Korte M, Kang H, Bonhoeffer T, Schuman E
Max-Planck-Instituti of Neurobiology, Munich-Martinsried, Germany.
Neuropharmacology. 1998 Apr-May;37(4-5):553-9. doi: 10.1016/s0028-3908(98)00035-5.
The neurotrophin family of growth factors has received enormous attention recently for its role in modulating synaptic strength in the developing and adult nervous system. Several recent studies have indicated a role for brain-derived neurotrophic factor (BDNF) in long-term potentiation (LTP), a form of long-lasting plasticity observed at synapses in the hippocampus and other brain areas. The late-phase (L-LTP; e.g. > 2 h) of LTP has been shown to require the synthesis of new proteins. We have examined whether BDNF or other TrkB ligands participate in L-LTP in two ways: by examining transgenic mice which lack BDNF or by acutely blocking TrkB function using function-blocking antibodies. Slices from BDNF knock-out animals or slices treated with TrkB antibodies failed to exhibit L-LTP, indicating that TrkB ligands participate in extending synaptic enhancement from a short-lasting to a long-lasting form.
神经营养因子家族的生长因子最近因其在调节发育中和成体神经系统突触强度中的作用而受到极大关注。最近的几项研究表明，脑源性神经营养因子（BDNF）在长时程增强（LTP）中发挥作用，LTP是在海马体和其他脑区突触处观察到的一种持久可塑性形式。已证明LTP的晚期（L-LTP；例如>2小时）需要合成新蛋白质。我们通过两种方式研究了BDNF或其他TrkB配体是否参与L-LTP：通过检查缺乏BDNF的转基因小鼠，或使用功能阻断抗体急性阻断TrkB功能。来自BDNF基因敲除动物的切片或用TrkB抗体处理的切片未能表现出L-LTP，这表明TrkB配体参与将突触增强从短暂形式扩展为持久形式。
