Modulation of benzodiazepine by lysine and pipecolic acid on pentylenetetrazol-induced seizures.

@article{Chang1988ModulationOB,
  title={Modulation of benzodiazepine by lysine and pipecolic acid on pentylenetetrazol-induced seizures.},
  author={Y. F. Chang and Virginia Hargest and Jay S. Chen},
  journal={Life sciences},
  year={1988},
  volume={43 15},
  pages={
          1177-88
        }
}
L-lysine, an essential amino acid for man and animals, and its metabolite pipecolic acid (PA) have been studied for their effects on pentylenetetrazol (PTZ)-induced seizures in mice. L-Lysine or L-PA i.p. significantly increased clonic and tonic latencies in a dose-dependent manner against 90 mg/kg PTZ-induced seizures. L-Lysine but not L-PA enhanced the anticonvulsant effect of diazepam (DZ) (0.2 mg/kg). L-PA (0.1 mmol/kg) i.c.v. showed a slight decrease in clonic latency; it did not enhance… 
Chronic L-lysine develops anti-pentylenetetrazol tolerance and reduces synaptic GABAergic sensitivity.
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After 15- and 20-day treatment, clonic and tonic seizures latencies and survival rate decreased, suggesting development of tolerance, and L-lysine enhanced the specific [35S]tert-butyl bicyclophosphorothionate binding in brain membranes dose dependently.
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Correlation between enhancement of [3H]flunitrazepam binding and suppression of pentylenetetrazol-induced seizures by L-lysine.
TLDR
L-Lysine, in a dose-dependent manner, suppressed seizures caused by PTZ at 50 or 60 mg/kg, or prolonged the time of seizure onset (seizure latency) caused by higher doses of PTZ (90 or 100mg/kg).
Plasma levels of pipecolic acid, both L- and D-enantiomers, in patients with chronic liver diseases, especially hepatic encephalopathy.
TLDR
The results suggest that plasma pipecolic acid, particularly D-acid, is produced from D-lysine by intestinal bacteria in liver cirrhotic patients and that pipe colic acid could be involved in the pathogenesis of hepatic encephalopathy.
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Administration of the charged amino acids, arginine, and glutamic acid can decrease the seizures of patients suffering from uncontrolled epilepsy.
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TLDR
Results suggest that OCTn1 is at least partially associated with PTZ-induced seizures, which is potentially deteriorated by treatment with homostachydrine, a newly identified food-derived OCTN1 substrate.
Enhancement of benzodiazepine receptor binding by L-lysine is chloride-dependent and due to increase in binding affinity.
TLDR
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Origin of D- and L-pipecolic acid in human physiological fluids: a study of the catabolic mechanism to pipecolic acid using the lysine loading test.
TLDR
The findings suggest that plasma pipecolic acid, particularly the D-isomer, originates mainly from the catabolism of dietary lysine by intestinal bacteria rather than by direct food intake and that D- and L-isomers may have different mechanisms of metabolism.
Determination of D- and L-Pipecolic Acid in Food Samples Including Processed Foods
TLDR
The findings suggest that plasma pipecolic acid, particularly the D-isomer, does not originate from direct food intake and that D- and L-pipecolic Acid can possibly be derived from intestinal bacterial metabolites.
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TLDR
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TLDR
L- or D-lysine appears to be metabolized in the rat brain via pipecolic acid to α-aminoadipic acid which differs from the major saccharopine pathway known to be operative in the liver or other mammalian tissues.
LYSINE METABOLISM IN THE RAT BRAIN: THE PIPECOLIC ACID‐FORMING PATHWAY
TLDR
The experimental evidences indicate that the pipecolic acid‐forming pathway is a significant route for lysine metabolism in the rat, and that the rat brain probably utilizes this pathway mainly for lYSine metabolism.
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