Intrinsic plasticity complements long-term potentiation in parallel fiber input gain control in cerebellar Purkinje cells.

A. Belmeguenai, E. Hosy, F. Bengtsson, C. M. Pedroarena, C. Piochon, E. Teuling, Q. He, G. Ohtsuki, M. T. G. De Jeu, Y. Elgersma, C. I. De Zeeuw, H. Jorntell, C. Hansel
Journal of Neuroscience. 2010-10-13; 30(41): 13630-13643
DOI: 10.1523/jneurosci.3226-10.2010

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1. J Neurosci. 2010 Oct 13;30(41):13630-43. doi: 10.1523/JNEUROSCI.3226-10.2010.

Intrinsic plasticity complements long-term potentiation in parallel fiber input
gain control in cerebellar Purkinje cells.

Belmeguenai A(1), Hosy E, Bengtsson F, Pedroarena CM, Piochon C, Teuling E, He Q,
Ohtsuki G, De Jeu MT, Elgersma Y, De Zeeuw CI, Jörntell H, Hansel C.

Author information:
(1)Department of Neuroscience, Erasmus University Medical Center, Rotterdam, The

Synaptic gain control and information storage in neural networks are mediated by
alterations in synaptic transmission, such as in long-term potentiation (LTP).
Here, we show using both in vitro and in vivo recordings from the rat cerebellum
that tetanization protocols for the induction of LTP at parallel fiber
(PF)-to-Purkinje cell synapses can also evoke increases in intrinsic
excitability. This form of intrinsic plasticity shares with LTP a requirement for
the activation of protein phosphatases 1, 2A, and 2B for induction. Purkinje cell
intrinsic plasticity resembles CA1 hippocampal pyramidal cell intrinsic
plasticity in that it requires activity of protein kinase A (PKA) and casein
kinase 2 (CK2) and is mediated by a downregulation of SK-type calcium-sensitive K
conductances. In addition, Purkinje cell intrinsic plasticity similarly results
in enhanced spine calcium signaling. However, there are fundamental differences:
first, while in the hippocampus increases in excitability result in a higher
probability for LTP induction, intrinsic plasticity in Purkinje cells lowers the
probability for subsequent LTP induction. Second, intrinsic plasticity raises the
spontaneous spike frequency of Purkinje cells. The latter effect does not impair
tonic spike firing in the target neurons of inhibitory Purkinje cell projections
in the deep cerebellar nuclei, but lowers the Purkinje cell signal-to-noise
ratio, thus reducing the PF readout. These observations suggest that intrinsic
plasticity accompanies LTP of active PF synapses, while it reduces at weaker,
nonpotentiated synapses the probability for subsequent potentiation and lowers
the impact on the Purkinje cell output.

DOI: 10.1523/JNEUROSCI.3226-10.2010
PMCID: PMC2968711
PMID: 20943904 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus