Disease relevance of delta-Amino-n-valeric acid

• Enzymatic reactions in the degradation of 5-aminovalerate by Clostridium aminovalericum [1].

Psychiatry related information on delta-Amino-n-valeric acid

• Since baclofen is known to bind to a subpopulation of GABA receptors (bicuculline-insensitive) and baclofen-induced catatonia was susceptible to reversal by homotaurine and delta-amino-n-valeric acid, it is suggested that this effect could be mediated through GABAB receptors [2].
• Baclofen's stimulatory action on motor activity was partially blocked by 5-aminovaleric acid, whereas 3-aminopropanesulphonic acid was without effect [3].

High impact information on delta-Amino-n-valeric acid

• Intraperitoneal injection of the cyclic imine 1-piperideine in mice resulted in measurable quantities of 5-aminopentanoic acid in brain [4].
• 1-Piperideine, 5-aminopentanoic acid, and its lactam, 2-piperidone, were identified as metabolites of cadaverine in 10,000 g mouse liver supernatants to which diamine oxidase had been added [5].
• Clostridium botulinum type F (proteolytic), C. ghoni, C. mangenoti and C. putrificum were found to reduce proline to 5-aminovaleric acid and to produce 2-aminobutyric acid, properties they shared with C. sporogenes and C. sticklandii [6].
• 5-Aminovaleric acid (5-AV; GABA(B) receptors antagonist, 20 mug) reduced KA-induced CA3 pyramidal cell death [7].
• It was found that the five-carbon 5-aminovaleric acid (delta), is suitable to span one base-pair (bp) of DNA when incorporated into a tandem polyamide [8].

Biological context of delta-Amino-n-valeric acid

• The selective GABAB antagonists 5-aminovaleric acid (1 mM) and homotaurine (100 microM) completely suppressed the inhibitory effect of GABA on field stimulation-induced vasoconstrictions [9].

Anatomical context of delta-Amino-n-valeric acid

• In vitro experiments with guinea pig ileum showed that the ability of THC to inhibit electrically evoked contractions was unaffected by delta-amino-n-valeric acid, a GABA(B) receptor antagonist, and that preparations rendered tolerant to GABA responded normally to THC [10].
• Intracisternal injection of 5-aminovaleric acid, a GABAB-receptor antagonist, did not alter basal gastric acid output, and it also failed to antagonize the acid secretory response to intracisternal PCPGABA [11].
• 5-Aminovaleric acid, a major free amino acid component of the anal sac secretion of the red fox, Vulpes vulpes [12].
• The potential interaction of 5-aminovaleric acid (5-AVA) on GABAA and GABAB receptors was investigated on the guinea-pig isolated ileum myenteric plexus preparation [13].

References