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Submitted on December 27, 2002
From the Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Ore. * To whom correspondence should be addressed. E-mail: aichers{at}ohsu.edu.
Abstract--The baroreceptor reflex is critical for homeostatic regulation of blood pressure and is initiated centrally by glutamate release from baroreceptive afferents onto neurons in the nucleus of the solitary tract that activates AMPA-type glutamate receptors. The GluR1 subunit of the AMPA receptor is located at postsynaptic sites within the nucleus of the solitary tract, particularly in dendritic spines, which are important sites for synaptic plasticity. We tested whether the distribution of GluR1 changes after sustained hypertension, which alters baroreceptor afferent activity. We examined the distribution of GluR1 in the nucleus of the solitary tract of both hypertensive (spontaneously hypertensive) and normotensive (Wistar-Kyoto) rats at the light microscopic and electron microscopic levels. There were more GluR1-containing dendritic spines in the nucleus of the solitary tract of hypertensive rats compared with normotensive rats, which was attributable to an increase in the proportion of dendritic spines containing GluR1 as well as an increase in the total number of dendritic spines. The differences were only seen after the development of hypertension and were not seen in rostral regions of the nucleus of the solitary tract. In the spontaneously hypertensive rat, many synapses on GluR1-containing dendrites had the morphological features of synapses undergoing dynamic changes, including the presence of perforated synapses. These results suggest that changes in afferent activity to the nucleus of the solitary tract during sustained hypertension alter both the dendritic structure and AMPA receptor content of some neurons. These structural changes may be a substrate for central resetting of the baroreceptor reflex.
Revised on January 24, 2003
Structural Changes in AMPA-Receptive Neurons in the Nucleus of the Solitary Tract of Spontaneously Hypertensive Rats
Sue A. Aicher*;
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