around quasars, investigate model implications from an observational standpoint, and test model predictions using new high-resolution spectroscopic observations of the broad absorption-line quasar SDSS J030000.56+004828.0 (J0300). Even with constant energy input from the wind, a bubble’s expansion decelerates over time as more ISM gas is swept up. Our new observations enable a direct search for this deceleration. We obtain the tightest reported 3σ limit on the average rest-frame deceleration (or acceleration) of a quasar outflow: |a| < 0.1 km s−1 yr−1 (<3 × 10−4 cm s−2) in the relatively low-velocity Ca ii outflow of J0300 over 9.65 rest-frame years. We can satisfy these limits with certain parameter choices in our model, but the large velocity range of the Ca ii absorption in J0300 rules out the hypothesis that such gas shares the velocity of the swept-up ISM gas in a self-similar shock bubble. We investigate the possibility of ram-pressure acceleration of preexisting ISM clouds and conclude that the velocity range seen in Ca ii in J0300 is potentially consistent with such an explanation. The Ca ii-absorbing gas clouds in J0300 have been inferred to have high densities by Choi et al., in which case they can only have been accelerated to their current speeds if they were originally at least an order of magnitude less dense than they are today. 

The cell adhesion molecule neuroligin2 (NLGN2) regulates GABAergic synapse development, but its role inneural circuit function in the adult hippocampus is unclear. We investigated GABAergic synapses and hippo-campus-dependent behaviors following viral-vector-mediated overexpression of NLGN2. Transducing hippo-campal neurons with AAV-NLGN2 increased neuronal expression of NLGN2 and membrane localization ofGABAergic postsynaptic proteins gephyrin and GABAARγ2, and presynaptic vesicular GABA transporter protein(VGAT) suggesting trans-synaptic enhancement of GABAergic synapses. In contrast, glutamatergic postsynapticdensity protein-95 (PSD-95) and presynaptic vesicular glutamate transporter (VGLUT) protein were unaltered.Moreover, AAV-NLGN2 significantly increased parvalbumin immunoreactive (PV+) synaptic boutons co-loca-lized with postsynaptic gephyrin+puncta. Furthermore, these changes were demonstrated to lead to cognitiveimpairments as shown in a battery of hippocampal-dependent mnemonic tasks and social behaviors.