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The Cerebellum

Erschienen in:

01.09.2008

Functional Crosstalk Between Cell-Surface and Intracellular Channels Mediated by Junctophilins Essential for Neuronal Functions

verfasst von: Sho Kakizawa, Shigeki Moriguchi, Atsushi Ikeda, Masamitsu Iino, Hiroshi Takeshima

Erschienen in: The Cerebellum | Ausgabe 3/2008

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Abstract

Junctophilins (JPs) contribute to the formation of junctional membrane complexes between the plasma membrane and the endoplasmic/sarcoplasmic reticulum, and provide a structural platform for channel communication during excitation–contraction coupling in muscle cells. In the brain, two neuronal JP subtypes are widely expressed in neurons. Recent studies have defined the essential role of neural JPs in the communication between cell-surface and intracellular channels, which modulates the excitability and synaptic plasticity of neurons in the cerebellum and hippocampus.

Pozzan T, Rizzuto R, Volpe P, Meldolesi J (1994) Molecular and cellular physiology of intracellular calcium stores. Physiol Rev 74:595–636PubMed

Berridge MJ (1998) Neuronal calcium signaling. Neuron 21:13–26PubMedCrossRef

Flucher BE (1992) Structural-analysis of muscle development—transverse tubules, sarcoplasmic-reticulum, and the triad. Dev Biol 154:245–260PubMedCrossRef

Tanabe T, Beam KG, Powell JA, Numa S (1988) Restoration of excitation–contraction coupling and slow calcium current in dysgenic muscle by dihydropyridine receptor complementary-DNA. Nature 336:134–139PubMedCrossRef

Takeshima H, Iino M, Takekura H, Nishi M, Kuno J, Minowa O et al (1994) Excitation–contraction uncoupling and muscular degeneration in mice lacking functional skeletal-muscle ryanodine-receptor gene. Nature 369:556–559PubMedCrossRef

Endo M (1985) Calcium release from sarcoplasmic-reticulum. Curr Top Membr Transp 25:181–230

Takekura H, Takeshima H, Nishimura S, Takahashi M, Tanabe T, Flockerzi V et al (1995) Coexpression in Cho cells of 2 muscle proteins involved in excitation–contraction coupling. J Muscle Res Cell Motil 16:465–480PubMedCrossRef

Suda N, Franzius D, Fleig A, Nishimura S, Bodding M, Hoth M et al (1997) Ca²⁺-induced Ca²⁺ release in Chinese hamster ovary (CHO) cells co-expressing dihydropyridine and ryanodine receptors. J Gen Physiol 109:619–631PubMedCrossRef

Franzini-Armstrong C, Pinconraymond M, Rieger F (1991) Muscle-fibers from dysgenic mouse in vivo lack a surface component of peripheral couplings. Dev Biol 146:364–376PubMedCrossRef

10.

Ikemoto T, Komazaki S, Takeshima H, Nishi M, Noda T, Iino M et al (1997) Functional and morphological features of skeletal muscle from mutant mice lacking both type 1 and type 3 ryanodine receptors. J Physiol-Lond 501:305–312PubMedCrossRef

11.

Takeshima H, Komazaki S, Nishi M, Iino M, Kangawa K (2000) Junctophilins: a novel family of junctional membrane complex proteins. Mol Cell 6:11–22PubMedCrossRef

12.

Ito K, Komazaki S, Sasamoto K, Yoshida M, Nishi M, Kitamura K et al (2001) Deficiency of triad junction and contraction in mutant skeletal muscle lacking junctophilin type 1. J Cell Biol 154:1059–1067PubMedCrossRef

13.

Nishi M, Sakagami H, Komazaki S, Kondo H, Takeshima H (2003) Coexpression of junctophilin type 3 and type 4 in brain. Mol Brain Res 118:102–110PubMedCrossRef

14.

Nishi M, Hashimoto K, Kuriyama K, Komazaki S, Kano M, Shibata S et al (2002) Motor discoordination in mutant mice lacking junctophilin type 3. Biochem Biophys Res Commun 292:318–324PubMedCrossRef

15.

Moriguchi S, Nishi M, Komazaki S, Sakagami H, Miyazaki T, Masumiya H et al (2006) Functional uncoupling between Ca²⁺ release and afterhyperpolarization in mutant hippocampal neurons lacking junctophilins. Proc Natl Acad Sci USA 103:10811–10816PubMedCrossRef

16.

Kakizawa S, Kishimoto Y, Hashimoto K, Miyazaki T, Furutani K, Shimizu H et al (2007) Junctophilin-mediated channel crosstalk essential for cerebellar synaptic plasticity. EMBO J 26:1924–1933PubMedCrossRef

17.

