Browsing by Author "Ahn, S."

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    Acute d-Amphetamine alters the temporal patterning of intermittent synchronized oscillations in hippocampal and prefrontal circuits of the rat
    (Office of the Vice Chancellor for Research, 2012-04-13) Ahn, S.; Lapish, C.C.; RUBCHINSKY, L.L.
    D-Amphetamine (d-AMPH) increases the bioavailability of numerous catecholamines, including dopamine, throughout the brain and modulates neural firing in cortical and subcortical regions. While a complex array of d-AMPH-mediated effects on firing have been reported, less is known regarding how d-AMPH affects the oscillatory properties of cortical circuits. In the current study, we simultaneously recorded local field potentials from electrode arrays implanted in the medial prefrontal cortex (PFC) and hippocampus (HC) of awake freely moving rats treated with saline, 1.0 mg/kg, or 3.3 mg/kg d-AMPH. The fine temporal structure of synchrony in delta, theta, beta, and gamma bands between these brain regions was examined to characterize how phase synchronization was altered by each dose of d-AMPH relative to saline. Differences were observed in the average level of phase-locking and in the variation of temporal patterns of synchrony on short (sub-second) time scales (including the distribution of durations of desynchronization events. In general, treatment with d-AMPH evoked higher levels of phase-locking. While this imperfect phase-locking can be potentially attained with both large number of short desynchronization episodes and small number of long desynchronization episodes, the data are marked by the dominance of short desynchronization episodes. These results suggest that within the HC and PFC, d-AMPH acts to increase synchronized oscillatory activity. The dominance of short desynchronization episodes suggests that the synchrony can be easily destabilized, yet it can be quickly re-established. The ease with which neural circuits can transition between synchronized and desynchronized dynamics may reflect altered information transfer regimes in these circuits and contribute to the spectrum of effects on cognition frequently observed with d-AMPH.
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    COMT Inhibition Alters Cue-Evoked Oscillatory Dynamics during Alcohol Drinking in the Rat
    (Society for Neuroscience, 2018-10-31) McCane, A. M.; Ahn, S.; Rubchinsky, L. L.; Janetsian-Fritz, S. S.; Linsenbardt, D. N.; Czachowski, C. L.; Lapish, C. C.; Psychology, School of Science
    Alterations in the corticostriatal system have been implicated in numerous substance use disorders, including alcohol use disorder (AUD). Adaptations in this neural system are associated with enhanced drug-seeking behaviors following exposure to cues predicting drug availability. Therefore, understanding how potential treatments alter neural activity in this system could lead to more refined and effective approaches for AUD. Local field potentials (LFPs) were acquired simultaneously in the prefrontal cortex (PFC) and nucleus accumbens (NA) of both alcohol preferring (P) and Wistar rats engaged in a Pavlovian conditioning paradigm wherein a light cue signaled the availability of ethanol (EtOH). On test days, the catechol-o-methyl-transferase (COMT) inhibitor tolcapone was administered prior to conditioning. Stimulus-evoked voltage changes were observed following the presentation of the EtOH cue in both strains and were most pronounced in the PFC of P rats. Phase analyses of LFPs in the θ band (5-11 Hz) revealed that PFC-NA synchrony was reduced in P rats relative to Wistars but was robustly increased during drinking. Presentation of the cue resulted in a larger phase reset in the PFC of P rats but not Wistars, an effect that was attenuated by tolcapone. Additionally, tolcapone reduced cued EtOH intake in P rat but not Wistars. These results suggest a link between corticostriatal synchrony and genetic risk for excessive drinking. Moreover, inhibition of COMT within these systems may result in reduced attribution of salience to reward paired stimuli via modulation of stimulus-evoked changes to cortical oscillations in genetically susceptible populations.