N-type calcium channel

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Calcium channel, voltage-dependent, N type, alpha 1B subunit
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols CACNA1B ; BIII; CACNL1A5; CACNN; Cav2.2; DYT23
External IDs OMIM601012 MGI88296 HomoloGene20184 IUPHAR: 533 ChEMBL: 4478 GeneCards: CACNA1B Gene
Orthologs
Species Human Mouse
Entrez 774 12287
Ensembl ENSG00000148408 ENSMUSG00000004113
UniProt Q00975 O55017
RefSeq (mRNA) NM_000718 NM_001042528
RefSeq (protein) NP_000709 NP_001035993
Location (UCSC) Chr 9:
137.88 – 138.12 Mb
Chr 2:
24.6 – 24.76 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. 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[1] which in humans is encoded by the CACNA1B gene.[2][3][4]

Clinical significance

Mutations in CACNA1B are associated to Myoclonus-Dystonia syndrome .[5]

Structure

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

Function

N-type ('N' for "Neural-Type" ) calcium channels are found primarily at presynaptic terminals and are involved in neurotransmission.[6] 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

Blockade of the N-type calcium channel is a potential therapeutic strategy for the treatment of alcoholism.[7][8] 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.

Blockers

References

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Further reading

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External links