Kainic acid, AMPA, and dihydrokainic acid effect on uptake and efflux ofd-[3H]aspartic acid in cerebellar slices

1996 ◽  
Vol 21 (12) ◽  
pp. 1527-1533 ◽  
Author(s):  
M. Bouazzaoui ◽  
C. Kannengieser ◽  
O. Procksch ◽  
G. Gombos
Keyword(s):  
Aspartic Acid ◽  
Kainic Acid ◽  
Acid Effect ◽  
Dihydrokainic Acid

Implication of p53 and caspase-3 in kainic acid but not in N -methyl- d -aspartic acid-induced apoptosis in organotypic hippocampal mouse cultures

2002 ◽  
Vol 327 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Myriam Djebaı̈li ◽  
Frédéric De Bock ◽  
Valérie Baille ◽  
Joël Bockaert ◽  
Gérard Rondouin
Keyword(s):  
Aspartic Acid ◽  
Kainic Acid ◽  
Caspase 3 ◽  
Induced Apoptosis

Blood–Brain Barrier Permeability and Brain Uptake Mechanism of Kainic Acid and Dihydrokainic Acid

2014 ◽  
Vol 40 (3) ◽  
pp. 542-549 ◽  
Author(s):  
Mikko Gynther ◽  
Aleksanteri Petsalo ◽  
Steen H. Hansen ◽  
Lennart Bunch ◽  
Darryl S. Pickering
Keyword(s):  
Kainic Acid ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Brain Uptake ◽  
Uptake Mechanism ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Dihydrokainic Acid

Breathing of awake goats during prolonged dysfunction of caudal M ventrolateral medullary neurons

1998 ◽  
Vol 84 (1) ◽  
pp. 129-140 ◽  
Author(s):  
H. V. Forster ◽  
L. G. Pan ◽  
T. F. Lowry ◽  
T. Feroah ◽  
W. M. Gershan ◽  
...  
Keyword(s):  
Amino Acid ◽  
Aspartic Acid ◽  
Kainic Acid ◽  
Excitatory Amino Acid ◽  
Neuronal Dysfunction ◽  
Excitatory Amino Acid Receptor ◽  
Acid Receptor ◽  
Awake State ◽  
Selective Antagonists ◽  
Medullary Neurons

Forster, H. V., L. G. Pan, T. F. Lowry, T. Feroah, W. M. Gershan, A. A. Whaley, M. M. Forster, and B. Sprtel. Breathing of awake goats during prolonged dysfunction of caudal M ventrolateral medullary neurons. J. Appl. Physiol.84(1): 129–140, 1998.—Cooling the caudal M ventrolateral medullary (VLM) surface for 30 s results in a sustained apnea in anesthetized goats but only a 30% decrease in breathing in awake goats. The purpose of the present study was to determine, in the awake state, the effect of prolonged (minutes, hours) caudal M neuronal dysfunction on eupneic breathing and CO2 sensitivity. Dysfunction was created by ejecting excitatory amino acid receptor antagonists or a neurotoxin on the VLM surface through guide tubes chronically implanted bilaterally on a 10- to 12-mm2portion of the caudal M VLM surface of 12 goats. Unilateral and bilateral ejections (1 μl) of selective antagonists for N-methyl-d-aspartic acid or non- N-methyl-d-aspartic acid receptors had no significant effect on eupneic breathing or CO2 sensitivity. Unilateral ejection of a nonselective excitatory amino acid receptor antagonist generally had no effect on eupneic breathing or CO2 sensitivity. However, bilateral ejection of this antagonist resulted in a significant 2-Torr hypoventilation during eupnea and a significant reduction in CO2 sensitivity to 60 ± 9% of control. Unilateral ejection of the neurotoxin kainic acid initially stimulated breathing; however, breathing then returned to near control with no incidence of apnea. After the kainic acid ejection, CO2 sensitivity was reduced significantly to 60 ± 7% of control. We conclude that in the awake state a prolonged dysfunction of caudal M VLM neurons results in compensation by other mechanisms (e.g., carotid chemoreceptors, wakefulness) to maintain near-normal eupneic breathing, but compensation is more limited for maintaining CO2 sensitivity.

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