ArticleBehavioral neuroscience2011
Exploration of cerebellar-dependent associative learning in schizophrenia: effects of varying and shifting interstimulus interval on eyeblink conditioning.
Article in Behavioral neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Cerebellar structure and function abnormalities in 16p11.2 microduplication mice.Brain communications · 2026Article
- Psychomotor slowing in schizophrenia is associated with aberrant postural control.Schizophrenia (Heidelberg, Germany) · 2024Article
- Local 5-HT signaling bi-directionally regulates the coincidence time window for associative learning.Neuron · 2023Article
- Consensus paper: Decoding the Contributions of the Cerebellum as a Time Machine. From Neurons to Clinical Applications.Cerebellum (London, England) · 2019Article
- Aberrant Middle Prefrontal-Motor Cortex Connectivity Mediates Motor Inhibitory Biomarker in Schizophrenia.Biological psychiatry · 2019Article
- What Can Different Motor Circuits Tell Us About Psychosis? An RDoC Perspective.Schizophrenia bulletin · 2017Review
- New Insights into the Nature of Cerebellar-Dependent Eyeblink Conditioning Deficits in Schizophrenia: A Hierarchical Linear Modeling Approach.Frontiers in psychiatry · 2016Article
- Hippocampal Non-Theta-Contingent Eyeblink Classical Conditioning: A Model System for Neurobiological Dysfunction.Frontiers in psychiatry · 2016Review
- Eyeblink conditioning: a non-invasive biomarker for neurodevelopmental disorders.Journal of autism and developmental disorders · 2015Review
- Eyeblink Conditioning in Schizophrenia: A Critical Review.Frontiers in psychiatry · 2015Review
- Eyeblink Conditioning and Novel Object Recognition in the Rabbit: Behavioral Paradigms for Assaying Psychiatric Diseases.Frontiers in psychiatry · 2015Review
- Impaired cerebellar-dependent eyeblink conditioning in first-degree relatives of individuals with schizophrenia.Schizophrenia bulletin · 2014Article
- Effects of OEF/OIF-related physical and emotional co-morbidities on associative learning: concurrent delay and trace eyeblink classical conditioning.International journal of environmental research and public health · 2014Article
- Cerebellar-motor dysfunction in schizophrenia and psychosis-risk: the importance of regional cerebellar analysis approaches.Frontiers in psychiatry · 2014Review
- Eyeblink conditioning in unmedicated schizophrenia patients: a positron emission tomography study.Psychiatry research · 2013Article
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Authors and funding
9 authors at 4 institutions in 1 country.
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Abstract
Eyeblink conditioning abnormalities have been reported in schizophrenia, but the extent to which these anomalies are evident across a range of delay intervals (i.e., interstimulus intervals; ISIs) is unknown. In addition, the effects of ISI shifts on learning are unknown, though such manipulations can be informative about the plasticity of cerebellar timing functions. Therefore, the primary purpose of the present study was to investigate the interactions between ISI manipulations and learning in schizophrenia. A standard delay eyeblink conditioning procedure with four different interstimulus intervals (ISIs; 250, 350, 550, 850 ms) was employed. Each eyeblink conditioning experiment was immediately followed by another with a different ISI, thus permitting the characterization of conditioned response (CR) learning at one ISI and the extent to which CRs could be generated at a different latency following an ISI shift. Collapsing across all conditions, the schizophrenia group (n = 55) had significantly fewer conditioned responses and longer onset latencies than age-matched controls (n = 55). Surprisingly, shifting to a new ISI had negligible effects on conditioned response rates in both groups. These findings contribute to evidence of robust eyeblink conditioning abnormalities in schizophrenia and suggest impaired cerebellar function, but underscore the need for more research to clarify the source of these abnormalities and their relationship to clinical manifestations of schizophrenia.
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