scholarly journals Effects of the AMPA-Receptor Antagonist, NBQX, on Neuron Loss in Dentate Hilus of the Hippocampal Formation after 8, 10, or 12 Min of Cerebral Ischemia in the Rat

1997 ◽  
Vol 17 (2) ◽  
pp. 147-152 ◽  
Author(s):  
Ping Hu ◽  
Nils Henrik Diemer ◽  
Torben Bruhn ◽  
Flemming Fryd Johansen
Keyword(s):  
Cerebral Ischemia ◽  
Receptor Antagonist ◽  
Ampa Receptor ◽  
Hippocampal Formation ◽  
Neuroprotective Effect ◽  
Pyramidal Cells ◽  
Ca1 Pyramidal Cells ◽  
Ampa Receptor Antagonist ◽  
Hippocampal Ca1 ◽  
Dentate Hilus

The α-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptor antagonist, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo( F)quinoxaline (NBQX), offers protection to hippocampal CA1 pyramidal cells after short episodes of transient cerebral ischemia. Besides CA1 pyramidal cells, neurons containing somatostatin (SS) and located in the dentate hilus of the hippocampal formation are lost after cerebral ischemia. We studied the protective effects of NBQX on SS neurons in the hilus and on hippocampal CA1 pyramidal cells following 8, 10, or 12 min of four-vessel occlusion ischemia during systemic hypotension. NBQX was administered 3 × 30 mg/kg at 0, 10, and 25 after induction of ischemia or sham, and all rats survived for 7 days. NBQX given to control rats without ischemia had no influence on number or morphology of hilar SS neurons and CA1 pyramidal cells. After 8 min of ischemia, NBQX prevented loss of hilar SS neurons. After 10 and 12 min of ischemia, NBQX had no significant effects on loss of SS neurons in the dentate hilus. However, in all ischemic groups, NBQX significantly reduced loss of CA1 pyramidal cells as compared to control rats. This neuroprotective effect decreased gradually and significantly as the time of ischemia increased. Our results support the observation that SS neurons in hilus are among the most ischemia-vulnerable neurons in the brain. We found that administration of NBQX in generally accepted dosages can protect the rapidly dying SS neurons in hilus from only brief episodes of ischemia.

scholarly journals Neuroprotective Effect of the AMPA Receptor Antagonist LY-293558 in Focal Cerebral Ischemia in the Cat

1994 ◽  
Vol 14 (3) ◽  
pp. 466-471 ◽  
Author(s):  
R. Bullock ◽  
D. I. Graham ◽  
S. Swanson ◽  
J. McCulloch
Keyword(s):  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Receptor Antagonist ◽  
Ampa Receptor ◽  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Ischemic Damage ◽  
Physiological Variables ◽  
Ampa Receptor Antagonist

The effects of the glutamate α-amino-3-hydroxy 5-methyl-4-isoxazole propionate (AMPA) receptor antagonist LY-293558 in reducing ischemic brain damage have been assessed in halothane-anesthetized cats. Focal cerebral ischemia was produced by permanent occlusion of one middle cerebral artery, and the animals were killed 6 h later. The amount of early irreversible ischemic damage was assessed at 16 predetermined stereotactic planes by an observer blinded to treatment paradigm employed. Treatment with LY-293558 (15 mg/kg i.v., plus infusion of 7 mg/kg/h) initiated 30 min prior to middle cerebral artery occlusion reduced significantly (p < 0.02) the volume of ischemic damage (from 3,423 ± 212 mm3 of the cerebral hemisphere in vehicle-treated cats to 2,822 ± 569 mm3 in LY-293558-treated cats). The present data demonstrate that an AMPA receptor antagonist can reduce focal ischemic damage in a gyrencephalic species in which key physiological variables have been controlled and monitored throughout the postischemic period. These data provide additional support for the clinical evaluation of AMPA receptor antagonists in focal cerebral ischemia in humans.

