Pipecolic acid: a new type of α-amino acid possessing bicuculline-sensiti action in the mammalian brain

Takahama, Kazuo; Miyata, Takeshi; Hashimoto, Tadatoshi; Okano, Yoshiro; Hitoshi, Taizo; Kasé, Yoshitoshi

doi:10.1016/0006-8993(82)90855-1

Cited by 30 publications

(12 citation statements)

References 15 publications

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“…The apparent CNS synaptosomal localization of pipecolic acid further suggests that it may be responsible for the remarkable hypotonia characteristic of most CHRS and HPAS patients. For example, Takahama et a1 [73] recently described a gamma amino-butyric acid (GABA)-like, generally inhibitory activity of pipecolic acid on the central nervous system, possibly by pipecolate inhibition of GABA reuptake. Moreover, pipecolic acid has been shown to produce hypotonia in mice [44].…”

Section: Hyperpipecolic Acldemlamentioning

confidence: 99%

The cerebrohepatorenal syndrome of Zellweger, morphologic and metabolic aspects

Kelley

1983

Am. J. Med. Genet.

170

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The cerebrohepatorenal syndrome of Zellweger (CHRS) is remarkable not only for a distinctive combination of congenital anomalies, but also for an unusual variety of profound metabolic disturbances. After a discussion of the clinical diagnosis of CHRS, abnormalities in the metabolism of peroxisomes, mitochondria, iron, pipecolic acid, glycogen, bile acids, and organic acids are discussed and related to the clinical and other biochemical findings in the syndrome. Attention is also drawn to syndromes with biochemical or clinical abnormalities similar to those of CHRS. Although the biochemical findings indicate major abnormalities in oxidative metabolism, the primary defect remains obscure.

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Section: Hyperpipecolic Acldemlamentioning

confidence: 99%

The cerebrohepatorenal syndrome of Zellweger, morphologic and metabolic aspects

Kelley

1983

Am. J. Med. Genet.

170

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“…Therefore, L-PA pathway may be particularly important in the brain. Previous neurophysiological studies in the rat have suggested a possible relationship between L-PA and g-aminobutyric acid (GABA) synapses in cortical and hippocampal neurons (Takahama et al 1982). In addition, L-PA by itself did not affect the basic firing rate of cortical neurons (Takahama et al 1986), but L-PA was able to increase the release of GABA stimulated by mild depolarization with potassium from brain slices and decrease the uptake of GABA by brain slices (Gutierrez & Delgado-Coello 1989).…”

Section: Pipecolic Acidmentioning

confidence: 95%

“…In addition, L-PA by itself did not affect the basic firing rate of cortical neurons (Takahama et al 1986), but L-PA was able to increase the release of GABA stimulated by mild depolarization with potassium from brain slices and decrease the uptake of GABA by brain slices (Gutierrez & Delgado-Coello 1989). L-pipecolic acid may affect neuronal firing by enhancing the release and inhibiting the uptake of GABA (Takahama et al 1982). According to Takagi et al (2001), the intracerebroventricular injection of 1 mg of L-PA and D-PA significantly inhibited food intake during the 2 h following injection, whereas greater than 2 mg of L-Lys was required to inhibit food intake.…”

Section: Pipecolic Acidmentioning

confidence: 96%

“…Therefore, L‐PA pathway may be particularly important in the brain. Previous neurophysiological studies in the rat have suggested a possible relationship between L‐PA and γ‐aminobutyric acid (GABA) synapses in cortical and hippocampal neurons (Takahama et al. 1982).…”

Section: Orexigenic Factors Confirmed In Mammalsmentioning

confidence: 99%

“…1986), but L‐PA was able to increase the release of GABA stimulated by mild depolarization with potassium from brain slices and decrease the uptake of GABA by brain slices (Gutierrez & Delgado‐Coello 1989). L‐pipecolic acid may affect neuronal firing by enhancing the release and inhibiting the uptake of GABA (Takahama et al. 1982).…”

Section: Orexigenic Factors Confirmed In Mammalsmentioning

confidence: 99%

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Central regulation of food intake in the neonatal chick

Furuse

2002

Animal Science Journal

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Regulating food intake is complicated in animals including domestic birds. Just after hatching, neonatal chicks find their food by themselves and they can control food intake, since domestic chicken belongs to the precocial type of avian species. Thus, domestic chickens have relatively well‐developed mechanisms of food‐intake control at hatching. While many aspects of food‐intake regulation in chickens appear similar to that in mammals, there are some responses that are unique to chickens. For instance, some neurotransmitters such as neuropeptide Y (NPY), orexin‐A, orexin‐B, motilin, melanin‐concentrating hormone (MCH), galanin, growth hormone releasing factor (GRF) and ghrelin stimulate feeding in mammals. Only NPY strongly stimulates food intake in birds similar to that observed in mammals; however, both orexins, motilin, MCH and galanin failed to alter food intake of the chick. Moreover, GRF and ghrelin suppressed feeding of chicks. On the other hand, cholecystokinin (CCK), gastrin, glucagon‐like peptide‐1 (GLP‐1), corticotropin‐releasing factor (CRF), histamine, α‐melanocyte stimulating hormone (α‐MSH), leptin and bombesin are known to suppress feeding in mammals. These responses are similar to those of mammals except for leptin. Therefore, the inhibitory mechanisms for feeding are well conserved in chicks.

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