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  Lynn Churchill, Ph.D.

Research Associate Professor

E-Mail: lnchurch@vetmed.wsu.edu

Phone: (509) 335-8378
Office: Neuroscience Center 13

The reason why we sleep is not known.  Recent findings suggest that neuronal activity initiated during the wake state is processed during sleep in order to scale the synaptic plasticity.  Recent studies demonstrated that sleep regulatory substances applied to the cortex increase neuronal activation in the corticothalamic projection (Yasuda et al., 2004; Churchill et al., 2005).  Sleep promoting growth factors that are applied to the somatosensory cortex or injected intraparitoneally will increase other sleep promoting growth factors as well as the immediate early gene, fos, within a neuroanatomical network (Churchill et al., 2005).  Currently studies in collaboration with Dr. Dave Rector are evaluating the responses of the somatosensory evoked potentials to microinjection of the sleep regulatory substances. 

   

 

 

Preliminary data indicate that tumor necrosis factor alpha increases the evoked potentials while interleukin-1beta decreases these same responses.  Further analyses are necessary to evaluate the mechanisms that underlie these alterations.

 

Another route for investigating sleep function is to identify the immunochemical composition of neurons that respond to neuronal activation.  Whisker stimulation increases the activation the number of tumor necrosis factor-immunoreactive cells.  Preliminary data suggest that the number of immunoreactive cells with growth hormone releasing hormone receptor is also increased in the somatosensory cortex activated by whisker stimulation.  Recent preliminary data indicates that intraperitoneal administration of a sleep-inducing dose of interleukin-1 beta increases the activation of nuclear factor kappa B as well as the mRNA levels for the cytokine, tumor necrosis factor, within specific regions of the nucleus tractus solitarius, the brain region that receives vagal afferents from the gut.  Also, an immunochemical marker for GABAergic neurons has been localized in hypothalamic neurons that alter their calcium signals in response to cytokines and the growth hormone-releasing hormone.  These findings in collaboration with James Krueger, Alok De and Steve Simasko are the first demonstration of colocalization of receptors for sleep-promoting factors in GABAergic, hypothalamic neurons.

Lynn Churchill

Biographical Information

Lynn Churchill, Research Associate Professor, completed her B.S. in biophysical science at the University of Houston in 1969 and her Ph.D. in psychobiology at the University of California, Irvine, in 1973. She was an NIH postdoctoral fellow at the Medical Center at the University of Wisconsin, Madison, from 1973-1977, a research scientist at the University of Texas Health Sciences Center in Houston, and a research assistant professor at the University of Kansas Medical Center, Kansas City. She joined VCAPP in 1987.


Selected Recent Publications

Peterfi, Z., L. Churchill, I. Hajdu, F. Obal Jr., J.M. Krueger, A. Parducz. 2004.  Fos-Immunoreactivity in the Hypothalamus: Dependency on the diurnal Rhythm, Sleep, Gender, and Estrogen.  Neuroscience 124(3):695-707.

Nelson, S.E., D.L. Duricka, K. Campbell, L. Churchill, J.M. Krueger.  2004.  Homer1a and 1bc levels in the rat somatosensory cortex vary with the time of day and sleep loss.  Neurosci Lett. 367(1):105-108.

Brandt, J.A., L. Churchill, A. Rehman, G. Ellis, Sylvie Mémet, Alain Israël, and J.M. Krueger.  Sleep deprivation increases the activation of Nuclear Factor kappa B in lateral hypothalamic cells.  Brain Research, 1004(1-2):91-97.

De, A., L. Churchill, F. Obál, Jr., S.M. Simasko, and J.M. Krueger.  2002.  GHRH and IL1b increase cytoplasmic Ca2+ levels in cultured hypothalamic GABAergic neurons.  Brain Res. 949: 209-212.

Cearley, C., L. Churchill, and J.M. Krueger.  2003.  Time of day differences in IL-1β and TNFα mRNA levels in specific regions of the rat brain.  Neurosci. Lett 352: 61-63.

Brandt, J.A., L. Churchill, A. Rehman, G. Ellis, S. Memet, A. Israel, and J.M. Krueger. 2004. Sleep deprivation increases the activation of Nuclear Factor kappa B in lateral hypothalamic cells. Brain Res. 1004: 91-97.

Peterfi, Z., L. Churchill, I. Hajdu, F. Obal Jr., J.M. Krueger, and A. Parducz. 2004. Fos-immunoreactivity in the hypothalamus: dependency on the diurnal rhythm, sleep, gender and estrogen. Neuroscience 124(3): 695-707.

Nelson, S.E., D.L. Duricka, K. Campbell, L. Churchill, and J.M. Krueger. 2004. Home 1a and 1bc levels in the rat somatosensory cortex vary with the time of day and sleep loss, Neurosci. Lett. 367: 105-108.

Churchill, L., K. Yasuda, T. Yasuda, K. Blindheim, M. Falter, F. Garcia-Garcia, and J.M. Krueger. 2005. Unilateral cortical application of tumor necrosis factor alpha induces asymmetry in Fos-and Interleukin 1beta-immunoreactive cells within the corticothalamic projection. Brain Res. 1055:15-24.

Churchill, L.
Taishi, P., M. Wang, J. Brandt, C. Cearley, A. Rehman, and J.M. Krueger. 2006. Brain distribution of cytokine mRNA induced by systemic administration of interleukin-1beta or tumor necrosis factor alpha. Brain Res. 1120:64-73.


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