RT Journal Article
SR Electronic
T1 Localized Suppression of Cortical Growth Hormone-Releasing Hormone Receptors State-Specifically Attenuates Electroencephalographic Delta Waves
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 4151
OP 4159
DO 10.1523/JNEUROSCI.6047-09.2010
VO 30
IS 11
A1 Fan Liao
A1 Ping Taishi
A1 Lynn Churchill
A1 Marcus J. Urza
A1 James M. Krueger
YR 2010
UL http://www.jneurosci.org/content/30/11/4151.abstract
AB Growth hormone-releasing hormone (GHRH) promotes non-rapid eye movement sleep (NREMS), in part via a well characterized hypothalamic sleep-promoting site. However, GHRH may also act in the cortex to influence sleep. Application of GHRH to the surface of the cortex changes electroencephalographic (EEG) delta power. GHRH and the GHRH receptor (GHRHR) mRNAs are detectable in the rat cortex, and the expression of cortical GHRHR is activity dependent. Here, we microinjected a GHRH antagonist or GHRHR small interfering RNA (siGHRHR) onto the somatosensory cortex surface in rats. The unilateral application of the GHRH antagonist ipsilaterally decreased EEG delta wave power during NREMS, but not wakefulness, during the initial 40 min after injection. Similarly, the injection of siGHRHR reduced cortical expression of GHRHR and suppressed NREMS EEG delta wave power during 20–24 h after injection. Using the fura-2 calcium imaging technique, cultured cortical cells responded to GHRH by increasing intracellular calcium. Approximately 18% of the GHRH-responsive cells were GABAergic as illustrated by glutamic acid decarboxylase-67 (GAD67) immunostaining. Double labeling for GAD67 and GHRHR in vitro and in vivo indicated that only a minority of cortical GHRHR-containing cells were GABAergic. Our data suggest that endogenous cortical GHRH activates local cortical cells to affect EEG delta wave power state-specifically. Results are also consistent with the hypothesis that GHRH contributes to local network state regulation.