Releasing Hormone Receptor-Immunoreactive Cells Increase in the Barrel Field in
Response to Whisker Deflection in Rats.
Hall S, De A,
Fix C, Churchill L, Krueger JM
Dept. of Veterinary and
Comparative Anatomy, Pharmacology and Physiology, Program in Neuroscience,
Washington State University, Pullman, WA, USA
The homeostatic regulation of sleep involves
several sleep regulatory substances including growth hormone releasing hormone (GHRH).
Previous studies showed that microinjection of GHRH onto the surface of the
cortex increases EEG delta power during non-REM sleep and that cortical GHRH
receptor mRNA levels increase after 6 h of sleep deprivation during the dark.
These studies suggest that the GHRH receptor may be sensitive to stimulation of
whiskers that are mainly used during the dark. Whisker deflection increases fos
expression within specific barrels of the primary somatosensory cortex providing
an anatomical localization for a specific neuronal activation without invasion
into the brain. We hypothesized that activation of neuronal circuits enhances
release of sleep regulatory substances locally and such use-dependent molecules
provide a mechanism for state-specific EEG slow wave power and for micro
circuitry connectivity processes such as synaptic scaling. Six male Sprague-Dawley
rats (200-300g) were stimulated unilaterally by brushing with fingers the long
whiskers along the caudal edge of the whisker field for 2 h in the afternoon.
After 2 h of stimulation, the rats were perfused with 4% paraformaldehyde, the
brains post-fixed for 2 h, sunk in 20% sucrose and immunoreactivity (IR) for
GHRH receptor (GHRHR), fos and nerve growth factor (NGF) were analyzed. In
layer IV (the primary sensory input to the barrel field) as well as in layers
II-III, the number of GHRHR-IR cells increased in the barrel columns that showed
fos activation in an adjacent section. No changes in IR for NGF were observed in
adjacent sections. These data suggest that afferent activation of a cortical
column enhances the number of GHRH receptors in these cortical cells. These
data support our hypothesis that the GHRH receptor is functionally sensitive to
neuronal activation and are consistent with the Krueger-Obal theory of
use-dependent local sleep.
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