Colliculopulvinar contributions to alpha dysregulation and cognitive dysfunction in schizophrenia

NIH RePORTER · NIH · R21 · $245,850 · view on reporter.nih.gov ↗

Abstract

Schizophrenia (Sz) is a severe psychiatric disorder associated with core neurocognitive deficits. Although, traditional models of schizophrenia focus on dysfunction within cognitive and sensory processing cortical regions, increasing evidence has accumulated suggestive of subcortical processing impairments as well. Deficits along the subcortical visual pathways, especially involving the magnocellular visual pathway, have been tied to deficits in the generation of early cortical responses which, in turn, contribute to higher-order cortical impairments. These deficits, however, may not account for all visual information processing abnormalities in Sz. Recently, we have observed deficits in the modulation of ongoing scalp- recorded alpha activity, which appear independent of the traditional magno/parvocellular pathways, and which may be mediated by dysfunction of the “retinotectal” visual pathway, which involves the superior colliculus (SC) and the pulvinar nucleus of the thalamus (PuN), but which bypasses the lateral geniculate nucleus (LGN). At present, tools for the evaluation of the retinotectal system within neuropsychiatric populations remain limited. In this project we will conduct a side-by-side comparison of potential paradigms gleaned from the basic science literature to elicit PuN/SC activation and will study their feasibility and psychometric properties. These paradigms will then be used to assess the integrity of PuN/SC processing in Sz relative to alpha generation and cognitive performance.

Key facts

NIH application ID
10388226
Project number
5R21MH123875-02
Recipient
NATHAN S. KLINE INSTITUTE FOR PSYCH RES
Principal Investigator
Antigona Martinez
Activity code
R21
Funding institute
NIH
Fiscal year
2022
Award amount
$245,850
Award type
5
Project period
2021-04-15 → 2024-03-31