Literature DB >> 15466302

Brain mechanisms of extinction of the classically conditioned eyeblink response.

Karla Robleto1, Andrew M Poulos, Richard F Thompson.   

Abstract

It is well established that the cerebellum and its associated circuitry are essential for classical conditioning of the eyeblink response and other discrete motor responses (e.g., limb flexion, head turn, etc.) learned with an aversive unconditioned stimulus (US). However, brain mechanisms underlying extinction of these responses are still relatively unclear. Behavioral studies have demonstrated extinction as an active learning process distinct from acquisition. Experimental data in eyeblink conditioning suggest that plastic changes specific to extinction may play an important role in this process. Both cerebellar and hippocampal systems may be involved in extinction of these memories. The nature of this phenomenon and identification of the neural substrates necessary for extinction of originally learned responses is the topic of this review.

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Year:  2004        PMID: 15466302     DOI: 10.1101/lm.80004

Source DB:  PubMed          Journal:  Learn Mem        ISSN: 1072-0502            Impact factor:   2.460


  29 in total

1.  Lack of renewal effect in extinction of naturally acquired conditioned eyeblink responses, but possible dependency on physical context.

Authors:  J Claassen; L Mazilescu; A Thieme; V Bracha; D Timmann
Journal:  Exp Brain Res       Date:  2015-09-24       Impact factor: 1.972

Review 2.  Consolidation of motor memory.

Authors:  John W Krakauer; Reza Shadmehr
Journal:  Trends Neurosci       Date:  2005-11-14       Impact factor: 13.837

3.  Repeated acquisitions and extinctions in classical conditioning of the rabbit nictitating membrane response.

Authors:  E James Kehoe
Journal:  Learn Mem       Date:  2006-05-16       Impact factor: 2.460

Review 4.  Motor learning in the VOR: the cerebellar component.

Authors:  Dianne M Broussard; Heather K Titley; Jordan Antflick; David R Hampson
Journal:  Exp Brain Res       Date:  2011-02-19       Impact factor: 1.972

5.  Modulation of 7 T fMRI Signal in the Cerebellar Cortex and Nuclei During Acquisition, Extinction, and Reacquisition of Conditioned Eyeblink Responses.

Authors:  Thomas M Ernst; Markus Thürling; Sarah Müller; Fabian Kahl; Stefan Maderwald; Marc Schlamann; Henk-Jan Boele; Sebastiaan K E Koekkoek; Jörn Diedrichsen; Chris I De Zeeuw; Mark E Ladd; Dagmar Timmann
Journal:  Hum Brain Mapp       Date:  2017-05-05       Impact factor: 5.038

6.  A mouse model for MeCP2 duplication syndrome: MeCP2 overexpression impairs learning and memory and synaptic transmission.

Authors:  Elisa S Na; Erika D Nelson; Megumi Adachi; Anita E Autry; Melissa A Mahgoub; Ege T Kavalali; Lisa M Monteggia
Journal:  J Neurosci       Date:  2012-02-29       Impact factor: 6.167

7.  Retention and extinction of delay eyeblink conditioning are modulated by central cannabinoids.

Authors:  Adam B Steinmetz; John H Freeman
Journal:  Learn Mem       Date:  2011-09-22       Impact factor: 2.460

8.  Eyeblink conditioning in healthy adults: a positron emission tomography study.

Authors:  Krystal L Parker; Nancy C Andreasen; Dawei Liu; John H Freeman; Laura L Boles Ponto; Daniel S O'Leary
Journal:  Cerebellum       Date:  2012-12       Impact factor: 3.847

9.  Eyeblink conditioning in unmedicated schizophrenia patients: a positron emission tomography study.

Authors:  Krystal L Parker; Nancy C Andreasen; Dawei Liu; John H Freeman; Daniel S O'Leary
Journal:  Psychiatry Res       Date:  2013-10-01       Impact factor: 3.222

10.  GABAA receptor antagonism ameliorates behavioral and synaptic impairments associated with MeCP2 overexpression.

Authors:  Elisa S Na; Michael J Morris; Erika D Nelson; Lisa M Monteggia
Journal:  Neuropsychopharmacology       Date:  2014-02-19       Impact factor: 7.853

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