The PC12 cell line is a classical neuronal cell model due to its ability to acquire the sympathetic neurons features when deal with nerve growth factor (NGF). In the present study, the authors used a variety of different methods to induce PC12 cells, such as Opti-MEM medium containing different concentrations of fetal bovine serum (FBS) and horse serum compared with RPMI-1640 medium, and then observed the neurite length, differentiation, adhesion, cell proliferation and action potential, as well as the protein levels of axonal growth-associated protein 43 (GAP-43) and synaptic protein synapsin-1, among other differences. Compared with the conventional RPMI-1640 medium induction method, the new approach significantly improved the neurite length of induced cells (2.7 times longer), differentiation rate (30% increase), adhesion rate (21% increase) and expression of GAP-43 and synapsin-1 (three times), as well as reduced cell proliferation. The morphology of induced cells in Opti-MEM medium containing 0.5% FBS was more like that of neurons. Additionally, induced cells were also able to motivate the action potential after treatment for 6 days. Therefore, the research provided a novel, improved induction method of neural differentiation of PC12 cells using Opti-MEM medium containing 0.5% FBS, resulting in a better neuronal model cell line that can be widely used in neurobiology and neuropharmacology research.

Expression of the growth and plasticity associated protein GAP‐43 is closely related to synaptogenesis and synaptic remodeling in the developing as well as in the mature nervous system. We have studied the postnatal development of GAP‐43 mRNA expression in the auditory brainstem and determined the time course of its reexpression following deafening through cochlear ablation using a digoxigenin‐coupled mRNA probe. By the first postnatal day, GAP‐43 mRNA was expressed at high levels in all auditory brainstem nuclei. But whereas GAP‐43 mRNA is almost entirely lost in most of these nuclei in the adult animal, significant levels of this molecule are retained in the inferior colliculus and, most notably, in the lateral and medial superior olivary nucleus. As a consequence of unilateral cochleotomy, GAP‐43 mRNA rose dramatically in some neurons of the ipsilateral lateral superior olive, whereas the hybridization signal decreased in others. Using double staining protocols, we found that those olivary neurons that increase their level of GAP‐43 mRNA appear to be identical with the cells developing strong GAP‐43 immunoreactivity after cochleotomy. By combining axonal tracing with in situ hybridization, we proved that at least some of the cells with increased levels of GAP‐43 mRNA and protein are the cells of origin of olivocochlear projections. A substantial decrease of the level of GAP‐43 mRNA took place in the inferior colliculus contralateral to the lesioned cochlea. Our results led us to suggest that neurons in the superior olivary complex may play a crucial role in orchestrating auditory brainstem plasticity. J. Comp. Neurol. 412:353–372, 1999. © 1999 Wiley‐Liss, Inc.

Abstract. There are few diseases in modern biomedicine that have garnered as much scientific interest and public concern as Alzheimer's disease (AD). The amyloid hypothesis has become the dominant model of AD pathogenesis; however, the details of the hypothesis are changing over time. Recently, given the increasing recognition, subtle effects of amyloid β protein (Aβ) on synaptic efficacy may be critical to AD progression. Synaptic plasticity is the important neurochemical foundation of learning and memory. Recent studies have identified that soluble Aβ oligomers combine with certain receptors to impair synaptic plasticity in AD, which advanced the amyloid hypothesis. The aim of the present review was to summarize the role of Aβ-relevant receptors in regulating synaptic plasticity and their downstream signaling cascades, which may provide novel insights into the understanding of the pathogenesis of AD and the development of therapeutic strategies to slow down the progression of AD-associated memory decline in the early stages.

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