Involvement of the glutamatergic metabotropic receptors in the regulation of glutamate uptake and extracellular excitatory amino acid levels in the striatum of chloral hydrate-anesthetized rats

1996 ◽  
Vol 739 (1-2) ◽  
pp. 156-162 ◽  
Author(s):  
Denise Samuel ◽  
Pascale Pisano ◽  
Claude Forni ◽  
André Nieoullon ◽  
Lydia Kerkerian-Le Goff
Keyword(s):  
Amino Acid ◽  
Chloral Hydrate ◽  
Excitatory Amino Acid ◽  
Glutamate Uptake ◽  
Metabotropic Receptors ◽  
Anesthetized Rats ◽  
Amino Acid Levels

scholarly journals Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of 1H and 31P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

1992 ◽  
Vol 12 (3) ◽  
pp. 456-468 ◽  
Author(s):  
Hans Widmer ◽  
Hisashi Abiko ◽  
Alan I. Faden ◽  
Thomas L. James ◽  
Philip R. Weinstein
Keyword(s):  
Fatty Acid ◽  
Amino Acid ◽  
Energy Metabolism ◽  
Free Fatty Acid ◽  
Time Course ◽  
Excitatory Amino Acid ◽  
Serum Glucose ◽  
Peak Ratio ◽  
Amino Acid Levels ◽  
Complete Brain Ischemia

The effects of hyperglycemia on the time course of changes in cerebral energy metabolite concentrations and intracellular pH were measured by nuclear magnetic resonance (NMR) spectroscopy in rats subjected to temporary complete brain ischemia. Interleaved 31P and 1H NMR spectra were obtained every 5 min before, during, and for 2 h after a 30-min bilateral carotid occlusion preceded by permanent occlusion of the basilar artery. The findings were compared with free fatty acid and excitatory amino acid levels as well as with cations and water content in funnel-frozen brain specimens. One hour before occlusion, nine rats received 50% glucose (12 ml/kg i.p.) and five received 7% saline (12 ml/kg i.p.). Before ischemia, there were no differences in cerebral metabolite levels or pH between hyperglycemic rats and controls. During the carotid occlusion, the lactate/ N-acetylaspartate (Lac/NAA) peak ratio was higher (0.73–1.48 vs. 0.56–0.82; p < 0.05) and pH was lower (<6.0 vs. 6.45 ± 0.05; p < 0.05) in the hyperglycemic rats than in the controls. Phosphocreatine and adenosine triphosphate were totally depleted in both groups. Within 5–15 min after the onset of reperfusion, the Lac/NAA peak ratio increased further in all rats; however, only in extremely hyperglycemic rats (serum glucose > 960 mg/dl) did the lactic acidosis progress rather than recover later during reperfusion. Total free fatty acid and excitatory amino acid levels, but not cation concentration or water content, in brain correlated with serum glucose levels during and after ischemia and with NMR findings after 2 h of reperfusion. Although profound hyperglycemia (serum glucose of 970–1,650 mg/dl) appears to be associated with progression of anaerobic glycolysis and failure of cerebral energy metabolism to recover after temporary complete brain ischemia and with postischemic excitotoxic and lipolytic reactions thought to participate in delayed cellular injury, severe hyperglycemia (490–720 mg/dl) was associated with recovery of energy metabolism.

Relationship between apoE4 allele and excitatory amino acid levels after traumatic brain injury

2003 ◽  
Vol 31 (9) ◽  
pp. 2371-2379 ◽  
Author(s):  
Mary E. Kerr ◽  
M. Ilyas Kamboh ◽  
Kim Yookyung ◽  
Marilyn F. Kraus ◽  
Ava M. Puccio ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Amino Acid ◽  
Brain Injury ◽  
Excitatory Amino Acid ◽  
Apoe4 Allele ◽  
Amino Acid Levels

In vivo blockade of thalamic GABAB receptors increases excitatory amino-acid levels

1996 ◽  
Vol 318 (2-3) ◽  
pp. 295-300 ◽  
Author(s):  
Gabriella Nyitrai ◽  
Zsuzsa Emri ◽  
Vincenzo Crunelli ◽  
Katalin A. Kékesi ◽  
Árpád Dobolyi ◽  
...  
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Gabab Receptors ◽  
Amino Acid Levels

Changes in excitatory amino acid levels and tissue energy metabolites of neonate rat brain after hypoxia and hypoxia-ischemia

1998 ◽  
Vol 240 (2) ◽  
pp. 102-106 ◽  
Author(s):  
F Huguet ◽  
A Guerraoui ◽  
L Barrier ◽  
D Guilloteau ◽  
C Tallineau ◽  
...  
Keyword(s):  
Amino Acid ◽  
Rat Brain ◽  
Excitatory Amino Acid ◽  
Energy Metabolites ◽  
Hypoxia Ischemia ◽  
Amino Acid Levels ◽  
Neonate Rat

scholarly journals GABAA and excitatory amino acid receptors in dorsomedial hypothalamus and heart rate in rats

1991 ◽  
Vol 260 (1) ◽  
pp. R13-R20 ◽  
Author(s):  
R. P. Soltis ◽  
J. A. DiMicco
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Amino Acid ◽  
Receptor Antagonist ◽  
Excitatory Amino Acid ◽  
Cardiovascular Response ◽  
Dorsomedial Hypothalamus ◽  
Amino Acid Receptors ◽  
Anesthetized Rats ◽  
Gabaa Receptor Antagonist

We have previously shown that microinjection of drugs that interfere with the function of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) into the hypothalamus produces cardiorespiratory and behavioral changes resembling those seen in emotional stress. The purpose of this study was to determine whether excitatory amino acids (EAAs) can produce a cardiovascular response similar to that caused by the GABAA receptor antagonist bicuculline methiodide (BMI) when microinjected at the same hypothalamic site in urethan-anesthetized rats and to clarify the precise locus of action of these agents. N-methyl-D-aspartic acid (NMDA, 0.68-6.8 pmol/50 nl) and kainic acid (KA, 0.47-4.7 pmol/50 nl) produced dose-related increases in heart rate and blood pressure when injected at sites in the dorsomedial hypothalamus reactive to BMI (20 pmol/50 nl). Higher doses of NMDA (68 pmol), however, failed to elicit consistent increases in heart rate and blood pressure when injected at these same sites. The effects of NMDA were selectively blocked by the NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid, whereas the effects of KA were selectively blocked by the non-NMDA EAA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. These results demonstrate that 1) blockade of inhibitory amino acid receptors or stimulation of EAA receptors in the dorsomedial nucleus of the hypothalamus produces tachycardic and pressor responses in urethan-anesthetized rats and 2) use of high doses of EAAs may be an unreliable method of evoking local neuronal excitation in certain regions of the central nervous system.

Sign in / Sign up

Export Citation Format

Share Document