Accumulating evidence indicates that individuals with schizophrenia manifest abnormalities in structures (cerebellum and basal ganglia) and neurotransmitter systems (dopamine) linked to internal-timing processes. A single-cue tone delay eyeblink conditioning paradigm comprised of 100 learning and 50 extinction trials was used to examine cerebellar timing circuits in 13 medicated patients with schizophrenia and 13 age- and sex-matched controls. Patients with schizophrenia showed impaired learning of the conditioned response compared to controls and also greater within-subject variability in the timing of their responses. These findings are consistent with models of schizophrenia in which timing deficits underlie information-processing abnormalities and clinical features of the disorder.
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http://dx.doi.org/10.1016/j.bandc.2004.09.011 | DOI Listing |
Nat Commun
January 2025
Department of Neuroscience, Erasmus MC, Westzeedijk 353, 3015 AA, Rotterdam, the Netherlands.
Precise temporal control of sensorimotor coordination and adaptation is a fundamental basis of animal behavior. How different brain regions are involved in regulating the flexible temporal adaptation remains elusive. Here, we investigated the neuronal dynamics of the cerebellar interposed nucleus (IpN) and the medial prefrontal cortex (mPFC) neurons during temporal adaptation between delay eyeblink conditioning (DEC) and trace eyeblink conditioning (TEC).
View Article and Find Full Text PDFCommun Psychol
December 2024
Clinical Child and Adolescent Psychology, Mental Health Research and Treatment Center, Faculty of Psychology, Ruhr University Bochum, Bochum, Germany.
Associative learning is a key feature of adaptive behaviour and mental health, enabling individuals to adjust their actions in anticipation of future events. Comprehensive documentation of this essential component of human cognitive development throughout different developmental periods is needed. Here, we investigated age-related changes in associative learning in key developmental stages, including infancy, childhood, adolescence, and adulthood.
View Article and Find Full Text PDFClin Neurophysiol
December 2024
Department of Neurorehabilitation, Hospital of Vipiteno (SABES-ASDAA), Vipiteno-Sterzing, Italy; Department of Neurology, Neurocritical Care and Neurorehabilitation, Christian Doppler University Hospital, Centre for Cognitive Neuroscience, Paracelsus Medical University, Salzburg, Austria. Electronic address:
Objective: Blink reflexes following supraorbital nerve (SON) stimulation are typically modulated by conditioning stimuli (CS) to the index finger (D2) (low-intensity, prepulse inhibition paradigm) or SON (same intensity, paired-pulse paradigm). We aimed to disentangle whether CS-intensity or CS-induced motor responses define blink reflex modulation.
Methods: In 35 subjects, test SON stimuli (8 times sensory threshold, 8 × ST) were applied either alone or following CS.
J Psychopathol Clin Sci
November 2024
Department of Psychological and Brain Sciences, Indiana University Bloomington.
As clinical psychological science and biological psychiatry push to assess, model, and integrate heterogeneity and individual differences, approaches leveraging computational modeling, translational methods, and dimensional approaches to psychopathology are increasingly useful in establishing brain-behavior relationships. The field is ultimately interested in complex human behavior, and disruptions in such behaviors can arise through many different pathways, leading to heterogeneity in etiology for seemingly similar presentations. Parsing this complexity may be enhanced using "simple" tasks-which we define as those assaying elemental processes that are the building blocks to complexity.
View Article and Find Full Text PDFDespite the emerging consensus that microglia are critical to physiological and pathological brain function, it is unclear how microglial roles and their underlying mechanisms differ between brain regions. Microglia throughout the brain express common markers, such as the purinergic receptor P2Y12, that delineate them from peripheral macrophages. P2Y12 is a critical sensor of injury but also contributes to the sensing of neuronal activity and remodeling of synapses, with microglial loss of P2Y12 resulting in behavioral deficits.
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