Mechanisms underlying rapid experience-dependent plasticity in the human visual cortex

^*Human Cortical Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892; and ^†Neurologische Klinik, Universitätsklinikum, Aachen 52074, Germany

Edited by Jon H. Kaas, Vanderbilt University, Nashville, TN, and approved October 4, 2001 (received for review July 22, 2001)

Abstract

Visual deprivation induces a rapid increase in visual cortex excitability that may result in better consolidation of spatial memory in animals and in lower visual recognition thresholds in humans. γ-Aminobutyric acid (GABA)ergic, N-methyl-d-aspartate (NMDA), and cholinergic receptors are thought to be involved in visual cortex plasticity in animal studies. Here, we used a pharmacological approach and found that lorazepam (which enhances GABA_A receptor function by acting as a positive allosteric modulator), dextrometorphan (NMDA receptor antagonist), and scopolamine (muscarinic receptor antagonist) blocked rapid plastic changes associated with light deprivation. These findings suggest the involvement of GABA, NMDA, and cholinergic receptors in rapid experience-dependent plasticity in the human visual cortex.

Footnotes

↵ ‡ To whom reprint requests should be addressed. E-mail: cohenl{at}ninds.nih.gov.
This paper was submitted directly (Track II) to the PNAS office.
Abbreviations:

ACh,

acetylcholine;

DM,

dextrometorphan;

GABA,

γ-aminobutyric acid;

LTD,

long-term depression;

LTG,

lamotrigine;

LTP,

long-term potentiation;

LZP,

lorazepam;

NMDA,

N-methyl-d-aspartate;

PT,

phosphene threshold;

SCO,

scopolamine;

SLD,

sleep deprivation;

TMS,

transcranial magnetic stimulation