Behavioural and neurochemical interactions of the AMPA antagonist GYKI 52466 and the non-competitive NMDA antagonist dizocilpine in rats

1995 ◽  
Vol 101 (1-3) ◽  
pp. 115-126 ◽  
Author(s):  
M. Bubser ◽  
T. Tzschentke ◽  
W. Hauber
Keyword(s):  
Nmda Antagonist ◽  
Gyki 52466 ◽  
Ampa Antagonist

scholarly journals Synergism of the AMPA-antagonist NBQX and the NMDA-antagonist CPP with L-Dopa in models of Parkinson's disease

1991 ◽  
Vol 3 (3) ◽  
pp. 203-213 ◽  
Author(s):  
P. -A. Löschmann ◽  
K. W. Lange ◽  
M. Kunow ◽  
K. -J. Rettig ◽  
P. Jähnig ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nmda Antagonist ◽  
Ampa Antagonist

IN VITRO AND IN VIVO EFFECTS OF SOME NON-COMPETITIVE AMPA ANTAGONIST 2,3-BENZODIAZEPINES (GYKI 52466-HC1, 53405, 53655)

1996 ◽  
Vol 24 (4) ◽  
pp. 566S-566S ◽  
Author(s):  
A. D. Kovács ◽  
G. Gigler ◽  
Zs. Szücs ◽  
I. Gacsályi ◽  
T. Szabados ◽  
...  
Keyword(s):  
Gyki 52466 ◽  
Ampa Antagonist ◽  
In Vivo Effects

Nicotine-induced dopamine release in the nucleus accumbens is inhibited by the novel AMPA antagonist ZK200775 and the NMDA antagonist CGP39551

2004 ◽  
Vol 175 (1) ◽  
Author(s):  
AlexanderR. Kosowski ◽  
Gvido Cebers ◽  
Aleta Cebere ◽  
Ann-Charlott Swanhagen ◽  
Sture Liljequist
Keyword(s):  
Nucleus Accumbens ◽  
Dopamine Release ◽  
Nmda Antagonist ◽  
The Novel ◽  
Ampa Antagonist

scholarly journals Treatment with an AMPA Antagonist 12 Hours following Severe Normothermic Forebrain Ischemia Prevents CA1 Neuronal Injury

1993 ◽  
Vol 13 (6) ◽  
pp. 933-939 ◽  
Author(s):  
Hui Li ◽  
Alastair M. Buchan
Keyword(s):  
Nmda Receptor ◽  
Ampa Receptors ◽  
Wistar Rats ◽  
Neuronal Injury ◽  
Forebrain Ischemia ◽  
Neuroprotective Effects ◽  
Mk 801 ◽  
Gyki 52466 ◽  
Ampa Antagonist

The neuroprotective effects of 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo( f)quinoxaline (NBQX), GYKI 52466, and MK-801 were tested following severe forebrain ischemia. Wistar rats were subjected to 10 min of normothermic ischemia and reperfused for 7 days. Necrotic hippocampal CA1 neurons were counted and expressed as a percentage (mean ± SD). In Experiment 1, saline-treated rats sustained 81 ± 20% damage to dorsal CA1. Rats given NBQX 30 mg/kg i.p. x 3 lost 21 ± 27% (p < 0.01). Neither MK-801 1 mg i.p. x 3 alone, nor in combination with the cytoprotective dose of NBQX protected CA1, with 83 ± 18 and 54 ± 34% damage, respectively (NS). Giving NBQX 90 mg/kg i.v. did not protect cells (94 ± 5%) and resulted in nephrotoxicity. In Experiment 2, rats were given saline or three doses of NBQX 30 mg/kg i.p. immediately at reperfusion (RP) or after a 6-, 12-, or 24-h delay. Saline-treated rats suffered 79 ± 16% injury. NBQX given immediately resulted in 17 ± 17% injury, and even if treatment was delayed by either 6 or 12 h, there was marked protection with only 27 ± 32 and 25 ± 17% injury, respectively (all p < 0.01). Delaying the initiation of treatment to 24 h was not successful, resulting in 50 ± 28% injury (NS). In Experiment 3, saline-treated rats lost 81 ± 19% of CA1 cells, while those given GYKI 52466 10 mg/kg i.p. x 5 starting immediately following RP lost 80 ± 14%. Blocking α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors with NBQX postischemia is highly efficacious, indicating that delayed degeneration of CA1 cells is AMPA rather than N-methyl-d-aspartate (NMDA) receptor-linked and is reversible for CA1 cells for at least 12 h.

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