Michael D. Mauk
Research Subjects
Research Interests
Michael D. Mauk has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
Frank A. Riusech
1 shared publication- Javier F. Medina
Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA
1 shared publication - Tatsuya Ohyama
Keck Center for Neurobiology of Learning and Memory and Department of Neurobiology and Anatomy, University of Texas Medical School at Houston, Houston, Texas 77030, USA
1 shared publication William L. Nores
1 shared publication
Latest Publications
- Open Access
- 6 December 2006
- Published by Society for Neuroscience in The Journal of Neuroscience
- Vol. 26 (49) , 12656-12663
Learning-Induced Plasticity in Deep Cerebellar Nucleus
Evidence that cerebellar learning involves more than one site of plasticity comes from, in part, pavlovian eyelid conditioning, where disconnecting the cerebellar cortex abolishes one component of learning, response timing, but spares the expression of abnormally timed short-latency responses (SLRs). Here, we provide evidence that SLRs unmasked by cerebellar cortex lesions are mediated by an associative form of learning-induced plasticity in the anterior interpositus nucleus (AIN) of the cerebellum. We used pharmacological inactivation and/or electrical microstimulation of various sites afferent and efferent to the AIN to systematically eliminate alternative candidate sites of plasticity upstream or downstream from this structure. Collectively, the results suggest that cerebellar learning is mediated in part by plasticity in target nuclei downstream of the cerebellar cortex. These data demonstrate an instance in which an aspect of associative learning, SLRs, can be used as an index of plasticity at a specific site in the brain.
- 6 December 2006
- Published by Society for Neuroscience in The Journal of Neuroscience
- Vol. 26 (49) , 12656-12663
Open AccessLearning-Induced Plasticity in Deep Cerebellar Nucleus
Evidence that cerebellar learning involves more than one site of plasticity comes from, in part, pavlovian eyelid conditioning, where disconnecting the cerebellar cortex abolishes one component of learning, response timing, but spares the expression of abnormally timed short-latency responses (SLRs). Here, we provide evidence that SLRs unmasked by cerebellar cortex lesions are mediated by an associative form of learning-induced plasticity in the anterior interpositus nucleus (AIN) of the cerebellum. We used pharmacological inactivation and/or electrical microstimulation of various sites afferent and efferent to the AIN to systematically eliminate alternative candidate sites of plasticity upstream or downstream from this structure. Collectively, the results suggest that cerebellar learning is mediated in part by plasticity in target nuclei downstream of the cerebellar cortex. These data demonstrate an instance in which an aspect of associative learning, SLRs, can be used as an index of plasticity at a specific site in the brain.