Changes in Gene Expression in Adult Sympathetic Neurons after Axonal Injury

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This chapter summarizes the advances in the knowledge of the phenotype of axotomized peripheral neurons, concentrating on the phenotypic changes that occur in axotomized sympathetic neurons and the signals that trigger these changes. The decrease in tyrosine hydroxylase (TH) activity in axotomized sympathetic neurons is accompanied by a decrease in TH mRNA. Changes can also be found in the mRNA levels of other proteins involved in synaptic transmission. Decreases in transmitter synthesis also occur in axotomized sensory and motor neurons. In addition to changes in neurotransmitter-neuromodulator levels in peripheral neurons after axotomy, changes have been found in their complement of receptors for these signaling molecules. Axotomy of peripheral neurons also produces increases in expression of certain proteins known to be involved in regeneration, such as tubulin and growth-associated protein (GAP)-43. In addition, several neuropeptides, not normally expressed by these neurons, are induced in response to axotomy. Some of these peptides might promote neuronal survival and/or fiber outgrowth under conditions in which the neurons are deprived of their target-derived trophic factors. Two events involved in triggering these phenotypic changes following axotomy have been identified: the induction and release of leukemia inhibitory factor (LIF) in nonneuronal cells within the superior cervical ganglion (SCG) and/or at the site of nerve transection and the reduction in levels of nerve growth factor (NGF) in the SCG as a consequence of the disconnection of the neurons from their target tissues. Other evidence confirms that dramatic changes occur in the nonneuronal population of the SCG after axotomy. Evidence for an endogenous LIF-inducing factor has also been reported in the chapter. In addition to LIF induction, a reduction in NGF levels in the SCG also plays an important role in triggering these changes.

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    The reduced expression of pSTAT3 is likely a direct result of the reduced IL-6 and LIF expression, as it has previously been shown that gp130 signaling accounts for a majority of the STAT3 activation after injury (Hyatt Sachs et al., 2010). gp130 Signaling is known to drive the expression of the neuropeptides Vip, galanin, Pacap, and Cck (Habecker et al., 2009; Rao et al., 1993a; Sun and Zigmond, 1996a; Zigmond et al., 1998; Zigmond, 2011; Zigmond et al., 1996). Galanin and Pacap expression have been directly linked to axon regeneration, as a knockout or inhibition of these neuropeptides shows significantly impaired regeneration (Armstrong et al., 2008; Hobson et al., 2006; Holmes et al., 2000; Kerr et al., 2000).

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