Hostname: page-component-745bb68f8f-l4dxg Total loading time: 0 Render date: 2025-01-24T22:54:09.994Z Has data issue: false hasContentIssue false
  • English
  • Français

Receptive-field Size of S1 Cortical Neurones is Altered by Methaqualone via a GABA Mechanism

Published online by Cambridge University Press:  18 September 2015

T.P. Hicks ,
T. Kaneko  and
J.-I. Oka
T.P. Hicks*
Affiliation:
Department of Psychology, University of North Carolina at Greensboro, Greensboro, North Carolina
T. Kaneko
Affiliation:
Department of Psychology, University of North Carolina at Greensboro, Greensboro, North Carolina
J.-I. Oka
Affiliation:
Department of Psychology, University of North Carolina at Greensboro, Greensboro, North Carolina
*
Department of Psychology, University of North Carolina at Greensboro, 296 Eberhart Building, Greensboro, N.C., U.S.A. 27412-5001
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Methaqualone (Mtq; quaaludes or 'ludes) is a controlled substance, having a molecular structure related to the imidiazobenzodiazepine series of drugs, that has gained some notoriety recently due to its history of widespread abuse on the street. Users report experiencing peripheral paresthesia and transient numbness on body parts receiving dense cutaneous innervation (lips, fingertips, etc.). Since the receptive-field (RF)-sizes of many primary somatosensory (SI) cortical neurones are controlled by local, gamma-aminobutyric acid (GABA)-mediated inhibitory processes, we tested Mtq to see whether its clinical symptoms might have a basis in an action through central GABA-mediated synaptic processes. This report supports this contention and describes a likely pharmacological mechanism involved as one being related to the Ro 15-1788-sensitive benzodiazepine (Bzd) recognition site(s) of the GABA receptor complex.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 17 , Issue 1 , February 1990 , pp. 30 - 34
Copyright
Copyright © Canadian Neurological Sciences Federation 1990

References

REFERENCES

1.Brown, SS, Goenechea, S. Methaqualone: Metabolie, kinetic, and clinical pharmacologic observations. Clin Pharmacol Ther 1973; 14: 314–324.CrossRefGoogle Scholar
2.Soulairac, A, Gottesman, C. Experimental studies on sleep produced by methaqualone. Life Sei 1967; 6: 1229–1232.CrossRefGoogle ScholarPubMed
3.Williams, RL, Agnew, HW Jr. The effects of drugs on the EEG sleep patterns of normal humans. Exp Med Surg 1969; 27: 53–64.Google ScholarPubMed
4.Swift, JG, Dickens, EA, Becker, BA. Anticonvulsant and other pharmacological activities of tuazolone. Arch Int Pharmacodyn Ther 1960; 128: 112–125.Google ScholarPubMed
5.Marks, P. Methaqualone and peripheral neuropathy. Practitioner 1974; 212: 721–722.Google ScholarPubMed
6.Hoaken, PCS. Adverse effect of methaqualone. Can Med Assoc J 1975; 112: 685.Google ScholarPubMed
7.Kaneko, T, Hicks, TP. Baclofen and 7-aminobutyric acid differentially suppress the cutaneous responsiveness of primary somatosensory cortical neurones. Brain Res 1988; 443: 360–366.CrossRefGoogle Scholar
8.Hicks, TP, Dykes, RW. Receptive field size for certain neurons in primary somatosensory cortex is determined by GABA-mediated intracortical inhibition. Brain Res 1983; 274: 160–164.CrossRefGoogle ScholarPubMed
9.Dykes, RW, Landry, P, Metherate, R, et al. Functional role of GABA in cat primary somatosensory cortex: shaping receptive fields of cortical neurons. J Neurophysiol 1984; 52: 1066–1093.CrossRefGoogle ScholarPubMed
10.Alloway, KD, Burton, H. Bicuculline-induced alterations in neuronal responses to controlled tactile stimuli in the second somatosensory cortex of the cat: a microiontophoretic study. Somatosens Res 1986; 3: 197–211.CrossRefGoogle Scholar
11.Hicks, TP, Landry, P, Metherate, R, et al. Functional properties of neurons mediated by GABA in cat somatosensory cortex under barbiturate and urethane anesthesia. In: Rowe, MJ, Willis, WD, eds. Development, Organization and Processing in Somatosensory Pathways, New York: Alan R Liss Inc 1985; 265–276.Google Scholar
12.Hunkeler, W, Möhler, H, Pieri, L, et al. Selective antagonists of benzodiazepines. Nature 1981; 290: 514–516.CrossRefGoogle ScholarPubMed
13.Oka, J-I, Hicks, TP. Benzodiazepines and synaptic processing in the spatial domain within the cat’s primary somatosensory cortex. Submitted.Google Scholar
14.Gardiner, EP, Costanzo, RM. Spatial integration of multiple-point stimuli in primary somatosensory receptive fields of alert monkeys. J Neurophysiol 1980; 43: 420–433.CrossRefGoogle Scholar
15.Hicks, TP. The history and development of microiontophoresis in experimental neurobiology. Prog Neurobiol 1984; 22: 185–240.CrossRefGoogle ScholarPubMed
16.Oka, J-I, Jang, EK, Hicks, TP. Benzodiazepine receptor involvement in the control of receptive field size and responsiveness in primary somatosensory cortex. rain Res 1986; 376: 194–198.Google ScholarPubMed
17.Mueller, WE, Schlaefer, U, Wallen, U. Benzodiazepine receptor binding: the interactions of some non-benzodiazepine drugs with specific [3H] diazepam binding to rat brain synaptosomal membranes. Naunyn-Schmiedeberg’s Arch Pharmacol 1978; 305: 23–26.CrossRefGoogle Scholar
18.Mokier, DJ, Rech, RH. Effects of the benzodiazepine antagonist, Ro 15–1788 on Yelease of conditioned suppression by diazepam, pentobarbital and methaqualone. Pharmacologist 1982; 24: 125.Google Scholar
19.Koe, BK, Minor, E, Kondratas, ME, et al. Enhancement of benzodiazepine binding by methaqualone and related quinazolinones. Drug Devel Res 1986; 7: 255–268.CrossRefGoogle Scholar
20.Codding, PW, Muir, AKS. Molecular structure of Ro 15–1788 and a model for the binding of benzodiazepine receptor ligands. Structural identification of common features in antagonists. Mol Pharmacol 1985; 28: 178–184.Google Scholar