Format

Send to:

Choose Destination
See comment in PubMed Commons below
J Neural Transm. 1982;54(3-4):239-49.

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

Abstract

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.

PMID:
6127374
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Write to the Help Desk