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福尔马林后爪注射可诱导小鼠脑和脊髓特定区域中[³H]哌唑嗪与α1 -肾上腺素能受体结合的变化。

Formalin hindpaw injection induces changes in the [3H]prazosin binding to alpha1-adrenoceptors in specific regions of the mouse brain and spinal cord.

作者信息

Nalepa I, Vetulani J, Borghi V, Kowalska M, Przewłocka B, Pavone F

机构信息

Department of Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.

出版信息

J Neural Transm (Vienna). 2005 Oct;112(10):1309-19. doi: 10.1007/s00702-005-0279-3. Epub 2005 Feb 22.

DOI:10.1007/s00702-005-0279-3
PMID:15719155
Abstract

Involvement of the alpha1-adrenoceptor subtypes in early and late phases of formalin pain was investigated by quantitative in vitro autoradiography in the spinal cord and brain structures of CD-1 mice. Total alpha1-adrenoceptors binding (including all alpha1-adrenoceptor subtypes) was assessed with [3H]prazosin; alpha(1B)-adrenoceptor was assessed with [3H]prazosin in the presence of 10 nM WB4101 to mask remaining alpha1-adrenoceptor subtypes. Early after formalin injection the alpha1-adrenoceptors (mainly alpha1B receptor) binding was reduced in the contralateral hind limb area of the somatosensory cortex and in the secondary motor cortex. A reduction occurred also in the ipsilateral laminae I-III of the spinal cord (both alpha1B- and non-alpha1B-adrenoceptors). Lately an increase of alpha1-adrenoceptors binding (mostly subtypes other than alpha1B) appeared in discrete amygdaloid and thalamic nuclei. These results provide the first description of changes at the level of central alpha1-adrenoceptors' binding during the formalin-induced pain in mice. Their distribution suggests that they may have a functional meaning.

摘要

通过定量体外放射自显影技术,在CD-1小鼠的脊髓和脑结构中研究了α1-肾上腺素能受体亚型在福尔马林疼痛早期和晚期阶段的作用。用[3H]哌唑嗪评估总的α1-肾上腺素能受体结合(包括所有α1-肾上腺素能受体亚型);在存在10 nM WB4101以掩盖其余α1-肾上腺素能受体亚型的情况下,用[3H]哌唑嗪评估α(1B)-肾上腺素能受体。福尔马林注射后早期,体感皮层对侧后肢区域和次级运动皮层中的α1-肾上腺素能受体(主要是α1B受体)结合减少。脊髓同侧I-III层(α1B-和非α1B-肾上腺素能受体)也出现减少。后期,离散的杏仁核和丘脑核中出现α1-肾上腺素能受体结合增加(主要是α1B以外的亚型)。这些结果首次描述了小鼠福尔马林诱导疼痛期间中枢α1-肾上腺素能受体结合水平的变化。它们的分布表明它们可能具有功能意义。

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Stimulation of alpha(1)-adrenoceptors reduces glutamatergic synaptic input from primary afferents through GABA(A) receptors and T-type Ca(2+) channels.α1肾上腺素能受体的刺激通过GABA(A)受体和T型Ca(2+)通道减少来自初级传入神经的谷氨酸能突触输入。
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