N-type calcium channel

N-type calcium channel
Calcium channel, voltage-dependent, N type, alpha 1B subunit
Symbols CACNA1B; BIII; CACNL1A5; CACNN; Cav2.2
External IDs OMIM601012 MGI88296 HomoloGene20184 IUPHAR: Cav2.2 GeneCards: CACNA1B Gene
Species Human Mouse
Entrez 774 12287
Ensembl ENSG00000148408 ENSMUSG00000004113
UniProt Q00975 O55017
RefSeq (mRNA) NM_000718 NM_007579
RefSeq (protein) NP_000709 NP_031605
Location (UCSC) Chr 9:
140.77 – 141.02 Mb
Chr 2:
24.46 – 24.62 Mb
PubMed search [1] [2]
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. Like the others of this class, 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[1] which in humans is encoded by the CACNA1B gene.[2][3][4]



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 neurotransmitter release.[5] 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.[1]

Therapeutic Potential

Recently, blockade of the N-type calcium channel has emerged as a potential therapeutic strategy for the treatment of alcoholism.[6][7]



  1. ^ a b Williams ME, Brust PF, Feldman DH, Patthi S, Simerson S, Maroufi A, McCue AF, Veliçelebi G, Ellis SB, Harpold MM (July 1992). "Structure and functional expression of an omega-conotoxin-sensitive human N-type calcium channel". Science 257 (5068): 389–95. doi:10.1126/science.1321501. PMID 1321501. 
  2. ^ "Entrez Gene: CACNA1B calcium channel, voltage-dependent, N type, alpha 1B subunit". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=774. 
  3. ^ Diriong S, Lory P, Williams ME, Ellis SB, Harpold MM, Taviaux S (December 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. 
  4. ^ Catterall WA, Perez-Reyes E, Snutch TP, Striessnig J (December 2005). "International Union of Pharmacology. XLVIII. Nomenclature and structure-function relationships of voltage-gated calcium channels". Pharmacol. Rev. 57 (4): 411–25. doi:10.1124/pr.57.4.5. PMID 16382099. 
  5. ^ Kurihara T, Tanabe T (April 2003). "N-type Ca2+ channel". Nippon Yakurigaku Zasshi. Folia Pharmacologica Japonica 121 (4): 211–22. PMID 12777840. http://joi.jlc.jst.go.jp/JST.JSTAGE/fpj/121.211?lang=en&from=PubMed. 
  6. ^ a b Newton PM, Zeng L, Wang V, Connolly J, Wallace MJ, Kim C, Shin HS, Belardetti F, Snutch TP, Messing RO (November 2008). "A blocker of N- and T-type voltage-gated calcium channels attenuates ethanol-induced intoxication, place preference, self-administration, and reinstatement". J. Neurosci. 28 (45): 11712–9. doi:10.1523/JNEUROSCI.3621-08.2008. PMID 18987207. Lay summary – Pychology Today. 
  7. ^ Newton PM, Messing RO (2009). "The N-type calcium channel is a novel target for treating alcohol use disorders". Channels (Austin) 3 (2): 77–81. PMID 19372737. 

Further reading

External links

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