Elsevier

Brain Research

Volume 138, Issue 1, 9 December 1977, Pages 169-174
Brain Research

Cis-3-aminocyclohexanecar☐ylic acid: a substrate for the neuronal GABA transport system

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    It has been suggested that DAB might contribute to the pathogenesis of neuronal cell loss linked to neurolathyrism and neuroexcitation [56,62,123]. It was shown that DAB was promptly absorbed by cells, such as tumor, ganglion and liver [119,124,125]. Ganglion cells of the cerebellum and the cerebral cortex, when exposed to DAB, demonstrated focal degenerative alteration as they appeared shrunken and pyknotic [15,119,125].

  • Distinguishing the cyanobacterial neurotoxin β-N-methylamino-l-alanine (BMAA) from its structural isomer 2,4-diaminobutyric acid (2,4-DAB)

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    2,4-DAB has been identified as having “strong neurotoxic action” in the rat with 7 mmol/kg producing behaviors including hyperirritability, weakness in hind legs, tremors in the upper extremities and convulsions leading to death (Riggs et al., 1954; Ressler et al., 1961; O’Neal et al., 1968; Chen et al., 1972). Cells (e.g. tumor and liver) rapidly take up 2,4-DAB (Riggs et al., 1954; Neal and Bowery, 1977; Weitsch-Dick et al., 1978). When exposed to 2,4-DAB, the ganglion cells of the cerebellum and the cerebral cortex shrink and exhibit pyknosis (Riggs et al., 1954).

  • Structure-Activity Relationship and Pharmacology of γ-Aminobutyric Acid (GABA) Transport Inhibitors

    2006, Advances in Pharmacology
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    Like muscimol, these two compounds are naturally occurring and have proven to be lead structures in the development of highly potent GABA uptake inhibitors. The existence of at least two different transport systems was evidenced very early by the complementary substrate inhibitory effects of DABA/ACHC and β‐alanine, reflecting the neuronal and glial transport systems, respectively (Iversen and Kelly, 1975; Neal and Bowery, 1977). A highly glia‐selective compound was discovered by further modification of THPO.

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