1997
DOI: 10.1002/(sici)1097-4547(19970401)48:1<43::aid-jnr4>3.0.co;2-e
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Pharmacological characterisation of voltage-sensitive calcium channels and neurotransmitter release from mouse cerebellar granule cells in culture

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Cited by 12 publications
(6 citation statements)
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“…On the other hand Corvol et al [15] reported that CNQX and MK 801 did not alter the depolarization-induced phosphorylation of ERK in similar slices, perhaps reflecting that the tissue had been pre-incubated for 45 min in an artificial cerebrospinal solution before the K + -induced depolarization. Moreover, tetrodotoxin had been added to the incubation solution, which may have reduced any potential glutamate release [23]. The observed ability of depolarization to cause a glutamate-independent ERK phosphorylation is consistent with the present findings.…”
Section: Discussionsupporting
confidence: 92%
“…On the other hand Corvol et al [15] reported that CNQX and MK 801 did not alter the depolarization-induced phosphorylation of ERK in similar slices, perhaps reflecting that the tissue had been pre-incubated for 45 min in an artificial cerebrospinal solution before the K + -induced depolarization. Moreover, tetrodotoxin had been added to the incubation solution, which may have reduced any potential glutamate release [23]. The observed ability of depolarization to cause a glutamate-independent ERK phosphorylation is consistent with the present findings.…”
Section: Discussionsupporting
confidence: 92%
“…First, we investigated whether the loss of P/Q-type channel would affect the properties of GC action potential firing in postnatal 3-4 week old adolescent mice. Although P/Q-type channel is responsible for 40-50% of the total somatic Ca 2+ current in cultured GCs (Mintz et al, 1992; Pearson et al, 1995; Randall and Tsien, 1995; Doroshenko et al, 1997; Varming et al, 1997), the loss of P/Q-type channels in GCs does not lead to any change in action potential firing property in response to current injection, suggesting that P/Q-type channel do not contribute importantly to the firing property of mature GCs (Fig. 7F, G).…”
Section: Resultsmentioning
confidence: 99%
“…P/Q-type channel is responsible for 40-50% of the total somatic Ca 2+ current in cultured GCs (Mintz et al, 1992; Pearson et al, 1995; Randall and Tsien, 1995; Doroshenko et al, 1997; Varming et al, 1997) and is the major Ca 2+ channel at PF-PC synapse, along with some contribution of N-type and residual-type Ca 2+ channels (Mintz et al, 1995; Empson and Knopfel, 2010; Myoga and Regehr, 2011). A reduction in P/Q-type channels and/or a change in the contribution of other Ca 2+ channels at the presynaptic terminal would result in alteration of synaptic transmission and its profile of short-term synaptic plasticity (Catterall and Few, 2008; Neher and Sakaba, 2008).…”
Section: Resultsmentioning
confidence: 99%
“…The effectiveness of different L-type specific antagonists varied. A saturating dose of the DHP nifedipine (100 M) (Varming et al 1997) reduced the current amplitude only by 21.8 Ϯ 7.3% (n ϭ 10). But another L-type channel blocker, the benzothiazepine (ϩ) diltiazem (100 M) (Kraus et al 1998) reduced the current by 51.3 Ϯ 9.1% (n ϭ 21).…”
Section: Pharmacological Identification Of the Voltage-gated Ca 2ϩ Cumentioning
confidence: 98%