August 2016
Volume 16, Issue 12
Open Access
Vision Sciences Society Annual Meeting Abstract  |   September 2016
Reduced steady-state following responses in primary visual cortex in an animal model of schizophrenia
Author Affiliations
  • Alexander Schielke
    Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102, USA
  • Bart Krekelberg
    Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102, USA
Journal of Vision September 2016, Vol.16, 1227. doi:10.1167/16.12.1227
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to Subscribers Only
      Sign In or Create an Account ×
    • Get Citation

      Alexander Schielke, Bart Krekelberg; Reduced steady-state following responses in primary visual cortex in an animal model of schizophrenia. Journal of Vision 2016;16(12):1227. doi: 10.1167/16.12.1227.

      Download citation file:


      © 2017 Association for Research in Vision and Ophthalmology.

      ×
  • Supplements
Abstract

Schizophrenia (Sz) is a severe and disabling brain disorder that affects approximately 1% of the population. Even though the psychotic symptoms of schizophrenia are better known, patients display significant changes in visual processing and perception; these are stable throughout the course of the disease, better prodromal indicators of disease progression than many traditional neuropsychological tests, and thought to be related to aberrant neural dynamics in visual cortex. Specifically, we investigated the synchronization of cortical responses to the repetition rate of photic stimulation. In comparison to healthy subjects, patients with Sz show reduced power of steady state visually evoked potentials (SSVEP) at the stimulation frequency when the repetition rate is within the beta or gamma range. We hypothesized that hypofunction of the NMDA receptor – one of the neurotransmitter systems implicated in Sz – could underlie this phenomenon. To test this hypothesis, we injected two rhesus monkeys (m. mulatta) either with sub anesthetic doses of the NMDA-receptor antagonist ketamine (0.3mg/kg), or with saline (control). After the injection we presented whole-screen flicker at temporal frequencies of 0, 5, 11, 23, or 47 Hz and recorded evoked local field potentials using permanently implanted multi-electrode arrays in area V1. The SSVEP was assessed by determining the power at the visual stimulation frequency. Ketamine injections resulted in a reduction of the SSVEP. This finding was consistent across recording sites and sessions. Similar to the findings in patients with Sz, the largest SSVEP reductions were found for photic stimulation at 23 Hz (beta) and 47 Hz (gamma). Our findings support the view that NMDA hypofunction could underlie visual/cognitive deficits in Sz. In addition, these results show that visual processing in the macaque can be a fruitful model to investigate cellular mechanisms of schizophrenia.

Meeting abstract presented at VSS 2016

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×