Distribution of the ω-conotoxin receptor in rat brain. An autoradiographic mapping
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The organ-protective effect of N-type Ca<sup>2+</sup> channel blockade
2015, Pharmacology and TherapeuticsCitation Excerpt :Among the 10 different genes encoding α1 subunits, which include α1A, α1B, α1C, α1D, α1E, α1F, α1G, α1H, α1I and α1S, CACNA1B encodes the α1B subunit, which comprises the NCC (Y. Fujita et al., 1993; Williams et al., 1992). The α1B subunit is expressed widely in the nervous system, as suggested by experiments using ω-CTX- GVIA (Takemura et al., 1989; Mills et al., 1994; Whorlow et al., 1996). Although ω-CTX-GVIA has been used to elucidate physiological function of NCCs, ω-CTX-GVIA is a relatively large polypeptide whose distribution in tissue is somewhat limited, and it also appears to inhibit certain neuronal LCCs (Aosaki & Kasai, 1989; Williams et al., 1992).
Antinociceptive effects of the marine snail peptides conantokin-G and conotoxin MVIIA alone and in combination in rat models of pain
2009, NeuropharmacologyCitation Excerpt :Similar to antagonism of pre-synaptic central terminal NMDA receptors, block of pre-synaptic N-type Ca2+ channels inhibits transmitter release and decreases spinal cord tissue pathology due to ischemia (Burns et al., 1999; Smith et al., 2002). Also, N-type Ca2+ channel blockers applied to post-synaptic dorsal horn neurons in rat models of chronic pain reduce spontaneous activity and abnormal responses to peripheral stimuli (Heinke et al., 2004; Matthews and Dickenson, 2001; Takemura et al., 1989; Vanegas and Schaible, 2000; Yusaf et al., 2001). Blocking other Ca2+ channel subtypes, such as P/Q- and L-type, in the spinal cord has little effect on chronic pain behavior (Chaplan et al., 1994b).
Expression of voltage-dependent calcium channels in the embryonic rat midbrain
2002, Developmental Brain ResearchAutoradiographic localization of N-type VGCCs in gerbil hippocampus and failure of ω-conotoxin MVIIA to attenuate neuronal injury after transient cerebral ischemia
2001, Brain ResearchCitation Excerpt :Our experimental approach was to precisely localize and quantitate the density of N-type VGCCs in gerbil hippocampus and to evaluate in finer detail ω-MVIIA neuroprotective effects using the gerbil model of global ischemia. Using high-resolution receptor autoradiography, we show a different N-type VGCC density profile in hippocampus than previously described [25,42]. In the course of our experiments, however, we found that ω-MVIIA failed to attenuate CA1 hippocampal injury after 5 min of global ischemia.