Kappa 2 opioid receptors inhibit NMDA receptor-mediated synaptic currents in guinea pig CA3 pyramidal cells

Caudle, Robert M.; Chavkin, Charles; Dubner, Ronald

doi:10.1523/jneurosci.14-09-05580.1994

Cited by 76 publications

(35 citation statements)

References 43 publications

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“…On the basis of autoradiographic studies, it was reported that virtually no 1 receptor binding existed in the CA3 region of the guinea pig (Wagner et al, 1991(Wagner et al, , 1992; therefore, it was proposed that the receptor binding observed previously in s. lucidum (McLean et al, 1987) reflected the binding to 2 receptors (Caudle et al, 1994). Our electrophysiological results, however, suggest the presence of functional 1 receptors in the CA3 region.…”

Section: Discussioncontrasting

confidence: 43%

Characterizing the Site and Mode of Action of Dynorphin at Hippocampal Mossy Fiber Synapses in the Guinea Pig

et al. 1996

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Extracellular field potential recordings from the CA3 region in guinea pig hippocampal slices were used to study the release and action of dynorphin at the mossy fiber synapse. Dynorphin A(1-17) or U69593 inhibited mossy fiber synaptic responses in preparations in which the CA3 region was surgically isolated from the rest of the hippocampus. This inhibition was completely reversed by the 1 selective antagonist nor-BNI, thus establishing the presence of functional 1 receptors in CA3. Inhibitory effects of dynorphin on mossy fiber responses were unaltered in the presence of the N-or P-type Ca 2ϩ channel blockers, -CgTx or -Aga IVA, respectively. This indicates that the action of dynorphin is independent of the particular type of Ca 2ϩ channel that mediates transmitter release at the mossy fiber terminal. Heterosynaptic inhibition of mossy fiber responses was observed in the presence of nifedipine, -CgTx, or -Aga IVA, indicating that dynorphin release does not depend specifically on L-, N-, or P-type Ca 2ϩ channels. The blockade of heterosynaptic inhibition by the membranepermeant Ca 2ϩ chelator EGTA-AM suggests the involvement of a slow Ca 2ϩ -dependent process in dynorphin release. On the basis of a variety of experimental evidence, we propose that the time course of heterosynaptic inhibition is determined primarily by the time course of clearance of dynorphin in the extracellular space.

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Section: Discussioncontrasting

confidence: 43%

Characterizing the Site and Mode of Action of Dynorphin at Hippocampal Mossy Fiber Synapses in the Guinea Pig

et al. 1996

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“…Suramin and Reactive Blue 2 blocked both excitatory synaptic transmission to the pyramidal cells as well as the action of applied glutamate. A classical P2y-purinoceptor in the postsynaptic membrane may therefore modulate the glutamate receptors perhaps in a way similar to the modulation of these receptors by c2-opioid receptors (Caudle et al, 1994). Such a modulation may occur through several different mechanisms.…”

Section: Discussionmentioning

confidence: 98%

Effect of P₂‐purinoceptor antagonists on glutamatergic transmission in the rat hippocampus

Motin

Bennett

1995

British J Pharmacology

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1 A study has been made of the effects of P2-purinoceptor antagonists on the evoked excitatory postsynaptic currents (e.p.s.cs) generated in CAl pyramidal cells on stimulation of Schaffer collaterals and in CA3 pyramidal cells on stimulation of mossy fibres. The effects of these antagonists on currents generated in the cells on application of glutamate has also been determined. 2 Suramin blocked the evoked e.p.s.cs with an 50% inhibition (ID50) of 62 ± 8 Mm (mean±s.e.mean, n = 17), spontaneous miniature e.p.s.cs and the currents induced by application of 100 gM glutamate with an ID" = 121 ± 36 gM (n = 15) in all the cells studied.3 Reactive Blue 2 (RB-2) in a concentration of 200 gM decreased the e.p.s.cs by 80 10% (n = 6) and the glutamate-activated currents by 83 ± 3% (n = 6). 4 Pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) in the concentration-range of 40-500 gM decreased the amplitude of the e.p.s.cs in 12 out of 13 cells studied. PPADS at 200 gM reduced the amplitude of the e.p.s.cs by 60± 10% (n = 3). PPADS did not affect the glutamate-induced currents in 4 cells and produced potentiation of the current amplitude by 60± 10% in 4 other cells. 5 These results suggest that both presynaptic and postsynaptic P2-purinoceptors in the hippocampus can modulate the release and action of endogenous glutamate.

