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BRAINSTEM CONTROL OF SUBCORTICAL VISUAL INFORMATION

Award Number: R01EY011695
ORGANIZATION: NATIONAL EYE INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 12/01/1997
PERIOD OF PERFORMANCE END DATE: 01/31/2006

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BRAINSTEM CONTROL OF SUBCORTICAL VISUAL INFORMATION - DESCRIPTION (provided by applicant): The dorsal lateral geniculate nucleus (LGN) is a vital link in the chain of perception. Retinal ganglion cells encode the visual world and transmit it to the LGN. Most agree that gating of this information occurs at the retinogeniculate synapse, but a complete mechanism is elusive. Our recent findings demonstrate several new and exciting sources of dynamic control of visual information at the LGN. Two of these are known modulators of relay neurons: the cholinergic parabrachial brainstem (PBR) and the massive corticogeniculate (CG) feedback. The PBR releases nitric oxide (NO), and our data indicate an amazing difference in the way NO affects retinal and cortical inputs. NO has a powerful and selective inhibitory influence on retinogeniculate transmission in the LGN through interaction with the NMDA receptor; however, transmission through the CG pathway is enhanced by two separate mechanisms. The other great remaining mystery of thalamic function is the purpose of the cortical feedback to LGN from layer 6, which we now see as intimately linked with the PBR and NO. We propose a new series of experiments to reveal the contributions of the PBR, and cortical feedback influences, with a global hypothesis that vision requires cooperative activity patterns of both of these pathways. Aim 1: How does NO affect LGN relay cell membrane properties? NO suppresses NMDA receptor function in the retinogeniculate pathway. We hypothesize that NO also targets the low threshold Ca2+ current (I(T)) and a key K+ currents (I) (As)). We will probe I(T) and I(As) with intracellular patch recordings from slices of the LGN, while delivering NO donors and scavengers, and by stimulating intrinsic NO production through the enzyme bNOS. Aim 2: How does NO affect fast synaptic inputs to LGN relay cells? We will stimulate the retinal and CG pathways (to evoke GABAergic IPSP/JPSCs) and the CG pathway (to evoke glutamatergic EPSP/EPSCs) in slices while manipulating NO levels. We hypothesize a stark difference in how NO affects retinal and cortical EPSP/EPSCs; cortical EPSP/EPSCs are enhanced, indicating that the PBR, through NO, may shift the balance away from retinal feedforward processing and toward cortical feedback processing. Aim 3: How does the corticogeniculate projection control the thalamocortical dialog? Relay cells respond to retinal inputs in one of two modes, burst or tonic. We hypothesize that layer 6 promotes a visuotopic gradient of burst and tonic responses, and synchronous firing, in the LGN. We will record from thalamic ensembles during visual processing, while activating and inactivating layer 6 of visual cortex, and while activating brainstem pathways. The impact of retinal inputs to LGN is well known, but the field is struggling with the nature and scope of extraretinal synaptic influences. The answers to these questions will completely transform our view of thalamic function from that of a slave of the periphery to a partner with cortex in binding together the threads of visual perception.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2005 ( Subtotal = $335,256 )
2005	2005	WAKE FOREST UNIVERSITY HEALTH SCIENCES	MEDICAL CENTER BOULEVARD	WINSTON SALEM	NC	27157	FORSYTH	USA	Vision Research	000	8	1/28/2005	NON-COMPETING CONTINUATION	$335,256
														Subtotal = $335,256

Issue Date FY: 2004 ( Subtotal = $325,492 )
2004	2004	WAKE FOREST UNIVERSITY HEALTH SCIENCES	MEDICAL CENTER BOULEVARD	WINSTON SALEM	NC	27157	FORSYTH	USA	Vision Research	000	7	1/12/2004	NON-COMPETING CONTINUATION	$325,492
														Subtotal = $325,492

Issue Date FY: 2003 ( Subtotal = $316,009 )
2003	2003	WAKE FOREST UNIVERSITY HEALTH SCIENCES	MEDICAL CENTER BOULEVARD	WINSTON SALEM	NC	27157	FORSYTH	USA	Vision Research	000	6		NON-COMPETING CONTINUATION	$316,009
														Subtotal = $316,009

Issue Date FY: 2002 ( Subtotal = $253,908 )
2002	2002	WAKE FOREST UNIVERSITY SCHOOL OF MEDICINE	MEDICAL CENTER BOULEVARD	WINSTON-SALEM	NC	27157		USA	Vision Research	000	5	1/18/2002	COMPETING CONTINUATION	$253,908
														Subtotal = $253,908

Issue Date FY: 2001 ( Subtotal = $208,300 )
2001	2001	WAKE FOREST UNIVERSITY SCHOOL OF MEDICINE	MEDICAL CENTER BOULEVARD	WINSTON-SALEM	NC	27157		USA	Vision Research	000	4	1/5/2001	NON-COMPETING CONTINUATION	$208,300
														Subtotal = $208,300

Issue Date FY: 2000 ( Subtotal = $202,232 )
2000	2000	WAKE FOREST UNIVERSITY SCHOOL OF MEDICINE	MEDICAL CENTER BOULEVARD	WINSTON-SALEM	NC	27157		USA	Vision Research	000	3	12/3/1999	NON-COMPETING CONTINUATION	$202,232
														Subtotal = $202,232

Issue Date FY: 1999 ( Subtotal = $250,572 )
1999	1999	WAKE FOREST UNIVERSITY SCHOOL OF MEDICINE	MEDICAL CENTER BOULEVARD	WINSTON-SALEM	NC	27157		USA	Vision Research	000	2	11/13/1998	NON-COMPETING CONTINUATION	$250,572
														Subtotal = $250,572

Issue Date FY: 1998 ( Subtotal = $251,443 )
1998	1998	WAKE FOREST UNIVERSITY SCHOOL OF MEDICINE	MEDICAL CENTER BOULEVARD	WINSTON-SALEM	NC	27157		USA	Vision Research	000	1	11/28/1997	NEW	$251,443
														Subtotal = $251,443

Grand Total All Awards = $2,143,212

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BRAINSTEM CONTROL OF SUBCORTICAL VISUAL INFORMATION

Award Number: R01EY011695

ORGANIZATION: NATIONAL EYE INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 12/01/1997

PERIOD OF PERFORMANCE END DATE: 01/31/2006

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