Neuroprotective effect of the novel glutamate AMPA receptor antagonist YM872 assessed with in vivo MR imaging of rat MCA occlusion

1998 ◽  
Vol 811 (1-2) ◽  
pp. 63-70 ◽  
Author(s):  
Asta Håberg ◽  
Masayasu Takahashi ◽  
Tokio Yamaguchi ◽  
Mari Hjelstuen ◽  
Olav Haraldseth
Keyword(s):  
Mr Imaging ◽  
Receptor Antagonist ◽  
Ampa Receptor ◽  
Neuroprotective Effect ◽  
The Novel ◽  
Ampa Receptor Antagonist ◽  
Mca Occlusion

scholarly journals The Neuroprotective Effect of the Novel AMPA Receptor Antagonist PD152247 (PNQX) in Temporary Focal Ischemia in the Rat

Stroke ◽  
1999 ◽  
Vol 30 (7) ◽  
pp. 1472-1477 ◽  
Author(s):  
Gerald P. Schielke ◽  
Nancy C. Kupina ◽  
Peter A. Boxer ◽  
Christopher F. Bigge ◽  
Devin F. Welty
Keyword(s):  
Receptor Antagonist ◽  
Ampa Receptor ◽  
Neuroprotective Effect ◽  
Focal Ischemia ◽  
The Novel ◽  
Ampa Receptor Antagonist

scholarly journals Acetylcholine release inhibits distinct excitatory inputs onto hippocampal CA1 pyramidal neurons via different cellular and network mechanisms

2019 ◽  
Author(s):  
Priyodarshan Goswamee ◽  
A. Rory McQuiston
Keyword(s):  
Receptor Antagonist ◽  
Brain Slices ◽  
Pyramidal Cells ◽  
Inhibitory Interneuron ◽  
Stratum Radiatum ◽  
Synaptic Efficacy ◽  
Ach Release ◽  
Paired Pulse ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1

AbstractIn hippocampal CA1, muscarinic acetylcholine (ACh) receptor (mAChR) activation via exogenous application of cholinergic agonists has been shown to presynaptically inhibit Schaffer collateral (SC) glutamatergic inputs in stratum radiatum (SR), and temporoammonic (TA) and thalamic nucleus reuniens (RE) glutamatergic inputs in stratum lacunosum-moleculare (SLM). However, steady-state uniform mAChR activation may not mimic the effect of ACh release in an intact hippocampal network. To more accurately examine the effect of ACh release on glutamatergic synaptic efficacy, we measured electrically evoked synaptic responses in CA1 pyramidal cells (PCs) following the optogenetic release of ACh in genetically modified mouse brain slices. The ratio of synaptic amplitudes in response to paired-pulse SR stimulation (stimulus 2/stimulus 1) was significantly reduced by the optogenetic release of ACh, consistent with a postsynaptic decrease in synaptic efficacy. The effect of ACh release was blocked by the M3 receptor antagonist 4-DAMP, the GABAB receptor antagonist CGP 52432, inclusion of GDP-β-S, cesium, QX314 in the intracellular patch clamp solution, or extracellular barium. These observations suggest that ACh release decreased SC synaptic transmission through an M3 muscarinic receptor-mediated increase in inhibitory interneuron excitability, which activate GABAB receptors and inwardly rectifying potassium channels on CA1 pyramidal cells. In contrast, the ratio of synaptic amplitudes in response to paired-pulse stimulation in the SLM was increased by ACh release, consistent with presynaptic inhibition. ACh-mediated effects in SLM were blocked by the M2 receptor antagonist AF-DX 116, presumably located on presynaptic terminals. Therefore, our data indicate that ACh release differentially modulates excitatory inputs in SR and SLM of CA1 through different cellular and network mechanisms.

Long-term study of dendritic spines from hippocampal CA1 pyramidal cells, after neuroprotective melatonin treatment following global cerebral ischemia in rats

2007 ◽  
Vol 423 (2) ◽  
pp. 162-166 ◽  
Author(s):  
Ignacio González-Burgos ◽  
Graciela Letechipía-Vallejo ◽  
Elisa López-Loeza ◽  
Gabriela Moralí ◽  
Miguel Cervantes
Keyword(s):  
Cerebral Ischemia ◽  
Dendritic Spines ◽  
Pyramidal Cells ◽  
Global Cerebral Ischemia ◽  
Melatonin Treatment ◽  
Term Study ◽  
Ca1 Pyramidal Cells ◽  
Long Term Study ◽  
Hippocampal Ca1
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