Homeostatic maintenance in excitability of tree shrew hippocampal CA3 pyramidal neurons after chronic stress.
The experience of chronic stress induces a reversible regression of hippocampal CA3 apical neuron dendrites. Although such postsynaptic membrane reduction will obviously diminish the possibility of synaptic input, the consequences for the functional membrane properties of these cells are not well understood. We tested the hypothesis that chronic stress affects the input-output characteristics and excitability of CA3 pyramidal cells. Somatic whole-cell current-clamp recording with parallel intracellular biocytin labeling was performed on CA3 neurons from in vitro hippocampal slices from male tree shrews, which were collected after 28 days of psychosocial stress exposure and compared to recordings obtained from control animals. Post hoc morphometric analysis of biocytin-labeled CA3 cells revealed branch regression, by fewer dendritic crossings and length, limited to a distance of approximately 280-340 microm from the soma only. The results from whole-cell recording indicate that chronic stress surprisingly reduced the apparent membrane time constant and input resistance 20-25%, accompanied by increased amplitude of the hyperpolarization-induced voltage "sag." All active membrane properties, including depolarization-induced action potential kinetics, complex spiking patterns, and afterhyperpolarization voltages, were indistinguishable from control recordings. Although linear association analysis confirmed that differences in geometry, such as apical length or branch number, were correlated to functional variability in properties of the AP current and voltage threshold, these changes were too marginal to be reflected in the group differences. However, the individual adrenal hormone status was associated significantly with the selective changes in subthreshold excitability. Taken together, the data provide evidence that despite long-term stress induces morphological changes, upregulates cortisol release and shifts the intrinsic membrane properties, the efficacy of somatic excitability of CA3 pyramidal neurons is largely preserved.
Kole
Maarten H P
MH
Clinical Neurobiology Laboratory, German Primate Center, Göttingen, Germany. Maarten.Kole@physiologie.uni-freiburg.de
Czéh
Boldizsár
B
Fuchs
Eberhard
E
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001284:Atrophy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D002462:Cell Membrane / Q000502:physiology; D002908:Chronic Disease; D003712:Dendrites / Q000473:pathology / Q000502:physiology; D004195:Disease Models, Animal; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology*; D006706:Homeostasis / Q000502:physiology; D008239:Lysine / Q000031:analogs & derivatives*; D008297:Male; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology; D018408:Patch-Clamp Techniques; D017966:Pyramidal Cells / Q000473:pathology / Q000502:physiology*; D013315:Stress, Psychological / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000502:physiology; D014417:Tupaia
C013411:biocytin; D008239:Lysine