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Neurotrophins and Spinal Circuit Function

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Neurotrophins and Spinal Circuit Function View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Frontiers - Publisher Connector REVIEW ARTICLE published: 05 June 2014 NEURAL CIRCUITS doi: 10.3389/fncir.2014.00059 Neurotrophins and spinal circuit function Vanessa S. Boyce † and Lorne M. Mendell* Department of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA Edited by: Work early in the last century emphasized the stereotyped activity of spinal circuits Shawn Hochman, Emory University, based on studies of reflexes. However, the last several decades have focused on the USA plasticity of these spinal circuits. These considerations began with studies of the effects of Reviewed by: James W. Grau, Texas A&M monoamines on descending and reflex circuits. In recent years new classes of compounds University, USA called growth factors that are found in peripheral nerves and the spinal cord have been Sandra Garraway, Emory University shown to affect circuit behavior in the spinal cord. In this review we will focus on the School of Medicine, USA effects of neurotrophins, particularly nerve growth factor (NGF), brain derived neurotrophic *Correspondence: factor (BDNF) and neurotrophin-3 (NT-3), on spinal circuits. We also discuss evidence Lorne M. Mendell, Department of Neurobiology and Behavior, Stony that these molecules can modify functions including nociceptive behavior, motor reflexes Brook University, Stony Brook, 100 and stepping behavior. Since these substances and their receptors are normally present Nicolls Road, NY 11794-5230, in the spinal cord, they could potentially be useful in improving function in disease USA states and after injury. Here we review recent findings relevant to these translational e-mail: lorne.mendell@ stonybrook.edu issues. †Present address: Keywords: neurotrophin, spinal cord injury, motor neuron, stretch reflex, pain, c-Fos, locomotion, nociceptor Vanessa S. Boyce, 22 Highwoods Ct., Saint James, NY 11780, USA INTRODUCTION NEUROTROPHIN EFFECTS ON SENSORY NEURONS AND Classical studies of spinal cord function have centered on well- THEIR SPINAL PROJECTIONS defined neural pathways that were considered to mediate stereo- NGF typed automatic functions such as stretch and flexion reflexes, NGF was the first neurotrophin to be well characterized after and to distribute input from sensory fibers and from descending discovery of its ability to promote the growth of neurites when fibers to their appropriate targets. In the past several decades applied to explanted dorsal root ganglia (reviewed in Cowan, it has become apparent that these projections are modifiable 2001). Later, it was identified as a survival factor during the and that this plays an important role in the physiology and period of programmed cell death for small sensory neurons pathology of functions mediated by the spinal cord. Thus a expressing the trkA receptor (reviewed in Mendell, 1995; Mendell complete understanding the nature of spinal function as well et al., 1999b; Huang and Reichardt, 2001). In the immediate as spinal dysfunction requires knowledge of these processes. In postnatal period, NGF continues to act as a survival factor, and addition, such plasticity can serve potentially as a basis for revers- subjecting the animal to an anti NGF antibody leads to failure of ing pathological changes after injury or disease. Initial studies high threshold mechanoreceptors to survive (Lewin et al., 1992). of this type centered on the effects of monoamines on spinal Beginning about 2 days after birth, withdrawing NGF has little circuits because of the well-known projections of serotonergic effect on nociceptor survival. However, during this same postnatal and noradrenergic projections to the spinal cord from the raphe period, these cells begin to show sensitization of the response to and locus coeruleus, respectively (Jankowska et al., 2000). More noxious heat or capsaicin after application of NGF (Zhu et al., recently, a different class of molecule has been shown capable 2004). This switch, occurring in the immediate postnatal period, of altering spinal circuit function. These are the neurotrophins, is associated with upregulation of ERK1/2 and PI3K/P110 in the most studied of which are nerve growth factor (NGF), dorsal root ganglion (DRG) cells, and does not appear to be due to brain derived neurotrophic factor (BDNF), and neurotrophin- changes in expression of trkA or TRPV1 (Zhu and Oxford, 2011). 3 (NT-3). These molecules interact with neurons that express The sensitization elicited by NGF in adult nociceptive neurons the appropriate tropomyosin related kinase (trk) receptor- trkA in the DRG results from an increase in the current produced by (NGF), trkB (BDNF), and trkC (NT-3) as well as the p75 receptor TRPV1 receptor activation (Shu and Mendell, 1999a,b; Galoyan common to all trk- expressing neurons. The receptor biology and et al., 2003). This increase is not due to enhanced sensitivity of intracellular signaling associated with trk receptors is reviewed the TRPV1 receptors, but rather from recruitment of additional elsewhere (Chao and Hempstead, 1995; Huang and Reichardt, TRPV1 receptors from the interior of the cell (Zhang et al., 2001). 