N-type calcium channel

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Available structures
PDB Ortholog search: PDBe RCSB
Aliases CACNA1B, BIII, CACNL1A5, CACNN, Cav2.2, DYT23, calcium voltage-gated channel subunit alpha1 B
External IDs OMIM: 601012 MGI: 88296 HomoloGene: 20184 GeneCards: 774
Species Human Mouse
RefSeq (mRNA)



RefSeq (protein)



Location (UCSC) Chr 9: 137.88 – 138.12 Mb Chr 2: 24.6 – 24.76 Mb
PubMed search [1] [2]
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Illustration of the major elements in a prototypical synapse. Synapses allow nerve cells to communicate with one another through axons and dendrites, converting electrical impulses into chemical signals.
Neuron A (transmitting) to neuron B (receiving)
  • 1. Mitochondrion
  • 2. Synaptic vesicle with neurotransmitters
  • 3. Autoreceptor
  • 4. Synapse with neurotransmitter released (serotonin)
  • 5. Postsynaptic receptors activated by neuro-transmitter (induction of a postsynaptic potential)
  • 6. Calcium channel
  • 7. Exocytosis of a vesicle
  • 8. Recaptured neurotransmitter

The N-type calcium channel is a type of voltage-dependent calcium channel. As with other sub-types of voltage-gated calcium channel, the α1 subunit forms the pore through which calcium enters the cell and determines most of the channel's properties. The α1 subunit is also known as the calcium channel, voltage-dependent, N type, alpha 1B subunit (CACNA1B) or Cav2.2[3] which in humans is encoded by the CACNA1B gene.[4][5][6]

Clinical significance[edit]

Mutations in CACNA1B are associated to Myoclonus-Dystonia syndrome .[7]


In addition to the α1 subunit, the following subunits are present in the N-type calcium channel:


N-type ('N' for "Neural-Type" ) calcium channels are found primarily at presynaptic terminals and are involved in neurotransmission.[8] Strong depolarization by an action potential causes these channels to open and allow influx of Ca2+, initiating vesicle fusion and release of stored neurotransmitter. N-type channels are blocked by ω-conotoxin.[3]

Therapeutic Potential[edit]

Blockade of the N-type calcium channel is a potential therapeutic strategy for the treatment of alcoholism.[9][10] Blockade of N-type calcium channels in sensory neurons has therapeutic potential for the treatment of certain types of pain, particularly neuropathic pain. The peptide N-type calcium channel blocker ziconotide is given intrathecally for intractable pain.



  1. ^ "Human PubMed Reference:". 
  2. ^ "Mouse PubMed Reference:". 
  3. ^ a b Williams ME, Brust PF, Feldman DH, Patthi S, Simerson S, Maroufi A, McCue AF, Veliçelebi G, Ellis SB, Harpold MM (Jul 1992). "Structure and functional expression of an omega-conotoxin-sensitive human N-type calcium channel". Science. 257 (5068): 389–95. Bibcode:1992Sci...257..389W. doi:10.1126/science.1321501. PMID 1321501. 
  4. ^ "Entrez Gene: CACNA1B calcium channel, voltage-dependent, N type, alpha 1B subunit". 
  5. ^ Diriong S, Lory P, Williams ME, Ellis SB, Harpold MM, Taviaux S (Dec 1995). "Chromosomal localization of the human genes for alpha 1A, alpha 1B, and alpha 1E voltage-dependent Ca2+ channel subunits". Genomics. 30 (3): 605–9. doi:10.1006/geno.1995.1284. PMID 8825650. 
  6. ^ Catterall WA, Perez-Reyes E, Snutch TP, Striessnig J (Dec 2005). "International Union of Pharmacology. XLVIII. Nomenclature and structure-function relationships of voltage-gated calcium channels". Pharmacological Reviews. 57 (4): 411–25. doi:10.1124/pr.57.4.5. PMID 16382099. 
  7. ^ Groen JL, Andrade A, Ritz K, Jalalzadeh H, Haagmans M, Bradley TE, Jongejan A, Verbeek DS, Nürnberg P, Denome S, Hennekam RC, Lipscombe D, Baas F, Tijssen MA (Feb 2015). "CACNA1B mutation is linked to unique myoclonus-dystonia syndrome". Human Molecular Genetics. 24 (4): 987–93. doi:10.1093/hmg/ddu513. PMID 25296916. 
  8. ^ Kurihara T, Tanabe T (Apr 2003). "N-type Ca2+ channel". Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica. 121 (4): 211–22. doi:10.1254/fpj.121.211. PMID 12777840. 
  9. ^ a b Newton PM, Zeng L, Wang V, Connolly J, Wallace MJ, Kim C, Shin HS, Belardetti F, Snutch TP, Messing RO (Nov 2008). "A blocker of N- and T-type voltage-gated calcium channels attenuates ethanol-induced intoxication, place preference, self-administration, and reinstatement". The Journal of Neuroscience. 28 (45): 11712–9. doi:10.1523/JNEUROSCI.3621-08.2008. PMC 3045811free to read. PMID 18987207. Lay summaryPsychology Today. 
  10. ^ Newton PM, Messing RO (2009). "The N-type calcium channel is a novel target for treating alcohol use disorders". Channels. 3 (2): 77–81. doi:10.4161/chan.3.2.8037. PMID 19372737. 
  11. ^ Vega-Hernández A, Felix R (Apr 2002). "Down-regulation of N-type voltage-activated Ca2+ channels by gabapentin". Cellular and Molecular Neurobiology. 22 (2): 185–90. PMID 12363200. 
  12. ^ Lukyanetz EA, Shkryl VM, Kostyuk PG (Jan 2002). "Selective blockade of N-type calcium channels by levetiracetam". Epilepsia. 43 (1): 9–18. doi:10.1046/j.1528-1157.2002.24501.x. PMID 11879381. 
  13. ^ Wang SJ, Huang CC, Hsu KS, Tsai JJ, Gean PW (Nov 1996). "Inhibition of N-type calcium currents by lamotrigine in rat amygdalar neurones". NeuroReport. 7 (18): 3037–40. doi:10.1097/00001756-199611250-00048. PMID 9116235. 
  14. ^ Li SN, Bräter M, Andreas K (Feb 1999). "Nicardipine inhibits N-type calcium channels in dbcAMP-differentiated neuroblastoma x glioma hybrid cells (NG 108-15 cells)". Acta Pharmacologica Sinica. 20 (2): 117–120. PMID 10437156. 

Further reading[edit]

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