Pellegri G, Magistretti P J, Martin J L
Laboratoire de Recherche Neurologiche, Institut de Physiologie et Service de Neurologie du CHUV, Faculté de Médecine, Université de Lausanne, Switzerland.
Eur J Neurosci. 1998 Jan;10(1):272-80. doi: 10.1046/j.1460-9568.1998.00052.x.
In view of the neurotrophic effect of vasoactive intestinal peptide (VIP), the regulation of brain-derived neurotrophic factor (BDNF) expression by VIP and the related peptide pituitary adenylate cyclase-activating polypeptide (PACAP) was analysed by Northern blot in primary cultures of cortical neurones. Results reported in this article demonstrate that VIP and PACAP stimulate the expression of BDNF mRNA in primary cultures of cortical neurones and astrocytes. In primary cultures of cortical neurones, induction of BDNF mRNA by VIP and PACAP is completely inhibited by the N-methyl-D-aspartate (NMDA) receptor antagonists MK-801 and AP5, therefore indicating that VIP and PACAP do not stimulate BDNF expression directly but rather by potentiating the effect of glutamate tonically released by neurones and acting at NMDA receptors. In addition to its neurotrophic effects, BDNF has been shown to be involved in neuronal plasticity and results reported here suggest that by stimulating BDNF expression, VIP and PACAP could modulate synaptic plasticity in the cerebral cortex.
鉴于血管活性肠肽（VIP）的神经营养作用，我们通过Northern印迹法分析了在皮质神经元原代培养物中VIP及相关肽垂体腺苷酸环化酶激活肽（PACAP）对脑源性神经营养因子（BDNF）表达的调控。本文报道的结果表明，VIP和PACAP可刺激皮质神经元和星形胶质细胞原代培养物中BDNF mRNA的表达。在皮质神经元原代培养物中，VIP和PACAP对BDNF mRNA的诱导作用被N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK-801和AP5完全抑制，因此表明VIP和PACAP并非直接刺激BDNF表达，而是通过增强神经元持续释放的谷氨酸作用于NMDA受体的效应来实现。除了其神经营养作用外，BDNF还被证明与神经元可塑性有关，本文报道的结果表明，通过刺激BDNF表达，VIP和PACAP可能调节大脑皮质的突触可塑性。