2005; Stein et al., 2006). The ability of NGF to sensitize the Frontiers in Neural Circuits www.frontiersin.org June 2014 | Volume 8 | Article 59 | 1 Boyce and Mendell Neurotrophins and spinal circuit function response of nociceptors to noxious heat stimuli has important An additional property of BDNF is that its expression in behavioral significance, namely that exposure of adult rats to nociceptor somata is upregulated by exposure to NGF in the systemic NGF results in robust mechanical and thermal hyperal- periphery as part of the response to peripheral inflammation gesia. Thermal hyperalgesia has a strong peripheral component (Pezet and McMahon, 2006). Enhanced expression of BDNF in while mechanical hyperalgesia induced by exposure to NGF is the DRG results in increased levels of BDNF in the superficial mediated largely centrally (Lewin et al., 1994). The central effects dorsal horn (Lever et al., 2001). This is known to rapidly enhance elicited from peripheral exposure to NGF are mediated by another the synaptic action of nociceptive afferents on cells of lamina II neurotrophin, BDNF, whose expression in the DRG is enhanced via a mechanism involving NMDA receptors (Garraway et al., several hours after administration of NGF (reviewed in Pezet and 2003). It is interesting that NMDA receptors in these cells are not McMahon, 2006). The synaptic action of BDNF is discussed in subject to Mg block in the adult unlike those in motor neurons more detail below. (see above), presumably because their subunit composition differs (Arvanian et al., 2004). NT-3 BDNF also acutely strengthens the monosynaptic reflex path- NT-3 plays a role similar to NGF in the survival of sensory way in the isolated spinal cord of neonates. However, this reverses afferents, but in this case it is muscle spindle (group Ia) afferent into long lasting inhibition of transmission several minutes after fibers expressing trkC (reviewed in Huang and Reichardt, 2001). BDNF exposure (Arvanian and Mendell, 2001b). The inhibitory NT-3 also promotes the elaboration of their terminal projections effect is thought to be due to a presynaptic effect of BDNF in to motor neurons during late stages of development (Chen et al., contrast to the potentiation, which has a postsynaptic mechanism, 2003), and in addition potentiates the strength of the group Ia as is the case for NT-3 (reviewed in Mendell and Arvanian, 2002). synaptic projection to motor neurons. In intact afferents this has In agreement with these long lasting postnatal changes, exposure been studied by delivering the NT-3 systemically or intramus- of the prenatal rat to BDNF by i.p. injection of the mother reduces cularly (Arvanian et al., 2003; Petruska et al., 2010) and it is the monosynaptic EPSP measured postnatally, whereas prenatal difficult to determine the precise mode of action. For peripherally exposure to NT-3 increases it (Seebach et al., 1999). axotomized afferent fibers the NT-3 was delivered via a cuff on the cut nerve (Mendell et al., 1999). Because the effects were limited to SUMMARY the treated nerve, it seems likely that this was due to a direct effect In summary, there are several common features linking the of the NT-3 on the terminals of the fibers that were exposed to the effects of the different neurotrophins on sensory neurons. All NT-3, but possible mechanisms such as sprouting or facilitation sensory neurons express trk receptors whose identity determines of glutamate release could not be distinguished. which neurotrophin will influence their function. Neurotrophins The monosynaptic projections from spindle afferent fibers to all serve as survival factors during the period of programmed motor neurons also exhibit potentiation acutely when exposed cell death. They all affect the response of receptors to nat- to NT-3 in the isolated spinal cord (Arvanov et al., 2000). The ural stimulation, and finally they all are able to modify the acute effect is developmentally regulated because the postsynaptic synaptic effects of the affected sensory neurons. In the latter (motor neuron) NMDA receptors required for the action of NT- case the mechanisms are quite different. NGF elicits its effect 3 become inactive about 10–14 days after birth due to Mg block by upregulating another neurotrophin, BDNF, which elicits its (Arvanian and Mendell, 2001a; Arvanian et al., 2004). NT-3 also effect in the spinal cord by acting on NMDA receptors in cells enhances the mechanical sensitivity of the neuroma of spindle of the superficial dorsal horn. The effect of peripherally deliv- afferents that have been axotomized and capped with a Gore-Tex ered NT-3 is not established, but probably involves a presy- sleeve (Munson et al., 1999). naptic change in the affected fibers. However, studies of the acute action of NT-3 have also revealed the possibility of a BDNF postsynaptic NMDA receptor- mediated change as discussed for The effect of the trkB agonist BDNF on sensory neurons is BDNF.
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