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The impact of hemodynamic stress on sensory signal processing in the rodent lateral geniculate nucleus
Journal article   Open access   Peer reviewed

The impact of hemodynamic stress on sensory signal processing in the rodent lateral geniculate nucleus

Gerard A. Zitnik, Brain D. Clark and Barry D. Waterhouse
Brain research, v 1518, pp 36-47
26 Jun 2013
PMID: 23643838
url
https://europepmc.org/articles/pmc4529672View
Accepted (AM)Open Access (License Unspecified) Open

Abstract

Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology Science & Technology
Hemodynamic stress via hypotensive challenge has been shown previously to cause a corticotropin-releasing factor (CRF)-mediated increase in tonic locus coeruleus (LC) activity and consequent release of norepinephrine (NE) in noradrenergic terminal fields. Although alterations in LC-NE can modulate the responsiveness of signal processing neurons along sensory pathways, little is understood regarding how continuous CRF-mediated activation of LC-NE output due to physiologically relevant stressor affects downstream target cell physiology. The goal of the present study was to investigate the effects of a physiological stressor [hemodynamic stress via sodium nitroprusside (SNP) i.v.] on stimulus evoked responses of sensory processing neurons that receive LC inputs. In rat, the dorsal lateral geniculate nucleus (dLGN) of the thalamus is the primary relay for visual information and is a major target of the LC-NE system. We used extracellular recording techniques in the anesthetized rat monitor single dLGN neuron activity during repeated presentation of light stimuli before and during hemodynamic stress. A significant decrease in magnitude occurred, as well as an increase in latency of dLGN stimulus-evoked responses were observed during hemodynamic stress. In another group of animals the CRF antagonist DpheCRF(12-41) was infused onto the ipsilateral LC prior to SNP administration. This infusion blocked the hypotension-induced changes in dLGN stimulus-evoked discharge. These results show that CRF-mediated increases in LC-NE due to hemodynamic stress disrupts the transmission of information along thalamic-sensory pathways by: (1) initially reducing signal transmission during onset of the stressor and (2) decreasing the speed of stimulus evoked sensory transmission. (c) 2013 Elsevier B.V. All rights reserved.

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