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Differential modulation by carbachol of four separate excitatory afferent systems to the rat subiculum in vitro
Author(s) -
Kunitake Ayumi,
Kunitake Takato,
Stewart Mark
Publication year - 2004
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20016
Subject(s) - subiculum , neuroscience , chemistry , excitatory postsynaptic potential , methoctramine , carbachol , entorhinal cortex , population , stimulation , population spike , hippocampus , postsynaptic potential , endocrinology , medicine , antagonist , pirenzepine , receptor , biology , inhibitory postsynaptic potential , dentate gyrus , biochemistry , environmental health
The subiculum is a limbic cortical region that receives inputs from hippocampus and other parahippocampal regions. We used horizontal brain slices to study the modulatory effects of muscarinic receptor activation on excitatory afferent systems of the subiculum. Multiple inputs are preserved in these slices. Carbachol (CCh, applied to the bath) induced a decrease in the field responses (40–50% at 50 μM; 60% at 100 μM) to CA1, presubicular (PreS), and medial entorhinal (MEC) stimulation. Subicular responses to lateral entorhinal (LEC) stimuli were not depressed. The M 1 receptor antagonist pirenzepine at 1 μM was sufficient to reverse most of the CCh‐induced depression of afferent excitation, but 10 μM concentrations were required to eliminate the CCh‐induced firing in the isolated subiculum. A partial reversal of the CCh‐induced depression of afferent excitation was achieved by the M 2 receptor antagonist methoctramine (1 or 10 μM), but these concentrations did not prevent CCh‐induced firing. When CA1 afferents were repetitively activated with submaximal stimuli in the presence of CCh, population excitatory postsynaptic potentials (EPSPs) showed modest summation, but every response was smaller than a corresponding events in normal media. Population spikes, particularly late spikes in a train, showed pronounced facilitation during CCh exposure. The NMDA receptor antagonist CPP (10 μM) prevented facilitation of responses to repetitive stimulation in the presence of carbachol. We conclude that CA1, PreS, and MEC afferents to the subiculum exhibit CCh sensitivity similar to that established for area CA3 afferents to CA1, and LEC afferents to subiculum exhibit CCh resistance. Our data suggest that much of the hippocampal formation circuitry is modulated by CCh and the properties of this modulation can explain some specific firing characteristics of hippocampal formation neurons in “cholinergic” versus “noncholinergic” brain states. © 2004 Wiley‐Liss, Inc.