Memory trace of motor learning shifts transsynaptically from cerebellar cortex to nuclei for consolidation

Shutoh, Fumihiro; Ohki, Masafumi; Kitazawa, Hiromasa; Itohara, Shigeyoshi; Nagao, Soichi

doi:10.1016/j.neuroscience.2005.12.035

Cited by 198 publications

(225 citation statements)

References 46 publications

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“…Interestingly, a more natural form of cerebellar learning such as VOR adaptation does not display robust savings (Miles and Lisberger, 1981), perhaps because mossy fiber synapses onto the vestibular nuclei already exist. Nonetheless, recent studies of VOR adaptation showing that the effects of reversible cerebellar cortex lesions depend on the amount of training are generally consistent with these findings, further underscoring the parallels between eyelid conditioning and VOR adaptation (Kassardjian et al, 2005;Shutoh et al, 2006).…”

Section: Functional Contributions Of Plasticity In the Ainsupporting

confidence: 60%

Learning-Induced Plasticity in Deep Cerebellar Nucleus

Ohyama¹,

Nores²,

Medina³

et al. 2006

J. Neurosci.

139

131

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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.

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Section: Functional Contributions Of Plasticity In the Ainsupporting

confidence: 60%

Learning-Induced Plasticity in Deep Cerebellar Nucleus

Ohyama¹,

Nores²,

Medina³

et al. 2006

J. Neurosci.

139

131

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“…5A shows that the daily gain changes ([end gain] Ϫ [start gain]) did not show significant differences between the WT and G-substrate knockout mice throughout 5 days (two-way repeated measures ANOVA: F 1, 13 ϭ 0.019, P ϭ 0.893). The increase in the daily gain recovered within 24 hr; however, the start gain before the 1-hr oscillation gradually increased at days 2-5 compared with the start gain at day 1, which we call long-term adaptation (30). Fig.…”

Section: Resultsmentioning

confidence: 78%

“…5B). This long-term adaptation is caused by a slowly developed potentiation of synaptic transmission or an intrinsic excitability in vestibular relay neurons (30). The partial impairment of long-term VOR adaptation was also reported to occur in Purkinje cell-specific PKGI-deficient mice with normal short-term adaptation (24).…”

Section: Discussionmentioning

confidence: 97%

“…OKR adaptation is an increase of OKR gain induced by continuous oscillation of a screen around a stationary animal and is abolished by gene knockout (28) or pharmacological inhibition of neural NOS (28,29). As very recently reported, OKR adaptation (30), as well as vestibulo-ocular reflex (VOR) adaptation (31), has 2 distinct phases underlain by different neural mechanisms. The shortterm adaptation occurring during 1 h of training has its memory site in the cerebellar cortex of the flocculus, whereas the long-term adaptation accumulated during repeated 5-day training sessions is an event that takes place somewhere else, because the latter is maintained even after a glutamate antagonist (31) or lidocaine (30) has blocked cerebellar cortical activity.…”

mentioning

confidence: 92%

“…The shortterm adaptation occurring during 1 h of training has its memory site in the cerebellar cortex of the flocculus, whereas the long-term adaptation accumulated during repeated 5-day training sessions is an event that takes place somewhere else, because the latter is maintained even after a glutamate antagonist (31) or lidocaine (30) has blocked cerebellar cortical activity. There is some evidence indicating that long-term OKR adaptation has its memory site in vestibular nuclear neurons (30).…”

mentioning

confidence: 99%

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Dual involvement of G-substrate in motor learning revealed by gene deletion

Endo

Shutoh²,

Dinh³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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In this study, we generated mice lacking the gene for G-substrate, a specific substrate for cGMP-dependent protein kinase uniquely located in cerebellar Purkinje cells, and explored their specific functional deficits. G-substrate-deficient Purkinje cells in slices obtained at postnatal weeks (PWs) 10 -15 maintained electrophysiological properties essentially similar to those from WT littermates. Conjunction of parallel fiber stimulation and depolarizing pulses induced long-term depression (LTD) normally. At younger ages, however, LTD attenuated temporarily at PW6 and recovered thereafter. In parallel with LTD, short-term (1 h) adaptation of optokinetic eye movement response (OKR) temporarily diminished at PW6. Young adult G-substrate knockout mice tested at PW12 exhibited no significant differences from their WT littermates in terms of brain structure, general behavior, locomotor behavior on a rotor rod or treadmill, eyeblink conditioning, dynamic characteristics of OKR, or short-term OKR adaptation. One unique change detected was a modest but significant attenuation in the long-term (5 days) adaptation of OKR. The present results support the concept that LTD is causal to short-term adaptation and reveal the dual functional involvement of G-substrate in neuronal mechanisms of the cerebellum for both short-term and long-term adaptation.cerebellum ͉ long-term depression ͉ optokinetic response ͉ Purkinje cell

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Cerebellar Plasticity

Ito

2012

Encyclopedia of Life Sciences

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The remarkable recuperative capability of the cerebellum to compensate for lesion‐induced functional deficits has long been known. A well‐studied example is the vestibular compensation that follows unilateral labyrinthectomy, involving the cerebellar flocculus. More recently, however, the implications of cerebellar plasticity have expanded to include changes induced experience‐dependently. Various forms of motor adaptation and motor learning in physiological ranges are included in this term. For example, the vestibuloocular reflex exhibits a marked cerebellum‐mediated adaptability to a change imposed on the visual–vestibular relationship. Many other reflexes and voluntary movements exhibit similar plasticity via respective areas of the cerebellum. Moreover, certain morphological changes have been noted to occur under behavioural and social impositions as evidence of a role of cerebellar plasticity at such a high level of control. These various forms of cerebellar plasticity appear to be triggered by performance errors, which provoke synaptic plasticity in neuronal circuits of the cerebellum. Key Concepts: In general terms, plasticity implies the capability of the nervous system to change its structure and function to adapt to new bodily and environmental conditions. The history of research on the cerebellum contains rich cases of compensatory recovery that occurred after lesioning the cerebellum or other tissues of the brain and body, which represent cerebellar plasticity in the original sense. The notion of cerebellar plasticity has now been expanded to include physiological changes occurring in cerebellar neurons under certain functional and environmental impositions, broadly embracing various forms of motor adaptation and motor learning. The various forms of cerebellar plasticity appear to be commonly underlain by unique error‐learning mechanisms of cerebellar neuronal circuits based on plasticity at individual synapses (synaptic plasticity).

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Memory trace of motor learning shifts transsynaptically from cerebellar cortex to nuclei for consolidation

Cited by 198 publications

References 46 publications

Learning-Induced Plasticity in Deep Cerebellar Nucleus

Learning-Induced Plasticity in Deep Cerebellar Nucleus

Dual involvement of G-substrate in motor learning revealed by gene deletion

Cerebellar Plasticity

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