ω-Agatoxin IVA identifies a single calcium channel subtype which contributes to the potassium-induced release of acetylcholine, 5-hydroxytryptamine, dopamine, γ-aminobutyric acid and glutamate from rat brain slices

Harvey, Janette; Wedley, Susan; Findlay, Jeremy; Sidell, Mark R.; Pullar, Ian A.

doi:10.1016/0028-3908(96)00010-x

Cited by 38 publications

(22 citation statements)

References 35 publications

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“…However, electrophysiological evidence suggests that neuronal transmission in a variety of synapses is controlled by more than one type of Ca 2+ -channel (Takahashi & Momiyama, 1993). Furthermore, pharmacological studies have demonstrated that neurotransmission in a variety of synapses, including glutamatergic corticostriatal synapses, is controlled by more than one Ca 2+ -channel Graham & Burgoyne, 1995;Huston et al, 1995;Ambrosio et al, 1996;Harvey et al, 1996). Indeed, the IC 50 value of 330 nM obtained by Kimura et al (1995) may suggest a loss of selectivity of oaga-IVA for P-type channels and an action on Q-type channels Randall & Tsien, 1995).…”

Section: O-aga-iva-sensitive Glutamate Releasementioning

confidence: 99%

Control of glutamate release by calcium channels and κ‐opioid receptors in rodent and primate striatum

Hill¹,

Brotchie²

1999

British J Pharmacology

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1 The modulation of depolarization (4-aminopyridine, 2 mM)-evoked endogenous glutamate release by k-opioid receptor activation and blockade of voltage-dependent Ca 2+ -channels has been investigated in synaptosomes prepared from rat and marmoset striatum. 2 4-Aminopyridine (4-AP)-stimulated, Ca 2+ -dependent glutamate release was inhibited by enadoline, a selective k-opioid receptor agonist, in a concentration-dependent and norbinaltorphimine (nor-BNI, selective k-opioid receptor antagonist)-sensitive manner in rat (IC 50 =4.4+0.4 mM) and marmoset (IC 50 =2.9+0.7 mM) striatal synaptosomes. However, in the marmoset, there was a signi®cant (&23%) nor-BNI-insensitive component. -channels in the marmoset. 6 In conclusion, the results presented suggest that there are species dierences in the control of glutamate release by k-opioid receptors and Ca 2+ -channels.

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Section: O-aga-iva-sensitive Glutamate Releasementioning

confidence: 99%

Control of glutamate release by calcium channels and κ‐opioid receptors in rodent and primate striatum

Hill¹,

Brotchie²

1999

British J Pharmacology

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“…depolarization)-evoked neuronal catecholamine release (Hirota et al 2000b;Harvey et al 1996), we showed that K + -evoked glutamate release was dependent on [K + ]. Miao et al (1995Miao et al ( , 1998 have demonstrated a K + depolarizationinduced increase in intracellular Ca 2+ resulting from Ca 2+ influx through VSCCs, and that K + -evoked glutamate release is related linearly to intracellular Ca 2+ .…”

Section: Discussionmentioning

confidence: 78%

“…Similarly, in a previous study dopamine and noradrenaline release from rat striatal slices is blocked partially by N-type VSCC blockers, but more markedly so by ω-agatoxin IV A and ω-conotoxin MVII C (Hirota et al 2000b). Harvey et al (1996) have also shown that K + -evoked glutamate release is inhibited substantially by ω-agatoxin IV A and ω-conotoxin MVII C , but not by ω-conotoxin GVI A . These data indicate that glutamate release may be mediated predominantly through P/Q-type VSCCs.…”

Section: Discussionmentioning

confidence: 93%

“…Miao et al (1995Miao et al ( , 1998 have demonstrated a K + depolarizationinduced increase in intracellular Ca 2+ resulting from Ca 2+ influx through VSCCs, and that K + -evoked glutamate release is related linearly to intracellular Ca 2+ . Moreover, Harvey et al (1996) have reported that the response to K + differs for each neurotransmitter, but that K + -evoked dopamine, acetylcholine, serotonin or glutamate release from brain slices is mediated predominantly through VSCCs and is at least 85% dependent on extracellular Ca 2+ . In the present study, K + evoked-glutamate release was inhibited completely by Cd 2+ and ω-conotoxin MVII C , and substantially reduced by ω-agatoxin IV A .…”

Section: Discussionmentioning

confidence: 98%

“…In addition, evidence suggests that glutamate receptors and transmission may also be involved in the mechanism of general anaesthetic action (Miao et al 1995(Miao et al , 1998Buggy et al 2000). For instance, Miao et al (1995Miao et al ( , 1998 have reported that K + -evoked glutamate release is Ca 2+ dependent and mediated through VSCCs and Harvey et al (1996) have shown that ω-agatoxin IV A and ω-conotoxin MVII C inhibit K + -evoked glutamate release from rat cortical and striatal slices. In addition, several reports have suggested a link between VSCCs and GABA A receptors (Hansen et al 1992;Heidelberger and Mathews 1991).…”

Section: Masatou Kitayama · Kazuyoshi Hirota · Mihoko Kudo · Tsuyoshimentioning

confidence: 98%

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Inhibitory effects of intravenous anaesthetic agents on K + -evoked glutamate release from rat cerebrocortical slices. Involvement of voltage-sensitive Ca 2+ channels and GABA A receptors