Konnerth A, Llano I, Armstrong CM (1990) Synaptic currents in cerebellar Purkinje-cells. Proc Natl Acad Sci USA 87:2662–2665PubMedCrossRef

18.

Ito M (2006) Cerebellar circuitry as a neuronal machine. Prog Neurobiol 78:272–303PubMedCrossRef

19.

Kano M, Hashimoto K, Watanabe M, Kurihara H, Offermanns S, Jiang HP et al (1998) Phospholipase C beta 4 is specifically involved in climbing fiber synapse elimination in the developing cerebellum. Proc Natl Acad Sci USA 95:15724–15729PubMedCrossRef

20.

Kakizawa S, Yamasaki M, Watanabe M, Kano M (2000) Critical period for activity-dependent synapse elimination in developing cerebellum. J Neurosci 20:4954–4961PubMed

21.

Kakizawa S, Yamada K, Iino M, Watanabe M, Kano M (2003) Effects of insulin-like growth factor I on climbing fibre synapse elimination during cerebellar development. Eur J Neurosci 17:545–554PubMedCrossRef

22.

Kakizawa S, Miyazaki T, Yanagihara D, Iino M, Watanabe M, Kano M (2005) Maintenance of presynaptic function by AMPA receptor-mediated excitatory postsynaptic activity in adult brain. Proc Natl Acad Sci USA 102:19180–19185PubMedCrossRef

23.

Hashimoto K, Kano M (2005) Postnatal development and synapse elimination of climbing fiber to Purkinje cell projection in the cerebellum. Neurosci Res 53:221–228PubMedCrossRef

24.

Schmolesky MT, Weber JT, De Zeeuw CI, Hansel C (2002) The making of a complex spike: ionic composition and plasticity. Ann NY Acad Sci 978(1):359–390PubMedCrossRef

25.

Pedarzani P, Mosbacher J, Rivard A, Cingolani LA, Oliver D, Stocker M et al (2001) Control of electrical activity in central neurons by modulating the gating of small conductance Ca²⁺-activated K⁺ channels. J Biol Chem 276:9762–9769PubMedCrossRef

26.

Knaus HG, Schwarzer C, Koch ROA, Eberhart A, Kaczorowski GJ, Glossmann H et al (1996) Distribution of high-conductance Ca²⁺-activated K⁺ channels in rat brain: targeting to axons and nerve terminals. J Neurosc 16:955–963

27.

Womack MD, Khodakhah K (2002) Characterization of large conductance Ca²⁺-activated K⁺ channels in cerebellar Purkinje neurons. Eur J Neurosci 16:1214–1222PubMedCrossRef

28.

Edgerton JR, Reinhart PH (2003) Distinct contributions of small and large conductance Ca²⁺-activated K⁺ channels to rat Purkinje neuron function. J Physiol-Lond 548:53–69PubMedCrossRef

29.

Kohler M, Hirschberg B, Bond CT, Kinzie JM, Marrion NV, Maylie J et al (1996) Small-conductance, calcium-activated potassium channels from mammalian brain. Science 273:1709–1714PubMedCrossRef

30.

Sailer CA, Kaufmann WA, Marksteiner J, Knaus HG (2004) Comparative immunohistochemical distribution of three small-conductance Ca²⁺-activated potassium channel subunits, SK1, SK2, and SK3 in mouse brain. Mol Cell Neurosci 26:458–469PubMedCrossRef

31.

Bond CT, Herson PS, Strassmaier T, Hammond R, Stackman R, Maylie J et al (2004) Small conductance Ca²⁺-activated K⁺ channel knock-out mice reveal the identity of calcium-dependent afterhyperpolarization currents. J Neurosci 24:5301–5306PubMedCrossRef

32.

Grunnet M, Jensen BS, Olesen SP, Klaerke DA (2001) Apamin interacts with all subtypes of cloned small-conductance Ca²⁺-activated K⁺ channels. Pflugers Archiv European Journal of Physiology 441:544–550PubMedCrossRef

33.

Linden DJ, Connor JA (1995) Long-term synaptic depression. Annu Rev Neurosci 18:319–357PubMedCrossRef

34.

Weber JT, De Zeeuw CI, Linden DJ, Hansel C (2003) Long-term depression of climbing fiber-evoked calcium transients in Purkinje cell dendrites. Proc Natl Acad Sci USA 100:2878–2883PubMedCrossRef

35.

Coesmans M, Weber JT, De Zeeuw CI, Hansel C (2004) Bidirectional parallel fiber plasticity in the cerebellum under climbing fiber control. Neuron 44:691–700PubMedCrossRef

36.

Ikeda A, Miyazaki T, Kakizawa S, Okuno Y, Tsuchiya S, Myomoto A et al (2007) Abnormal features in mutant cerebellar Purkinje cells lacking junctophilins. Biochem Biophys Res Commun 363:835–839PubMedCrossRef

37.

