Antagonism by Folic Acid of Presynaptic Inhibition in the Rat Cuneate Nucleus

Hill, R.G.; Miller, A A

doi:10.1111/j.1476-5381.1974.tb09619.x

Cited by 21 publications

(5 citation statements)

References 4 publications

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“…Despite the fact that most studies have focused on the metabolism and nucleic acid synthesis-dependent mechanisms for folate action in the nervous system, other studies have found that folate also engages acute signaling in neurons. Folate induces epileptiform activity when applied in the brain of mice and rats (Spector, 1972; Baxter et al, 1973; Hill and Miller, 1974), and enhances neuronal excitability in the cat cerebral cortex (Davies and Watkins, 1973). Acute application of folate in rat hippocampal slices inhibits GABAergic transmission, enhancing excitation by blocking the postsynaptic response to GABA (Otis et al, 1985) as well as by inhibiting presynaptic GABA receptors in the rat cuneate nucleus (Hill and Miller, 1974).…”

Section: Folate and Neural Functionmentioning

confidence: 99%

Folate action in nervous system development and disease

Balashova

Visina²,

Borodinsky³

2018

Developmental Neurobiology

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The vitamin folic acid has been recognized as a crucial environmental factor for nervous system development. From the early fetal stages of the formation of the presumptive spinal cord and brain to the maturation and maintenance of the nervous system during infancy and childhood, folate levels and its supplementation have been considered influential in the clinical outcome of infants and children affected by neurological diseases. Despite the vast epidemiological information recorded on folate function and neural tube defects, neural development and neurodegenerative diseases, the mechanisms of folate action in the developing neural tissue have remained elusive. Here we compiled studies that argue for a unique role for folate in nervous system development and function and its consequences to neural disease and repair. © 2018 Wiley Periodicals, Inc. Develop Neurobiol 78: 391-402, 2018.

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Section: Folate and Neural Functionmentioning

confidence: 99%

Folate action in nervous system development and disease

Balashova

Visina²,

Borodinsky³

2018

Developmental Neurobiology

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“…It has been suggested that the reduction in presynaptic inhibition induced by folates in the rat cuneate nucleus reflects blockade of GABA receptors by the folates (Hill and Millar, 1974). This mechanism seems untenable since (a) folates do not inhibit the binding of 3H-GABA to GABA receptors in vivo (Ruck et al, 1980) and (b) in the present study the effects of the folates were not blocked by the GABA antagonist picrotoxin.…”

Section: Discussionmentioning

confidence: 58%

The effect of folates on the reflex activity in the isolated hemisected frog spinal cord

Loots

Kramer

Brennan

1982

J. Neural Transmission

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Folates may play a role in epileptic phenomena and may also be involved in synaptic events. Recently methyltetrahydrofolate was found to be a potent competitor for 3H-kainic acid binding sites in the cerebellum. The effects of 1 mM methyltetrahydrofolate (MTHF), 1 mM formyl-tetra-hydrofolate (FTHP) and 1 mM Na-folate (Na-F) were tested on the reflex activity of the isolated hemisected frog spinal cord. MTHF and FTHP were found to have an initial excitatory effect on the evoked ventral root responses. This was followed by a gradual decrease in the amplitudes of the ventral root responses. Sodium folate had only an inhibitory effect on these responses. When the evoked ventral root responses were totally inhibited by the folates the preparations did not respond to any of the following substances: (a) Kainic acid (KA), (b) L-glutamic acid (LG), (c) picrotoxin or (d) strychnine. All the folates had an inhibitory effect on the dorsal root responses. In most preparations neuronal activity was only partially restored by perfusion with normal Ringer solution. When the isolated spinal cords were bathed in either 0,5 mM KA or 1 mM LG similar results were obtained to that found with MTHF and FTHF. Glutamic acid diethyl ester (GDEE, 1 mM), however, yielded similar results to that seen with Na-F. It seems that the glutamates and related substances differ in their ability as neuroexcitants, but all share the common ability to inhibit synaptic activity when nervous tissue is exposed to the substances for long periods. Some of the folates share with KA some degree of neurotoxicity. These experiments could also not point out a separate kainic receptor in the frog spinal cord.

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“…The P wave reflects the prolonged depolarization of DC terminals (Andersen et al, 1964~). The GABA antagonist bicuculline (Davidson and Reisine, 1971;Banna et al, 1972) as well as other convulsants (Banna and Hazbun, 1969;Banna and Jabbur, 1970;Hill and Miller, 1974;Davidson et al, 1977;Simmonds, 1978;Pickles and Simmonds, 1980;Harrison and Simmonds, 1983) have been shown to block presynaptic inhibition in the DCN, although a bicucullineresistant component in recordings from rat gracile nucleus in vivo (Hayes et al, 1977) and in vitro (Newberry and Simmonds, 1984b) has been reported. The sites where these antagonists exert their action may not be identical.…”

Section: -Aminobutyric Acid (Gaba)mentioning

confidence: 99%

Neurochemical Transmission in the Dorsal Column Nuclei

Banna

Jabburt

1989

Somatosensory & Motor Research

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The transmitter chemistry of the dorsal column nuclei is reviewed, with special emphasis on the monosynaptic component of the dorsal column-medial lemniscal pathway. It is maintained that in this anatomically addressed system concerned mainly with fast, secure sensory transmission, amino acids represent the predominant mechanism used for chemical relay of primary afferent impulses. The major excitatory primary afferent transmitter is most likely glutamic acid, whereas gamma-aminobutyric acid (GABA) fulfills adequately the role of transmitter of recurrent, postsynaptic and presynaptic inhibition. Recent immunohistochemical and physiological evidence indicates that 5-hydroxytryptamine, originating mainly from neurons of the raphé nuclei, plays a modulatory role in dorsal column transmission of innocuous sensory information. The basic synaptic elements involved in transmission across this relay, along with their corresponding chemical identities, are presented in the form of a speculative model.

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Antagonism by Folic Acid of Presynaptic Inhibition in the Rat Cuneate Nucleus

Cited by 21 publications

References 4 publications

Folate action in nervous system development and disease

Folate action in nervous system development and disease

The effect of folates on the reflex activity in the isolated hemisected frog spinal cord

Neurochemical Transmission in the Dorsal Column Nuclei

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