Biology Reference
In-Depth Information
Table 1
Summary of the pore-forming subunits of voltage-gated calcium channels
Chromosomal
localiszation
Type
Ca
v
name
Old name
Exemplary characteristic inhibitors
High voltage-activated calcium channels (HVA)
Ca
v
subfamily
L
L
L
L
Ca
v
1.1
Ca
v
1.2
Ca
v
1.3
Ca
v
1.4
α
1S
1q31-q32
12p13.3
3p14.3
Xp11.23s
L-type Ca
2+
channel blockers, such
as 1,4-dihydropyridines
(e.g., nifedipin), phenylalkylam-
ine (e.g., verapamil) or benzothi-
azepines (e.g., diltiazem)
α
1C
α
1D
α
1F
Ca
v
subfamily
P/Q
N
E/R
Ca
v
2.1
Ca
v
2.2
Ca
v
2.3
α
1A
19p13.1-q13.2
9q34
1q25-q31
ω
-Aga-IVA
α
1B
ω
-CgTx-GVIA
SNX-482
α
1E
Low voltage-activated calcium channels (LVA)
T
T
T
Ca
v
3.1
Ca
v
3.2
Ca
v
3.3
a1G
a1H
a1I
17q22
16p13.3
22q12.3-q13.2
a
a
Different antagonists, such as milbefradil, amilorid, or kurtoxin, have initially thought to be specifi c T-type
blocker, but they also antagonize other voltage-gated Ca
2+
currents. Divalent ions, such as Ni
2+
, were used to
identify T-type Ca
2+
currents, but they also block E/R-type and to a lower extent N-, P/Q-Ca
2+
channel
Ca
2+
channels contains the Ca
v
2 subfamily with the ion-conducting
subunit of the P/Q-type Ca
2+
channels (Ca
v
2.1), N-type Ca
2+
chan-
nels (Ca
v
2.2), and E-/R-type Ca
2+
channels (Ca
v
2.3). P/Q- and
N-type Ca
2+
channels exhibit a lower averaged conductance than
L-type Ca
2+
channels (about 9-19 pS respectively 12-20 pS) and
inactivate at lower membrane potentials. Electrophysiologically,
E-/R-type Ca
2+
channels have an interim position between high-
and low voltage-activated Ca
2+
channels. The three T-type (“T” for
tiny or transient) Ca
2+
channel subunits Ca
v
3.1 (
α
1G), Ca
v
3.2
(
1I) constitute the group of the low voltage-
activated Ca
2+
channels, which activate after a low voltage shift to
voltages more positive than −70 mV (
10-13
).
α
1H), and Ca
v
3.3 (
α
Molecular-biological studies support a central role of ion chan-
nels at the genesis of cerebral vasospasm following SAH, but how
they are involved remains complex and incomprehensive.
Evaluation of voltage-gated ion channels, especially of the role of
voltage-gated calcium channels, is critical for our understanding
of the molecular mechanisms underlying SAH-related cerebral
vasospasm and includes all forms of ion channel assessment.
Here, important implications of ion channel assessment should
be discussed against the background of the recent studies as well
as the what, why, where, when, and how to examine changes in
1.3. Aim of
This Chapter
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