Edeline J M
Laboratoire de Neurobiologie de l'Apprentissage et de la Mémoire, CNRS URA 1491, Université Paris-Sud, Orsay, France.
Exp Brain Res. 1995;107(2):221-40. doi: 10.1007/BF00230044.
Idazoxan (IDA), an alpha 2 antagonist of adrenoceptors, has been shown to increase cortical release of norepinephrine (NE) by an action mediated primarily by the alpha 2 autoreceptors located on the NE terminals. In the present experiment, IDA application was used to increase the cortial concentration of NE. Single unit activity (n = 107) was recorded in the rat auditory cortex, and the neurons' frequency receptive fields (FRF) were determined before and after systemic (intraperitoneal or intravenous) or local application of IDA. In the whole population (n = 107) there was a decrease in spontaneous activity and/or evoked activity for 84% of the recordings (90/107 cells). Decreased tone-evoked responses were obtained after systemic injections (n = 39), as well as after local applications (n = 68) of IDA. These effects were not observed after either systemic injections (n = 13) or local applications (n = 9) of saline. The signal-to-noise ratio (the mean evoked responses divided by the spontaneous activity) was slightly decreased after systemic injections and slightly increased after local applications. However, after both systemic and local injections the frequency selectivity of the neuronal responses was increased. For a group of neurons (n = 27), testing the FRF at three intensities indicated that this increased selectivity can be expressed at high or middle range intensity but not at low intensity. For 37 cells, the intensity function was tested at the best frequency before and after IDA application, and the threshold for excitatory responses was determined in 28 cases. An increased threshold was observed in 16 of 28 cases after IDA application. Thus, using a pharmacological procedure to increase the extracellular concentration of NE, the dominant inhibitory effect on the auditory cortex neurons led to an enhancement of the frequency selectivity, but also an increase in the threshold of these neurons.
伊达唑啉（IDA）是一种肾上腺素能α2受体拮抗剂，已表明它可通过主要由去甲肾上腺素（NE）末梢上的α2自身受体介导的作用来增加皮质中NE的释放。在本实验中，使用IDA来提高NE的皮质浓度。在大鼠听觉皮质中记录单单位活动（n = 107），并在全身（腹腔内或静脉内）或局部应用IDA之前和之后确定神经元的频率感受野（FRF）。在整个群体（n = 107）中，84%的记录（90/107个细胞）的自发活动和/或诱发活动有所下降。全身注射（n = 39）以及局部应用IDA（n = 68）后，纯音诱发反应均降低。在全身注射生理盐水（n = 13）或局部应用生理盐水（n = 9）后未观察到这些效应。全身注射后信噪比（平均诱发反应除以自发活动）略有下降，局部应用后略有增加。然而，全身和局部注射后，神经元反应的频率选择性均增加。对于一组神经元（n = 27），在三种强度下测试FRF表明，这种增加的选择性可在高或中强度范围表达，但在低强度时则不然。对于37个细胞，在应用IDA之前和之后在最佳频率下测试强度函数，并在28例中确定兴奋性反应的阈值。应用IDA后，28例中有16例观察到阈值升高。因此，通过药理学方法提高细胞外NE浓度，对听觉皮质神经元的主要抑制作用导致频率选择性增强，但这些神经元的阈值也增加。
