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Activation of α-adrenoceptors depresses synaptic transmission of myelinated afferents and inhibits pathways mediating primary afferent depolarization (PAD) in the in vitro mouse spinal cord.
Experimental Brain Research ( IF 2 ) Pub Date : 2020-04-22 , DOI: 10.1007/s00221-020-05805-y
Elvia Mena-Avila 1 , Jonathan J Milla-Cruz 1 , Jorge R Calvo 1 , Shawn Hochman 2 , Carlos M Villalón 3 , José-Antonio Arias-Montaño 1 , Jorge N Quevedo 1
Affiliation  

Somatosensory afferent transmission strength is controlled by several presynaptic mechanisms that reduce transmitter release at the spinal cord level. We focused this investigation on the role of α-adrenoceptors in modulating sensory transmission in low-threshold myelinated afferents and in pathways mediating primary afferent depolarization (PAD) of neonatal mouse spinal cord. We hypothesized that the activation of α-adrenoceptors depresses low threshold-evoked synaptic transmission and inhibits pathways mediating PAD. Extracellular field potentials (EFPs) recorded in the deep dorsal horn assessed adrenergic modulation of population monosynaptic transmission, while dorsal root potentials (DRPs) recorded at root entry zone assessed adrenergic modulation of PAD. We found that noradrenaline (NA) and the α1-adrenoceptor agonists phenylephrine and cirazoline depressed synaptic transmission (by 15, 14 and 22%, respectively). DRPs were also depressed by NA, phenylephrine and cirazoline (by 62, 30, and 64%, respectively), and by the α2-adrenoceptor agonist clonidine, although to a lower extent (20%). We conclude that NA depresses monosynaptic transmission of myelinated afferents onto deep dorsal horn neurons via α1-adrenoceptors and inhibits interneuronal pathways mediating PAD through the activation of α1- and α2-adrenoceptors. The functional significance of these modulatory actions in shaping cutaneous and muscle sensory information during motor behaviors requires further study.

中文翻译:

α-肾上腺素受体的激活抑制髓鞘传入神经突触传递,并抑制介导体外小鼠脊髓原发传入去极化(PAD)的途径。

体感传入传递强度由几种突触前机制控制,这些机制可减少脊髓水平的递质释放。我们将这项研究的重点放在α-肾上腺素受体在调节低阈值髓鞘传入神经和介导新生小鼠脊髓原发传入去极化(PAD)的途径中的感觉传递中的作用。我们假设,α-肾上腺素受体的激活抑制了低阈值诱发的突触传递并抑制了介导PAD的途径。在背背深角记录的细胞外场电位(EFP)评估了群体单突触传递的肾上腺素能调节,而在根进入区记录的背根电位(DRPs)则评估了PAD的肾上腺素能调节。我们发现去甲肾上腺素(NA)和α1-肾上腺素受体激动剂去氧肾上腺素和西拉唑啉抑制突触传递(分别降低15%,14%和22%)。NA,去氧肾上腺素和西拉唑啉(分别降低62%,30%和64%)和α2-肾上腺素能受体激动剂可乐定也降低了DRPs,尽管降低的程度较小(20%)。我们得出的结论是,NA通过α1-肾上腺素能受体抑制了髓鞘传入神经到深背角神经元的单突触传递,并抑制了通过激活α1-和α2-肾上腺素能介导PAD的神经元间通路。这些调节作用在运动行为中影响皮肤和肌肉感觉信息形成的功能意义需要进一步研究。苯肾上腺素和西拉唑啉(分别减少62%,30%和64%),以及α2-肾上腺素能受体激动剂可乐定,尽管程度较低(20%)。我们得出的结论是,NA通过α1-肾上腺素能受体抑制了髓鞘传入神经到深背角神经元的单突触传递,并抑制了通过激活α1-和α2-肾上腺素能介导PAD的神经元间通路。这些调节作用在运动行为中影响皮肤和肌肉感觉信息形成的功能意义需要进一步研究。苯肾上腺素和西拉唑啉(分别减少62%,30%和64%),以及α2-肾上腺素能受体激动剂可乐定,尽管程度较低(20%)。我们得出的结论是,NA通过α1-肾上腺素能受体抑制了髓鞘传入神经到深背角神经元的单突触传递,并抑制了通过激活α1-和α2-肾上腺素能介导PAD的神经元间通路。这些调节作用在运动行为中影响皮肤和肌肉感觉信息形成的功能意义需要进一步研究。我们得出的结论是,NA通过α1-肾上腺素能受体抑制了髓鞘传入神经到深背角神经元的单突触传递,并抑制了通过激活α1-和α2-肾上腺素能介导PAD的神经元间通路。这些调节作用在运动行为中影响皮肤和肌肉感觉信息形成的功能意义需要进一步研究。我们得出的结论是,NA通过α1-肾上腺素能受体抑制了髓鞘传入神经到深背角神经元的单突触传递,并抑制了通过激活α1-和α2-肾上腺素能介导PAD的神经元间通路。这些调节作用在运动行为中影响皮肤和肌肉感觉信息形成的功能意义需要进一步研究。
更新日期:2020-04-22
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