Molecular determinants mediating effects of acute stress on hippocampus-dependent synaptic plasticity and learning.
The understanding of the molecular events underlying the neuroendocrine and behavioral sequelae of the response to stress has advanced rapidly over recent years. The hippocampus is a target of stress hormones, and we are beginning to dissect the molecular players in the modulation of synaptic plasticity and learning and memory involving this region of the brain. Given the wealth of data obtained from electrophysiological and behavioral experiments and in view of the importance to use identical experimental protocols in order to correlate the results obtained under both experimental conditions, this review focuses primarily on those contributions, which combine both approaches. From these studies it is evident that a single stressful event elicits responses in the hippocampus with different time-spans ranging from rapid changes in glutamatergic neurotransmission (i.e., N-methyl-d-aspartate receptor signaling), activation of second messenger cascades by corticotropin-releasing factor to long-lasting transcriptional changes of acetylcholinesterase. The relative contribution of these molecular targets to the stress response, the relation to hippocampal synaptic plasticity and memory formation, and the possible interaction of the underlying processes are discussed.
Blank
Thomas
T
Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D-37075 Goettingen, Germany. blank@em.mpg.de
Nijholt
Ingrid
I
Spiess
Joachim
J
D000208:Acute Disease; D000818:Animals; D006624:Hippocampus / Q000201:enzymology / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D007858:Learning / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D013315:Stress, Psychological / Q000201:enzymology / Q000378:metabolism*; D013569:Synapses / Q000201:enzymology / Q000378:metabolism / Q000502:physiology