Verkhratsky A (2002) The endoplasmic reticulum and neuronal calcium signalling. Cell Calcium 32:393–404PubMedCrossRef

38.

Rose CR, Konnerth A (2001) Stores not just for storage: intracellular calcium release and synaptic plasticity. Neuron 31:519–522PubMedCrossRef

39.

Bardo S, Cavazzini MG, Emptage N (2006) The role of the endoplasmic reticulum Ca²⁺ store in the plasticity of central neurons. Trends Pharmacol Sci 27:78–84PubMedCrossRef

40.

Finch EA, Augustine GJ (1998) Local calcium signalling by inositol-1,4, 5-trisphosphate in Purkinje cell dendrites. Nature 396:753–756PubMedCrossRef

41.

Takechi H, Eilers J, Konnerth A (1998) A new class of synaptic response involving calcium release in dendritic spines. Nature 396:757–760PubMedCrossRef

42.

Kano M, Garaschuk O, Verkhratsky A, Konnerth A (1995) Ryanodine receptor-mediated intracellular calcium-release in rat cerebellar Purkinje neurons. J Physiol-Lond 487:1–16PubMed

43.

Garaschuk O, Yaari Y, Konnerth A (1997) Release and sequestration of calcium by ryanodine-sensitive stores in rat hippocampal neurones. J Physiol-Lond 502:13–30PubMedCrossRef

44.

Llano I, Dipolo R, Marty A (1994) Calcium-induced calcium-release in cerebellar Purkinje-cells. Neuron 12:663–673PubMedCrossRef

45.

Verkhratsky A (2005) Physiology and pathophysiology of the calcium store in the endoplasmic reticulum of neurons. Physiol Rev 85:201–279PubMedCrossRef

46.

Furuichi T, Furutama D, Hakamata Y, Nakai J, Takeshima H, Mikoshiba K (1994) Multiple types of ryanodine receptor Ca²⁺ release channels are differentially expressed in rabbit brain. J Neurosci 14:4794–4805PubMed

47.

Furuichi T, Simonchazottes D, Fujino I, Yamada N, Hasegawa M, Miyawaki A et al (1993) Widespread expression of inositol 1,4,5-trisphosphate receptor type-1 gene (Insp3r1) in the mouse central-nervous-system. Recept Channels 1:11–24PubMed

48.

Inoue T, Kato K, Kohda K, Mikoshiba K (1998) Type 1 inositol 1,4,5-trisphosphate receptor is required for induction of long-term depression in cerebellar Purkinje neurons. J Neurosci 18:5366–5373PubMed

49.

Miyata M, Finch EA, Khiroug L, Hashimoto K, Hayasaka S, Oda SI et al (2000) Local calcium release in dendritic spines required for long-term synaptic depression. Neuron 28:233–244PubMedCrossRef

50.

Furutani K, Okubo Y, Kakizawa S, Iino M (2006) Postsynaptic inositol 1,4,5-trisphosphate signaling maintains presynaptic function of parallel fiber-Purkinje cell synapses via BDNF. Proc Natl Acad Sci USA 103:8528–8533PubMedCrossRef

51.

Kohda K, Inoue T, Mikoshiba K (1995) Ca²⁺ release from Ca²⁺ stores, particularly from ryanodine-sensitive Ca²⁺ stores, is required for the induction of Ltd in cultured cerebellar Purkinje-cells. J Neurophysiol 74:2184–2188PubMed

52.

Iino M (1990) Biphasic Ca²⁺ dependence of inositol 1,4,5-trisphosphate-induced Ca release in smooth-muscle cells of the guinea-pig taenia ceci. J Gen Physiol 95:1103–1122PubMedCrossRef

53.

Bezprozvanny I, Watras J, Ehrlich BE (1991) Bell-shaped calcium-response curves of Ins(1,4,5)P3-gated and calcium-gated channels from endoplasmic-reticulum of cerebellum. Nature 351:751–754PubMedCrossRef

54.

Wang SSH, Denk W, Hausser M (2000) Coincidence detection in single dendritic spines mediated by calcium release. Nat Neurosci 3:1266–1273PubMedCrossRef

Titel: Functional Crosstalk Between Cell-Surface and Intracellular Channels Mediated by Junctophilins Essential for Neuronal Functions
verfasst von: Sho Kakizawa
Shigeki Moriguchi
Atsushi Ikeda
Masamitsu Iino
Hiroshi Takeshima
Publikationsdatum: 01.09.2008
Verlag: Springer-Verlag
Erschienen in: The Cerebellum / Ausgabe 3/2008
Print ISSN: 1473-4222
Elektronische ISSN: 1473-4230
DOI: https://doi.org/10.1007/s12311-008-0040-1

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