
Acute stress and hippocampal output: exploring dorsal CA 1 and subicular synaptic plasticity simultaneously in anesthetized rats
Author(s) -
MacDougall Matthew J.,
Howland John G.
Publication year - 2013
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.1002/phy2.35
Subject(s) - hippocampal formation , neuroscience , subiculum , long term potentiation , synaptic plasticity , hippocampus , neural facilitation , plasticity , electrophysiology , stimulation , neuroplasticity , biology , medicine , excitatory postsynaptic potential , dentate gyrus , physics , inhibitory postsynaptic potential , receptor , thermodynamics
The Cornu Ammonis‐1 ( CA 1) subfield and subiculum ( SUB ) serve as major output structures of the hippocampal formation. Exploring forms of synaptic plasticity simultaneously within these two output regions may improve understanding of the dynamics of hippocampal circuitry and information transfer between hippocampal and cortical brain regions. Using a novel dual‐channel electrophysiological preparation in urethane‐anesthetized adult male S prague‐ D awley rats in vivo, we examined the effects of acute restraint stress (30 min) on short‐ and long‐term forms of synaptic plasticity in both CA 1 and SUB by stimulating the CA 3 region. Paired‐pulse facilitation was disrupted in SUB but not CA 1 in the dual‐channel experiments following exposure to acute stress. Disruptions in CA 1 PPF were evident in subsequent single‐channel experiments with a more anterior recording site. Acute stress disrupted long‐term potentiation induced by high‐frequency stimulation (10 bursts of 20 pulses at 200 Hz) in both CA 1 and SUB . Low‐frequency stimulation (900 pulses at 1 Hz) did not alter CA 1 plasticity while a late‐developing potentiation was evident in SUB that was disrupted following exposure to acute stress. These findings highlight differences in the sensitivity to acute stress for distinct forms of synaptic plasticity within synapses in hippocampal output regions. The findings are discussed in relation to normal and aberrant forms of hippocampal‐cortical information processing.