Faculty Articles
Glutamate-mediated neuroplasticity in a limbic input to the hypothalamus
Document Type
Article
Publication Date
3-1-2006
Publication Title
Stress
Volume
9
Issue/Number
1
First Page
13
ISSN
1025-3890
Last Page
19
Abstract/Excerpt
Emotionally-salient stressors are processed by cortical and limbic circuits that provide important regulatory input to the hypothalamic-pituitary-adrenal (HPA) axis. However, exposure to chronic or severe stress may cause disregulation of the axis and a variety of physiological and psychological symptoms. The mechanisms that underlie stress-induced alterations in HPA axis function are not well characterized, but one possibility is that severe stress causes plastic changes in limbic inputs to the hypothalamus. We examined plasticity within the bed nucleus of stria terminalis (BNST) and the hypothalamic paraventricular nucleus (PVN) with a stimulating electrode in the BNST and a recording electrode in the PVN. High-frequency BNST stimulation produced long-lasting suppression of evoked field potentials recorded from the PVN, and this effect was blocked by administration of MK-801. Accordingly, rapid glutamate-mediated neuroplasticity in the BNST to PVN neurocircuitry may contribute to plasticity in limbic regulation of the HPA axis.
DOI
10.1080/10253890600556481
NSUWorks Citation
Tartar, J. L.,
King, M.,
Devine, D.
(2006). Glutamate-mediated neuroplasticity in a limbic input to the
hypothalamus. Stress, 9(1), 13-19.
Available at: https://nsuworks.nova.edu/cps_facarticles/1209
