Literature DB >> 17134698

Reversible attenuation of neuropathic-like manifestations in rats by lesions or local blocks of the intralaminar or the medial thalamic nuclei.

N E Saadé1, H Al Amin, S Abdel Baki, S Chalouhi, S J Jabbur, S F Atweh.   

Abstract

BACKGROUND AND AIM: Thalamic somatosensory nuclei have been classified into medial and lateral systems based on their role in nociception. An imbalance between these two systems may result in abnormal somatic sensations and spontaneous pain. This study aims to investigate the effects of transient or permanent block of the medial and intralaminar nuclear groups on the neuropathic-like behavior in a rat model for mononeuropathy.
METHODS: Neuropathy was induced on one hind paw in different groups of rats following the spared nerve injury model. When the resulting hyperalgesia and allodynia (tactile and cold) reached a maximum plateau, the rats received either chemical or electrolytic lesion or lidocaine (2%) microperfusion, placed in the various thalamic nuclear groups.
RESULTS: All procedures produced transient but significant decrease of neuropathic manifestations. The magnitude and duration of decrease depended on the type and the site of the block. These effects can be ranked in increasing order as follows, electrolytic<chemical<lidocaine micro-perfusion according to the procedure, and as rostro-medial<ventro-median<parafascicular nuclei, according to the site of the block. Thermal hyperalgesia was the most affected while cold allodynia showed the least attenuation. Neuropathic manifestations returned to their pre-lesion levels after 2-3 weeks, along with frequently observed delayed hyper-responsiveness to the hotplate test.
CONCLUSION: The observed results demonstrate the involvement of the medial and intralaminar thalamic nuclei in the processing of neuropathic-like manifestations, and the reversibility of the effects suggests the flexibility of the neural network involved in supraspinal processing of nociceptive information.

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Year:  2006        PMID: 17134698     DOI: 10.1016/j.expneurol.2006.10.009

Source DB:  PubMed          Journal:  Exp Neurol        ISSN: 0014-4886            Impact factor:   5.330


  11 in total

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