Premium
Adolescent stress alters synaptic plasticity: Is PKMzeta the mediator?
Author(s) -
Serrano Peter A,
Hernandez Alejandro Ivan,
Schrott Lisa M
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.810.7
Subject(s) - long term potentiation , synaptic plasticity , hippocampus , synaptic fatigue , synaptic augmentation , hippocampal formation , neurotransmission , synaptic scaling , chemistry , neuroscience , medicine , endocrinology , biology , metaplasticity , receptor
PKMζ has a fundamental role in the retention of long‐term memories and synaptic plasticity. We examined the behavioral consequences of stress and the concomitant changes in PKMζ protein expression. Our results show that adolescent (38 day‐old) male rats given an acute stress significantly elevated corticosterone in blood sera, increased PKMζ protein expression within the hippocampus, and produced a translocation of the GluR2 subunit to the synaptic membrane. Immediately following an acute stress condition (45 min of elevated platform stress) PKMζ protein increased within the synaptic and cytosolic fractions. The GluR2 receptor subunit increased significantly in the synaptic fraction (p>.05). In contrast, seven days following acute stress PKMζ levels continued to be significantly elevated in the cytosolic fraction but not in the synaptic fraction compared to age matched, unstressed controls. Hippocampal slices made from rats immediately after acute stress show depressed levels of synaptic potentiation (long‐term potentiation; LTP) in area CA1 of the hippocampus, but increased levels of depression (long‐term depression; LTD) as compared to unstressed controls. These results showing an increase in PKMζ and the GluR2 subunit in the synaptic region are consistent with PKMζ induced trafficking of this receptor during synaptic plasticity and LTP.