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Long‐term Depression of Horizontal Connections in Rat Motor Cortex
Author(s) -
Hess Grzegorz,
Donoghue John P.
Publication year - 1996
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1996.tb01251.x
Subject(s) - term (time) , neuroscience , depression (economics) , long term depression , motor cortex , psychology , cortex (anatomy) , physical medicine and rehabilitation , medicine , physics , economics , nmda receptor , keynesian economics , receptor , quantum mechanics , stimulation , ampa receptor
The possibility for long‐term depression (LTD) of synaptic transmission in layer 11/11 I horizontal connections within motor cortex was investigated using field potentials and intracellular recordings in rat brain slices. The LTD was induced by low‐frequency stimulation at 2 Hz for 10 min in sites displaced horizontally by 0.5 mm from the stimulating electrode. Response amplitude measured 25‐30 min after 2 Hz stimulation ended was 79% of baseline values ( n = 13) at half maximal stimulation and 59% when 2 Hz stimulus intensity was doubled ( n = 10). In 13/15 tested cases LTD in horizontal connections was specific to the activated pathway. Intracellular recordings from six neurons confirmed synaptic character of response depression. Horizontal connections in which LTD was induced retained the capability of increasing synaptic strength. Long‐term potentiation could be induced in previously depressed pathways by simultaneous theta burst stimulation of two converging horizontal inputs combined with transient local application of GABAA receptor antagonist bicuculline methiodide (mean increase: 45 ± 8%, n = 6) or by simultaneous theta burst stimulation of converging horizontal and vertical inputs (mean change: 26 5 6%, n = 5). These data demonstrate that activity‐dependent mechanisms may regulate bidirectionally the effectiveness of horizontal synaptic coupling between cortical neurons, thus forming a potential mechanism for plasticity of cortical connections and the representation patterns they support.