The provocative finding that there are 10-fold more corticothalamic (CT) than thalamocortical axons reinforces the long-standing view that the cerebral cortex dynamically regulates its own input via CT neurons. However, the role of corticothalamic circuitry remains a deep mystery. This is because a substantial proportion, perhaps even a majority, of CT cells are silent under standard experimental conditions. Recently, we have found in rat primary somatosensory cortex that weakly responsive CT cells, and even some that are otherwise silent, become more responsive to tactile stimulation of facial whiskers during pharmacologically- induced facilitation of the topographically corresponding area of motor cortex. Thus, inputs from other, functionally related neocortical areas can directly influence the excitability of CT neurons in sensory cortex and hence the processing of afferent, sensory signals in thalamocortical circuits. Understanding the nature of information that is potentially transmitted by these strategically located neurons will likely provide new and important insights into cortical function and its regulation during sensorimotor behaviors. The research plan employs a combination of in vivo and in vitro approaches to examine intrinsic electrophysiological properties, synaptic inputs and receptive fields of CT neurons in the rat somatosensory system. Novel findings will be obtained from two different types of corticothalamic projection systems long-postulated to play distinctly different roles in sensory processing during active touch. The research plan should lead to new insights into how - and perhaps, why - the cerebral cortex regulates its own activity during information processing states.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS058758-03
Application #
7591204
Study Section
Special Emphasis Panel (ZRG1-IFCN-F (04))
Program Officer
Chen, Daofen
Project Start
2007-05-15
Project End
2011-03-31
Budget Start
2009-04-01
Budget End
2010-03-31
Support Year
3
Fiscal Year
2009
Total Cost
$322,293
Indirect Cost
Name
University of Pittsburgh
Department
Biology
Type
Schools of Medicine
DUNS #
004514360
City
Pittsburgh
State
PA
Country
United States
Zip Code
15213
Yang, Qizong; Chen, Chia-Chien; Ramos, Raddy L et al. (2014) Intrinsic properties of and thalamocortical inputs onto identified corticothalamic-VPM neurons. Somatosens Mot Res 31:78-93
Orner, David A; Chen, Chia-Chien; Orner, Daniella E et al. (2014) Alterations of dendritic protrusions over the first postnatal year of a mouse: an analysis in layer VI of the barrel cortex. Brain Struct Funct 219:1709-20
Steger, Rob; Kamal, Arifa; Lutchman, Sara et al. (2014) Chronic caffeine ingestion causes microglia activation, but not proliferation in the healthy brain. Brain Res Bull 106:39-46
Barrera, Kyrstle; Chu, Philip; Abramowitz, Jason et al. (2013) Organization of myelin in the mouse somatosensory barrel cortex and the effects of sensory deprivation. Dev Neurobiol 73:297-314
Mangaru, Zareema; Salem, Elsaid; Sherman, Matthew et al. (2013) Neuronal migration defect of the developing cerebellar vermis in substrains of C57BL/6 mice: cytoarchitecture and prevalence of molecular layer heterotopia. Dev Neurosci 35:28-39
Steger, R M; Ramos, R L; Cao, R et al. (2013) Physiology and morphology of inverted pyramidal neurons in the rodent neocortex. Neuroscience 248C:165-179
Chen, Chia-Chien; Tam, Danny; Brumberg, Joshua C (2012) Sensory deprivation differentially impacts the dendritic development of pyramidal versus non-pyramidal neurons in layer 6 of mouse barrel cortex. Brain Struct Funct 217:435-46
Chen, Chia-Chien; Lu, Hui-Chen; Brumberg, Joshua C (2012) mGluR5 knockout mice display increased dendritic spine densities. Neurosci Lett 524:65-8
Rocco-Donovan, Mary; Ramos, Raddy L; Giraldo, Sandra et al. (2011) Characteristics of synaptic connections between rodent primary somatosensory and motor cortices. Somatosens Mot Res 28:63-72
Dummula, Krishna; Vinukonda, Govindaiah; Chu, Philip et al. (2011) Bone morphogenetic protein inhibition promotes neurological recovery after intraventricular hemorrhage. J Neurosci 31:12068-82

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