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Title

Sensory modulation of hippocampal transmission. II. Evidence for a cholinergic locus of inhibition in the Schaffer-CA1 synapse

AuthorsHerreras, Óscar CSIC ORCID ; Solís, José M.; Herranz, Antonio S.; Martín del Río, Rafael; Lerma Gómez, Juan
KeywordsNeuronal transmission
Brain dialysis
Presynaptic inhibition
Cholinergic mechanism
Hippocampus
Sensory input
Theta-rhythm
Issue Date4-Oct-1988
PublisherElsevier
CitationBrain Research 461(2): 303-313 (1988)
AbstractThe present work studied the neurotransmitter mediating the depressive effect of sensory stimulation on the Schaffer-CA1 transmission. Field responses of the CA1 region evoked by ipsilateral CA3 stimuli were recorded in paralyzed, locally anesthetized rats following the same experimental paradigm as in the previous work. The tissue zone under recording was perfused in vivo by an implanted hollow fiber (brain dialysis device) with either Krebs-Ringer bicarbonate (KRB), or KRB with penicillin, atropine, acetylcholine or eserine. Results were the following: (1) atropine-increased the field excitatory postsynaptic potential (EPSP) amplitude in a dose-dependent manner and totally abolished the modulatory action of sensory stimulation; (2) both the field EPSP and the modulatory action of sensory stimulation remained unaltered during the blockade of GABAergic activity by penicillin; (3) acetylcholine as well as eserine induced a great diminution of both field EPSP and population spike amplitudes, without altering the effect of sensory stimulation; (4) penicillin and atropine induced multiple population spikes, reversing the effect of sensory stimulation and increasing the cell excitability. These results demonstrate that the sensory modulation of information transfer through the Schaffer-CA1 synapse is mediated by a muscarinic cholinergic mechanism. The dose-dependent increase in the field EPSP by muscarinic blockade is evidence for the existence of a cholinergic presynaptic inhibition on the Schaffer collateral terminals.
Description11 páginas, 7 figuras.
Publisher version (URL)http://dx.doi.org/10.1016/0006-8993(88)90260-0
URIhttp://hdl.handle.net/10261/32484
DOI10.1016/0006-8993(88)90260-0
ISSN0006-8993
Appears in Collections:(IC) Artículos

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