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“…Selective antagonists to the NMDAR completely block the effects of Dyn A in producing hindlimb paralysis, loss of tail-flick reflex, decrease in spinal cord blood flow and barrel-rolling [13, 14, 15, 16, 17]. At the cellular level, Dyn A 1-17 has been shown to have an excitatory action on NMDA-mediated synaptic currents in guinea pig hippocampus [18]. These findings suggest that Dyn may bind directly to the NMDAR to activate or potentiate its function.…”

Section: Discussionmentioning

confidence: 99%

Dynorphin Stimulates Corticotropin Release from Mouse Anterior Pituitary AtT-20 Cells through Nonopioid Mechanisms

Cheng

Birk²,

Gershengorn³

et al. 2000

Neuroendocrinology

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Dynorphin (Dyn) peptides were previously shown to increase plasma corticotropin (ACTH) in the ovine fetus, but the site of its action remains unclear. In the present study, Dyn A_1-17 was found to stimulate ACTH release from mouse anterior pituitary tumor AtT-20 cells in a dose-dependent manner. Naloxone did not block the effect of Dyn A_1-17 and the selective ĸ-opioid receptor agonist U50488H did not stimulate ACTH release. Dyn A_2-17, a degradative peptide fragment that does not bind to opioid receptors, also stimulated ACTH release from AtT-20 cells. Although the nonopioid effects of Dyn have previously been attributed to N-methyl-D-aspartate (NMDA) receptors, the ACTH-releasing effects of Dyn A_1-17 in AtT-20 cells were not affected by co-administration of NMDA receptor antagonist LY235959. The ACTH response to Dyn A_1-17 could not be blocked by α-helical CRH (CRH antagonist) and was additive with a maximal stimulatory dose of CRH, suggesting different mechanisms of action. These results show that the release of ACTH by Dyn A_1-17 in AtT-20 cells is not mediated by ĸ-opioid receptors or by the NMDA receptor.

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Kappa 2 opioid receptors inhibit NMDA receptor-mediated synaptic currents in guinea pig CA3 pyramidal cells

Cited by 76 publications

References 43 publications

Characterizing the Site and Mode of Action of Dynorphin at Hippocampal Mossy Fiber Synapses in the Guinea Pig

Characterizing the Site and Mode of Action of Dynorphin at Hippocampal Mossy Fiber Synapses in the Guinea Pig

Effect of P₂‐purinoceptor antagonists on glutamatergic transmission in the rat hippocampus

Dynorphin Stimulates Corticotropin Release from Mouse Anterior Pituitary AtT-20 Cells through Nonopioid Mechanisms

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Kappa 2 opioid receptors inhibit NMDA receptor-mediated synaptic currents in guinea pig CA3 pyramidal cells

Cited by 76 publications

References 43 publications

Characterizing the Site and Mode of Action of Dynorphin at Hippocampal Mossy Fiber Synapses in the Guinea Pig

Characterizing the Site and Mode of Action of Dynorphin at Hippocampal Mossy Fiber Synapses in the Guinea Pig

Effect of P2‐purinoceptor antagonists on glutamatergic transmission in the rat hippocampus

Dynorphin Stimulates Corticotropin Release from Mouse Anterior Pituitary AtT-20 Cells through Nonopioid Mechanisms

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Effect of P₂‐purinoceptor antagonists on glutamatergic transmission in the rat hippocampus