Won Sohn N, Greenberg J H, Hand P J
Cerebrovascular Research Center, School of Medicine, 429 Johnson Pavilion, 3610 Hamilton Walk, University of Pennsylvania, Philadelphia, PA 19104, USA.
Brain Res. 1999 Jan 23;816(2):396-404. doi: 10.1016/s0006-8993(98)01161-5.
Nitric oxide (NO) has been proposed as an intercellular messenger mediating postsynaptic to presynaptic information transfer in the induction of long-term potentiation. A number of studies support the possible involvement of NO in synaptic plasticity. NO may have a role in synaptogenesis and synaptic plasticity in developing rat brain and may play a fundamental part in the process of regeneration, plasticity, and retargeting of axons following injury. We examined the possible role of NO on plasticity in the rat first somatosensory cortex with [14C]2-deoxyglucose (2-DG) autoradiography in rats treated daily with l-nitroarginine (l-NA) following neonatal unilateral vibrissae deafferentation. After 6 weeks of l-NA treatment, the local cerebral glucose utilization (LCGU) and the spatial extent of the metabolic activation following stimulation of the spared whisker was measured. NOS catalytic activity exhibited significant inhibition throughout the treatment period. Vibrissae deafferentation produced a small but not statistically significant increase of LCGU in the vibrissa activated C3 barrel, and l-NA treatment did not alter the activation of LCGU in the deafferented cortex following whisker stimulation. Additionally, l-NA treatment did not alter the area of metabolic activation on either the non-deafferented side or the deafferented side. Deafferentation produced a 298% increase in the metabolic representation of the spared C3 barrel following stimulation in the saline treated animals, a 257% increase in the chronically l-NA treated animals, and a 256% increase in the short-term treated animals, all with respect to the response in the non-deafferented cortex. Metabolic plasticity in the barrel cortex was not attenuated by l-NA treatment. These results show that nitric oxide does not play a major role on developmental cortical plasticity induced by vibrissae deafferentation in the rat.
一氧化氮（NO）被认为是一种细胞间信使，在长时程增强的诱导过程中介导从突触后到突触前的信息传递。许多研究支持NO可能参与突触可塑性。NO可能在发育中的大鼠大脑的突触形成和突触可塑性中发挥作用，并且可能在损伤后轴突的再生、可塑性和重新靶向过程中起重要作用。我们通过[14C]2-脱氧葡萄糖（2-DG）放射自显影术，在新生大鼠单侧触须去传入后每日用L-硝基精氨酸（L-NA）处理的大鼠中，研究了NO对大鼠第一体感皮层可塑性的可能作用。在L-NA处理6周后，测量了局部脑葡萄糖利用（LCGU）以及刺激留存触须后代谢激活的空间范围。在整个治疗期间，NOS催化活性表现出显著抑制。触须去传入在触须激活的C3桶状区引起LCGU有小幅增加，但无统计学意义，并且L-NA处理并未改变触须刺激后去传入皮层中LCGU的激活情况。此外，L-NA处理并未改变非去传入侧或去传入侧的代谢激活区域。在盐水处理的动物中，去传入后刺激留存的C3桶状区的代谢表征增加了298%，在长期接受L-NA处理的动物中增加了257%，在短期处理的动物中增加了256%，所有这些均相对于非去传入皮层中的反应。L-NA处理并未减弱桶状皮层中的代谢可塑性。这些结果表明，一氧化氮在大鼠触须去传入诱导的发育性皮层可塑性中不发挥主要作用。
