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Glutamate uptake is attenuated in spinal deep dorsal and ventral horn in the rat spinal nerve ligation model.
Brain Res. 2005 Apr 11; 1041(1):38-47.BR

Abstract

Alteration of glutamatergic (GLU) neurotransmission within the spinal cord contributes to hyperalgesic and allodynic responses following nerve injury. In particular, changes in expression and efficacy of glutamate transporters have been reported. Excitatory, pain transmitting primary afferent neurons utilizing glutamate as an excitatory neurotransmitter project to both superficial (I-II) and deep (III-V) laminae of the dorsal horn. These experiments were designed to examine changes in glutamate uptake occurring concomitantly within the spinal deep dorsal and ventral horn in situ after experimentally induced neuropathic pain. In vivo voltammetry, using microelectrode arrays configured for enzyme-based detection of GLU were employed. Sprague-Dawley rats had either sham surgery or tight ligation of L5 and L6 spinal nerves (SNL). Four to six weeks later, the L4-L6 spinal cord of chloral hydrate-anesthetized animals was exposed, and ceramic-based glutamate microelectrodes equipped with glass micropipettes 50 microm from the recording surfaces were placed stereotaxically at sites within the spinal cord. Pressure ejection of GLU into the ipsilateral L5-L6 spinal cord resulted in a 72% reduction of GLU uptake in SNL rats compared to sham controls in the ipsilateral L5-L6 deep dorsal horn and a 96% reduction in the ventral horn. In contrast, in the same animals, the contralateral L5-L6 or the ipsilateral L4 spinal cord showed no change in glutamate uptake. The data suggest that spinal nerve ligation produced attenuated glutamate uptake activity extending into the deep dorsal and ventral horn. The study suggests that plasticity related to spinal nerve injury produces widespread alteration in glutamate transporter function that may contribute to the pathophysiology of neuropathic pain.

Authors+Show Affiliations

Department of Physiology and Cell Biology, 304 Hamilton Hall, 1645 Neil Avenue, The Ohio State University, Columbus, OH 43210, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15804498

Citation

Binns, Brian C., et al. "Glutamate Uptake Is Attenuated in Spinal Deep Dorsal and Ventral Horn in the Rat Spinal Nerve Ligation Model." Brain Research, vol. 1041, no. 1, 2005, pp. 38-47.
Binns BC, Huang Y, Goettl VM, et al. Glutamate uptake is attenuated in spinal deep dorsal and ventral horn in the rat spinal nerve ligation model. Brain Res. 2005;1041(1):38-47.
Binns, B. C., Huang, Y., Goettl, V. M., Hackshaw, K. V., & Stephens, R. L. (2005). Glutamate uptake is attenuated in spinal deep dorsal and ventral horn in the rat spinal nerve ligation model. Brain Research, 1041(1), 38-47.
Binns BC, et al. Glutamate Uptake Is Attenuated in Spinal Deep Dorsal and Ventral Horn in the Rat Spinal Nerve Ligation Model. Brain Res. 2005 Apr 11;1041(1):38-47. PubMed PMID: 15804498.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glutamate uptake is attenuated in spinal deep dorsal and ventral horn in the rat spinal nerve ligation model. AU - Binns,Brian C, AU - Huang,Y, AU - Goettl,Virginia M, AU - Hackshaw,Kevin V, AU - Stephens,Robert L,Jr PY - 2004/11/19/received PY - 2005/01/25/revised PY - 2005/01/26/accepted PY - 2005/4/5/pubmed PY - 2005/9/13/medline PY - 2005/4/5/entrez SP - 38 EP - 47 JF - Brain research JO - Brain Res VL - 1041 IS - 1 N2 - Alteration of glutamatergic (GLU) neurotransmission within the spinal cord contributes to hyperalgesic and allodynic responses following nerve injury. In particular, changes in expression and efficacy of glutamate transporters have been reported. Excitatory, pain transmitting primary afferent neurons utilizing glutamate as an excitatory neurotransmitter project to both superficial (I-II) and deep (III-V) laminae of the dorsal horn. These experiments were designed to examine changes in glutamate uptake occurring concomitantly within the spinal deep dorsal and ventral horn in situ after experimentally induced neuropathic pain. In vivo voltammetry, using microelectrode arrays configured for enzyme-based detection of GLU were employed. Sprague-Dawley rats had either sham surgery or tight ligation of L5 and L6 spinal nerves (SNL). Four to six weeks later, the L4-L6 spinal cord of chloral hydrate-anesthetized animals was exposed, and ceramic-based glutamate microelectrodes equipped with glass micropipettes 50 microm from the recording surfaces were placed stereotaxically at sites within the spinal cord. Pressure ejection of GLU into the ipsilateral L5-L6 spinal cord resulted in a 72% reduction of GLU uptake in SNL rats compared to sham controls in the ipsilateral L5-L6 deep dorsal horn and a 96% reduction in the ventral horn. In contrast, in the same animals, the contralateral L5-L6 or the ipsilateral L4 spinal cord showed no change in glutamate uptake. The data suggest that spinal nerve ligation produced attenuated glutamate uptake activity extending into the deep dorsal and ventral horn. The study suggests that plasticity related to spinal nerve injury produces widespread alteration in glutamate transporter function that may contribute to the pathophysiology of neuropathic pain. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/15804498/Glutamate_uptake_is_attenuated_in_spinal_deep_dorsal_and_ventral_horn_in_the_rat_spinal_nerve_ligation_model_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(05)00192-7 DB - PRIME DP - Unbound Medicine ER -