• About
  • Keywords

Toxoplasma gondii & Human Phenotype

Compendium of Known Effects and Ongoing Research

cortex

Humans with latent toxoplasmosis display altered reward modulation of cognitive control

December 8, 2017
Stock, A. K., Dajkic, D., Kohling, H. L., von Heinegg, E. H., Fiedler, M., Beste, C.
Scientific Reports 2017;7: 10.1038/s41598-017-10926-6
Click for abstract
Latent infection with Toxoplasma gondii has repeatedly been shown to be associated with behavioral changes that are commonly attributed to a presumed increase in dopaminergic signaling. Yet, virtually nothing is known about its effects on dopamine-driven reward processing. We therefore assessed behavior and event-related potentials in individuals with vs. without latent toxoplasmosis performing a rewarded control task. The data show that otherwise healthy young adults with latent toxoplasmosis show a greatly diminished response to monetary rewards as compared to their noninfected counterparts. While this selective effect eliminated a toxoplasmosis-induced speed advantage previously observed for non-rewarded behavior, Toxo-positive subjects could still be demonstrated to be superior to Toxo-negative subjects with respect to response accuracy. Event-related potential (ERP) and source localization analyses revealed that this advantage during rewarded behavior was based on increased allocation of processing resources reflected by larger visual late positive component (LPC) amplitudes and associated activity changes in the right temporo-parietal junction (BA40) and left auditory cortex (BA41). Taken together, individuals with latent toxoplasmosis show superior behavioral performance in challenging cognitive control situations but may at the same time have a reduced sensitivity towards motivational effects of rewards, which might be explained by the presumed increase in dopamine.

Tagged: cortex, dual-task performance, goal activation, gondii infection leads, human brain, multicomponent behavior, neural

BehaviorCognitive functions

Paranoid Schizophrenia May Be Caused by Dopamine Hyperactivity of Ca1 Hippocampus

November 8, 1991
Krieckhaus EE, Donahoe JW, Morgan MA
Biological Psychiatry 1992; 31: 560-570
Click for abstract
Explicit consolidation of memory, or fixation of declarative belief, appears to be physically represented in changes of synaptic conductances of neurons in the parietal-temporal-occipital association cortex (PTO) of the mammalian forebrain. This fixation of belief in PTO is postulated to be critically dependent on a diffuse reinforcement signal via the inferior temporal cortex (ITC) ultimately caused by an increased output of the CA1 pyramidal cells of hippocampus. Analogous to the reinforcing mechanisms of other forebrain systems, this updating of the connection weights of the neural nets in PTO by the output of the critical neurons in CA1 is directly related to concentrations of dopamine (DA). We propose that the delusions (i.e., unreasonable beliefs) of paranoid schizophrenia are caused by a hyperactivity of the same DA-sensitive CA1 neurons that are responsible for the fixation of normal beliefs. The dramatic reduction in delusions with administration of neuroleptics, as DA D2 blockers, in schizophrenics may thus be explained by their acting to ameliorate the hyperactivity of these CA1 DA D2 receptors.

Tagged: amnesia, autoradiographic localization, brain, cortex, d2 receptors, disorder, long-term potentiation, memory impairment, modulation, psychosis

Mental health

Topics

  • Behavior 105
  • Cognitive functions 64
  • Mental health 439
  • Morphology 6
  • Motor functions 10
  • Personality 36
  • Physical health 134
  • Reproduction 36
  • Reviews 40
  • Sensory functions 3
  • Uncategorized 2

Archives

Recent articles

  • Mortality Patterns of Toxoplasmosis and Its Comorbidities in Tanzania: A 10-Year Retrospective Hospital-Based Survey February 6, 2020
  • The role of latent toxoplasmosis in the aetiopathogenesis of schizophrenia–the risk factor or an indication of a contact with cat? February 6, 2020
  • The Association between Toxoplasma gondii Infection and Risk of Parkinson’s Disease: A Systematic Review and Meta-Analysis February 6, 2020

Recent Comments

    Meta

    • Log in
    • Entries feed
    • Comments feed
    • WordPress.org

    Copyright © 2023 Toxoplasma gondii & Human Phenotype.

    ToxoBehavior WordPress Theme by Jelena Braum