Boylan C B, Davis K, Bennett-Clarke C A, Rhoades R W
Department of Anatomy and Neurobiology, Medical College of Ohio, Toledo 43699, USA.
Exp Brain Res. 1996 Dec;112(3):475-84. doi: 10.1007/BF00227953.
Previous studies in adult animals have suggested that the peptides galanin and neuropeptide Y (NPY) may be upregulated in the same primary afferent neurons after peripheral axotomy. The present study was undertaken to determine whether such upregulation occurred in vibrissae-related primary afferent neurons and their axons after damage to the infraorbital nerve [ION; the trigeminal (V) branch that innervates the vibrissae follicles]. Double-labelling experiments demonstrated that approximately 75% of axotomized V ganglion cells and the central arbors of vibrissae-related primary afferents expressed both galanin and NPY after perinatal, but not adult, nerve damage. However, additional experiments demonstrated that the sensitive periods for lesion-induced upregulation of the two peptides and the period over which they were expressed after neonatal ION transection differed substantially. Staining for both peptides was increased after ION damage on P-0 through P-14, but only galanin staining was increased in vibrissae-related primary afferents after lesions on P-21. Galanin expression was elevated in vibrissae-related primary afferents in rats killed 3, 8, and 15 days after neonatal ION transection, while increased NPY was observed at only the middle time point. The lesion-induced increases in galanin and NPY in vibrissae-related ION primary afferents suggest that these peptides may modulate central V reorganization after such damage.
以往对成年动物的研究表明,在周围轴突切断后,甘丙肽和神经肽Y(NPY)可能在同一初级传入神经元中上调。本研究旨在确定在眶下神经[ION;支配触须毛囊的三叉神经(V)分支]受损后,与触须相关的初级传入神经元及其轴突中是否发生这种上调。双标记实验表明,在围产期而非成年期神经损伤后,约75%的轴突切断的V神经节细胞和与触须相关的初级传入神经元的中枢分支同时表达甘丙肽和NPY。然而,额外的实验表明,损伤诱导的两种肽上调的敏感期以及新生期ION横断后它们表达的时期有很大差异。在P-0至P-14期间ION损伤后,两种肽的染色均增加,但在P-21损伤后,仅甘丙肽染色在与触须相关的初级传入神经元中增加。在新生期ION横断后3、8和15天处死的大鼠中,与触须相关的初级传入神经元中甘丙肽表达升高,而仅在中间时间点观察到NPY增加。损伤诱导的与触须相关的ION初级传入神经元中甘丙肽和NPY的增加表明,这些肽可能在此类损伤后调节中枢V的重组。