The effect of iontophoretically administered GABA and glycine on the neuronal activity of mesencephalic reticular formation

Abstract

By recording the neuron unit discharges we have observed the effect of iontophoresis of gamma amino butyric acid (GABA) and glycine on the electrical activity of three different types of neurons in mesencephalic reticular formation (MRF). The results indicated that both GABA and glycine have a significant inhibitory effect on the spontaneous discharges of all three types of neurons and the pain discharges of the “pain excitatory type” neurons, and this inhibitory effect can be abolished by their corresponding antagonists, picrotoxin and strychnine. In combination with known histochemical data the results suggest that GABA and glycine might be endogenous transmitters in MRF.

Iontophoresis of picrotoxin and strychnine can abolish the inhibitory effect of electro-acupuncture (EA) of pain discharges. This suggests that in mesencephalon there might exist endogenous GABA and glycine which might participate in analgesic mechanism. However, equal amount of picrotoxin and strychnine has no significant effect on the pain inhibitory response of “pain inhibitory type” neurons. This indicates that this response might have no direct relation to GABA and glycine.

Keywords

neurotransmitter / iontophoresis / gamma amino butyric acid / glycine

References

[1] 1: 1 1977

[2] 20, 1979

[3] 22, 1979

[4] 24, 1979

[5] OjaSS, KontroP. Amino acid as inhibitory neurotransmitter. Progr Pharmacol, 1977, 1(3): 1-1

[6] Baxter CF: GABA in nervous system function, in Roberts E Ed, Reven Press, 1976

[7] ShankRP, AprisionMH. The metabolism in vivo of glycine and serine in eight areas of the rat central nervous system. J Neurochem, 1970, 171461-1461

[8] BondPA. The uptake of gamma-(₃H)-aminobutyric acid by slices from various regions of rat brain and the effect of lithium. J Neurochem, 1973, 20511-511

[9] Krnjevi-cK. Chemical nature of synaptic transmission in vertebrates. Physiol Rev, 1974, 54418-418

[10] SnyderSH. The glycine synaptic receptor in the mammalian central nervous system. Br J Pharmacol, 1975, 53473-473

[11] 2: 68, 1980

[12] 3: 136, 1973

[13] 1: 26, 1978

[14] 1: 27, 1978

[15] DavidAH, HenryJH. Morphine and methionine: Different effects on spontaneous and evoked neuronal firing in the mesencephalic reticular formation of the rat. J Pharmacol Exp Ther, 1980, 213355-355

[16] 1: 28, 1973

[17] TebēcisAK, IshikawaT. Glycine and GABA as inhibitory transmitters in the medullary reticular formation. Pflüger Arch Ges Physiol, 1973, 338273-273

[18] TebēcisAK. Transmitters and reticulospinal neurons. Exp Neurol, 1973, 40297-297

[19] TebēcisAK, MariaADI. Strychninesensitive inhibition in the medullary reticular formation: Evidence for glycine as an inhibitory transmitter. Brain Res, 1972, 40373-373

[20] HosliL, et al. . Depressant amino acids and possible antagonists on medullary reticular neurons. Experientia, 1971, 27732-732

[21] KanderaJ, et al. . Control of cerebral metabolite levels: I Amino acid uptake and levels in various areas of the rat brain. Biochem J., 1968, 126249-249

[22] ShawRK, BeineJD. Ninhydrin positive substances present in different areas of normal rat brain. J Neurochem, 1965, 12151-151

[23] StraughanDW. Convulsant drugs: Amino acid antagonism and central inhibition. Neuropharmacology, 1974, 13495-495

[24] HillRG, et al. . Amino acid antagonists and depression of cuneate neurons by γaminobutyric acid (GABA) and glycine. Br J Pharmacol, 1973, 47642-642

[25] HillRG, et al. . Antagonism of γ-aminobutyric acid and glycine by convulsants in the cuneate nucleus of rat. Br Pharmacol, 1976, 569-9

[26] 1: 78, 1978

[27] 1: 90, 1978

[28] 1: 89, 1978