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Long-term depression and other synaptic plasticity in the cerebellum.

Hirano T - Proc. Jpn. Acad., Ser. B, Phys. Biol. Sci. (2013)

Bottom Line: LTD occurs at excitatory synapses between parallel fibers and a Purkinje cell in the cerebellar cortex, and is expressed as reduced responsiveness to transmitter glutamate.In vivo experiments including those on mutant mice, have reported good correlation of LTD and motor learning.A possibility that cerebellar synaptic plasticity other than LTD compensates for the defective LTD has been proposed.

View Article: PubMed Central - PubMed

Affiliation: Department of Biophysics, Graduate School of Science, Kyoto University, Kyoto, Japan. thirano@neurosci.biophys.kyoto-u.ac.jp

ABSTRACT
Cerebellar long-term depression (LTD) is a type of synaptic plasticity and has been considered as a critical cellular mechanism for motor learning. LTD occurs at excitatory synapses between parallel fibers and a Purkinje cell in the cerebellar cortex, and is expressed as reduced responsiveness to transmitter glutamate. Molecular induction mechanism of LTD has been intensively studied using culture and slice preparations, which has revealed critical roles of Ca(2+), protein kinase C and endocytosis of AMPA-type glutamate receptors. Involvement of a large number of additional molecules has also been demonstrated, and their interactions relevant to LTD mechanisms have been studied. In vivo experiments including those on mutant mice, have reported good correlation of LTD and motor learning. However, motor learning could occur with impaired LTD. A possibility that cerebellar synaptic plasticity other than LTD compensates for the defective LTD has been proposed.

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Neuronal circuits regulating vestibulo-ocular reflex.
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fig05: Neuronal circuits regulating vestibulo-ocular reflex.

Mentions: Contribution of LTD to motor learning has been intensively studied in two models, adaptation of vestibulo-ocular reflex (VOR)1,14–16) and classical conditioning of eye blink response.17) VOR is a reflex to stabilize the visual image during head motion. Vestibular organs such as semi-circular canals detect head motion, and drive eye balls to move in the opposite direction of head motion so that the visual image becomes stable. The timing and amplitude of VOR needs to be fine-tuned so that it works adequately in daily life. The adaptation of VOR occurs when the eyeball motion fails to stabilize the visual image. Experimentally this condition is given by rotating a surrounding screen during the rotation of a head-fixed animal. When the screen is rotated in the same direction of an animal, the rotation of eyeballs gets smaller, and when the screen is rotated in the opposite direction of an animal, the rotation of eyeballs becomes larger. Such adaptive change of VOR has been regarded as a type of motor learning. In VOR a climbing fiber conveys the retinal slip information,75) which contributes to the LTD induction. Neuronal activity recording from a Purkinje cell in rabbits and monkeys showed VOR-related activities in the cerebellar flocculus,18,76–78) which constitutes a side pathway of VOR and regulates the timing and amplitude of the reflex (Fig. 5). There have been contradictory ideas about the importance of LTD in the VOR adaptation.15,16)


Long-term depression and other synaptic plasticity in the cerebellum.

Hirano T - Proc. Jpn. Acad., Ser. B, Phys. Biol. Sci. (2013)

Neuronal circuits regulating vestibulo-ocular reflex.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3722574&req=5

fig05: Neuronal circuits regulating vestibulo-ocular reflex.
Mentions: Contribution of LTD to motor learning has been intensively studied in two models, adaptation of vestibulo-ocular reflex (VOR)1,14–16) and classical conditioning of eye blink response.17) VOR is a reflex to stabilize the visual image during head motion. Vestibular organs such as semi-circular canals detect head motion, and drive eye balls to move in the opposite direction of head motion so that the visual image becomes stable. The timing and amplitude of VOR needs to be fine-tuned so that it works adequately in daily life. The adaptation of VOR occurs when the eyeball motion fails to stabilize the visual image. Experimentally this condition is given by rotating a surrounding screen during the rotation of a head-fixed animal. When the screen is rotated in the same direction of an animal, the rotation of eyeballs gets smaller, and when the screen is rotated in the opposite direction of an animal, the rotation of eyeballs becomes larger. Such adaptive change of VOR has been regarded as a type of motor learning. In VOR a climbing fiber conveys the retinal slip information,75) which contributes to the LTD induction. Neuronal activity recording from a Purkinje cell in rabbits and monkeys showed VOR-related activities in the cerebellar flocculus,18,76–78) which constitutes a side pathway of VOR and regulates the timing and amplitude of the reflex (Fig. 5). There have been contradictory ideas about the importance of LTD in the VOR adaptation.15,16)

Bottom Line: LTD occurs at excitatory synapses between parallel fibers and a Purkinje cell in the cerebellar cortex, and is expressed as reduced responsiveness to transmitter glutamate.In vivo experiments including those on mutant mice, have reported good correlation of LTD and motor learning.A possibility that cerebellar synaptic plasticity other than LTD compensates for the defective LTD has been proposed.

View Article: PubMed Central - PubMed

Affiliation: Department of Biophysics, Graduate School of Science, Kyoto University, Kyoto, Japan. thirano@neurosci.biophys.kyoto-u.ac.jp

ABSTRACT
Cerebellar long-term depression (LTD) is a type of synaptic plasticity and has been considered as a critical cellular mechanism for motor learning. LTD occurs at excitatory synapses between parallel fibers and a Purkinje cell in the cerebellar cortex, and is expressed as reduced responsiveness to transmitter glutamate. Molecular induction mechanism of LTD has been intensively studied using culture and slice preparations, which has revealed critical roles of Ca(2+), protein kinase C and endocytosis of AMPA-type glutamate receptors. Involvement of a large number of additional molecules has also been demonstrated, and their interactions relevant to LTD mechanisms have been studied. In vivo experiments including those on mutant mice, have reported good correlation of LTD and motor learning. However, motor learning could occur with impaired LTD. A possibility that cerebellar synaptic plasticity other than LTD compensates for the defective LTD has been proposed.

Show MeSH
Related in: MedlinePlus