Severe reduction of heat nociceptive sensitivity in a mutant mouse lacking the corticospinal pathway

Severe reduction of heat nociceptive sensitivity in a mutant mouse lacking the corticospinal pathway

Field: Sensory systems

Authors: Thelin, Jonas
Waldenström, Alexandra
Schachner, Melitta
Schouenborg, Jens

Address of presenting
author: Department of Physiological Sciences
Section for Neurophysiology
Lund University
Sölvegatan 19
S-223 62 Lund
Sweden

E-mail: jonas.thelin@mphy.lu.se

Phone: 046-2224651

Fax: 046-2224546

Text of abstract: To characterize the role of the corticospinal tract (CTS) in the maturation and plasticity of the spinal cord reflex pathways, we have studied the nociceptive withdrawal reflex system in a mutant mouse lacking the CST. This mutant mouse (L1^-, 129/SvEv / C57BL/6J) lacks the gene for the adhesion molecule L1 that seems to be of critical importance for guiding the CST caudal to the pyramidal decussation.
L1^- mice had, with few exceptions, abnormally low nociceptive heat sensitivity as compared to control (L1⁺).
In addition, some body parts such as the tail exhibited a strikingly uneven distribution of sensitivity. These mice showed no other signs of pain related behaviour, such as vocalization, when using high stimulation intensities on the insensitive skin areas.
The tactile thresholds on different parts of the body were only slightly elevated in the L1^- as compared to L1⁺. However, tactile stimuli between the central pads on the hind paw failed to elicit a characteristic toe spreading responses that was typical for normal mice. This may indicate a disturbed plantar reflex pattern, analogue to the Babinski sign in humans.
Normal somatopy and termination patterns of thin sensory fibres were found in the superficial part of the dorsal horn using WGA-HRP. Suggesting that a lack of the L1-gene does not eliminate thin fibre input.
The present result indicate that the adhesion molecule L1 has a critical role, possibly through eliminating CST, for the developing of a normal spinal nociceptive system.

Keywords: mutant, corticospinal tract, nociception, adhesion molecule, pain

	Severe reduction of heat nociceptive sensitivity in a mutant mouse lacking the corticospinal pathway
Field:	Sensory systems
Authors:	Thelin, Jonas Waldenström, Alexandra Schachner, Melitta Schouenborg, Jens
Address of presenting author:	Department of Physiological Sciences Section for Neurophysiology Lund University Sölvegatan 19 S-223 62 Lund Sweden
E-mail:	jonas.thelin@mphy.lu.se
Phone:	046-2224651
Fax:	046-2224546
Text of abstract:	To characterize the role of the corticospinal tract (CTS) in the maturation and plasticity of the spinal cord reflex pathways, we have studied the nociceptive withdrawal reflex system in a mutant mouse lacking the CST. This mutant mouse (L1^-, 129/SvEv / C57BL/6J) lacks the gene for the adhesion molecule L1 that seems to be of critical importance for guiding the CST caudal to the pyramidal decussation. L1^- mice had, with few exceptions, abnormally low nociceptive heat sensitivity as compared to control (L1⁺). In addition, some body parts such as the tail exhibited a strikingly uneven distribution of sensitivity. These mice showed no other signs of pain related behaviour, such as vocalization, when using high stimulation intensities on the insensitive skin areas. The tactile thresholds on different parts of the body were only slightly elevated in the L1^- as compared to L1⁺. However, tactile stimuli between the central pads on the hind paw failed to elicit a characteristic toe spreading responses that was typical for normal mice. This may indicate a disturbed plantar reflex pattern, analogue to the Babinski sign in humans. Normal somatopy and termination patterns of thin sensory fibres were found in the superficial part of the dorsal horn using WGA-HRP. Suggesting that a lack of the L1-gene does not eliminate thin fibre input. The present result indicate that the adhesion molecule L1 has a critical role, possibly through eliminating CST, for the developing of a normal spinal nociceptive system.

Keywords:	mutant, corticospinal tract, nociception, adhesion molecule, pain

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Created 2000-03-16

Department of Physiological Sciences, Lund University

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