Kitayama

Hirota

Kudo

et al. 2002

Naunyn-Schmiedeberg's Archives of Pharmacology

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It is widely accepted that most general anaesthetic agents depress the central nervous system (CNS) by potentiation or activation of the GABA(A) receptor-mediated Cl(-) conductance. These agents also reportedly inhibit voltage-sensitive Ca(2+) channels (VSCCs), thus depressing excitatory transmission in the CNS. However, in this regard there are few functional data at the level of neurotransmitter release. In this study we examined the effects of VSCC antagonists and a range of intravenous anaesthetic agents on K(+)(40 mM)-evoked glutamate release from rat cerebrocortical slices in the absence and presence of the GABA(A) receptor antagonist bicuculline (100 microM). We employed both selective and non-selective VSCC antagonists, the anaesthetic barbiturates thiopental, pentobarbital and phenobarbital, the non-anaesthetic barbiturate barbituric acid, the non-barbiturate anaesthetics alphaxalone, propofol and ketamine and the GABA(A) receptor agonist, muscimol. Glutamate released into the incubation medium was determined by a glutamate dehydrogenase-coupled assay. Omega-agatoxin IV(A) (P-type VSCC), omega-conotoxin MVII(C) (P/Q-type VSCC) and Cd(2+) (non-selective) essentially abolished glutamate release whilst nifedipine (L-type VSCC) and omega-conotoxin GVI(A) (N-type VSCC) reduced release by less than 30%. The concentrations producing 50% of the maximum inhibition (IC(50)) for thiopental, pentobarbital, phenobarbital, alphaxalone, propofol and ketamine were (in microM) 8.3, 22, 112, 6.3, 83 and 120, respectively. Barbituric acid produced a small (about 20%) inhibition. With the exception of ketamine, the IC(50) values for these anaesthetic agents were increased threefold by bicuculline (100 microM). In addition, muscimol significantly inhibited release by 26% with an IC(50) of 1.1 microM. In summary, a range of anaesthetic agents at clinically achievable concentrations inhibit glutamate release and this inhibition of release appears to be due mainly to direct inhibition of P/Q-type VSCCs, although activation of the GABA(A) receptor plays a role in this response.

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Activation of 5‐HT_1B/1D receptor in the periaqueductal gray inhibits nociception

Bartsch

Knight

Goadsby

2004

Annals of Neurology

175

120

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It is considered that the site of action of the abortive antimigraine compounds acting at serotonin, 5-HT(1B/1D,) receptors (triptans) is the trigeminovascular system. We tested whether there is a non-trigeminal site of action. The 5-HT(1B/1D) agonist, naratriptan, was microinjected into the ventrolateral periaqueductal gray (vlPAG), and activity in the trigeminal nucleus caudalis (TNC) was monitored. Recordings were made from 20 nociceptive neurons in the dorsal horn of the TNC that received convergent input from the dura mater and face. Responses of neurons to dural, facial cutaneous and corneal stimulation were studied before and after injection of naratriptan. Naratriptan decreased the excitability to electrical stimulation of the dura mater as the A-fiber response decreased by 24 +/- 4.1% (p < 0.001) and the C-fiber response decreased by 42 +/- 8.2% (p < 0.001). Spontaneous activity was decreased by 38 +/- 7.5% (p < 0.001). After injection, the mechanical thresholds of the dura mater increased from (n = 14, p < 0.01). Responses to stimulation of the face and cornea were not altered by injection of naratriptan. These results suggest that 5-HT(1B/1D) receptor activation in the vlPAG activates descending pain-modulating pathways that inhibit dural, but not facial and corneal nociceptive input. These findings have implications for the understanding of the action of triptans in migraine and cluster headache, suggesting that brain loci other than the trigeminal nucleus may play a role in the clinical action of triptans.

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ω-Agatoxin IVA identifies a single calcium channel subtype which contributes to the potassium-induced release of acetylcholine, 5-hydroxytryptamine, dopamine, γ-aminobutyric acid and glutamate from rat brain slices

Cited by 38 publications

References 35 publications

Control of glutamate release by calcium channels and κ‐opioid receptors in rodent and primate striatum

Control of glutamate release by calcium channels and κ‐opioid receptors in rodent and primate striatum

Inhibitory effects of intravenous anaesthetic agents on K + -evoked glutamate release from rat cerebrocortical slices. Involvement of voltage-sensitive Ca 2+ channels and GABA A receptors

Activation of 5‐HT_1B/1D receptor in the periaqueductal gray inhibits nociception

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ω-Agatoxin IVA identifies a single calcium channel subtype which contributes to the potassium-induced release of acetylcholine, 5-hydroxytryptamine, dopamine, γ-aminobutyric acid and glutamate from rat brain slices

Cited by 38 publications

References 35 publications

Control of glutamate release by calcium channels and κ‐opioid receptors in rodent and primate striatum

Control of glutamate release by calcium channels and κ‐opioid receptors in rodent and primate striatum

Inhibitory effects of intravenous anaesthetic agents on K + -evoked glutamate release from rat cerebrocortical slices. Involvement of voltage-sensitive Ca 2+ channels and GABA A receptors

Activation of 5‐HT1B/1D receptor in the periaqueductal gray inhibits nociception

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Activation of 5‐HT_1B/1D receptor in the periaqueductal gray inhibits nociception