Noteworthy is that the functional contribution of a7 towards modulating physiological systems may not be revealed unless the system is imbalanced as by genetic . Central auditory systems express a7 GFP . Central auditory nuclei identified by a7 GFP expression. (A) At E18.5 in this sagittal image of the entire otic complex and the adjacent basal brainstem is included. The cochlear nucleus (C) and the eighth cranial nerve (8n) are visible as is the fifth cranial nerve (5n), the trigeminal nucleus (TGN), and trigeminal ganglion (TGG). Also noted are cochlear ducts (asterisk) and a spiral ganglion (SG). (B) At P12, a7 GFP expression of cochlear complex reveals the strongly labeled cells of the ventralposterior cochlear nucleus (VCP). The dorsal cochlear nucleus (DC) and ventral-anterior cochlear nucleus (VCA) are identified and is the eighth nerve (8n) and a cochlear duct (asterisk). The inset shows the VCP at increased magnification. Cells clusters expressing a7 GFP (arrowhead) and individual cells that resemble the morphology of octopus cells described previously (Morley and Happe 2000; Morley 2005) to express a7 (arrow) are noted. (C) Another P12 sagittal section reveals a7 GFP expression in the ascending central auditory pathways. (D) The expression of a7 GFP in the inferior colliculus (CIC) of this horizontal section reveals staining of the commissural fibers (arrow). Structures identified are the brachium of the inferior colliculus (BIC); dentate gyrus (DG), inferior colliculus, central nucleus (CIC); lateral lemniscus, dorsal nucleus (DLL); lateral lemniscus, ventral nucleus (VLL); medial geniculate nucleus (MGN), and the substantia nigra (SN). Bars = 100 lm (A, B0; 20 lm (B-insert), and 1 mm (C, D). deficiencies, sustained exposure to pharmacological compounds, or other events such as inflammation (e.g., Faustman et al. 1992; Gahring and Rogers 2005; Venables et al. 2007; Albuquerque et al. 2009; Brown 2011; Severance et al. 2011) . For example, the dysfunction of a7 is implicated in several psychiatric syndromes associated with certain forms of autism and schizophrenia (particularly in patients who hallucinate) whose spectrum of disorders include abnormal sensitivity to sensory stimuli including an abnormal auditory gating phenotype (Khalfa et al. 2001; Veuillet et al. 2001; Araki et al. 2002; McEvoy and Allen 2002; Freedman et al. 2003; Lippiello 2006; Martin and Freedman 2007; Wallace and Porter 2011 and references therein) . Also, the association of certain auditory deficits and nicotine abuse, mostly associated with cigarette smoking, has further focused speculation on the role of a7 in these pathologies and the possible advantages of therapeutically targeting this receptor for symptomatic relief in these cases (Araki et al. 2002; McEvoy and Allen 2002; Simosky et al. 2002; Freedman et al. 2003; Levin et al. 2006; Lippiello 2006; Martin and Freedman 2007; Wallace and Porter 2011) . In this context, our results suggest additional lines of investigation. For example, in a 7Cre:DTA cell lineage ablation there are collapsed cochlear ducts and abnormal innervation indicating that the cells express a7 and the cells that do so contribute an obligatory role in the successful development and long-term function of these structures. The a7 receptor could also participate in auditory performance after birth, including functions related to the central auditory pathways. This study also adds the possibility of an effect by a7 on the performance of the spiral ligament. These cells exhibit a cholinergic response that is most often described in terms of muscarinic acetylcholine receptors (Khan et al. 2002; Maison et al. 2010) , and their dysfunction is related to several pathogenic auditory deficiencies (Spicer and Schulte 1991; Slepecky et al. 1995; Kikuchi et al. 2000; Sun et al. 2012) . The role of a7 has, to our knowledge, not been examined in these cells. Collectively, the potential for a7 functional pleiotropy in the auditory system is similar to other tissues we have recently examined . Thus, multiple defects that impact upon adult function could be expected depending upon the timing, duration, and nature of the receptor dysfunction. Identification of serum proteomic biomarkers for early porcine reproductive and respiratory syndrome (PRRS) infection BACKGROUND: Porcine reproductive and respiratory syndrome (PRRS) is one of the most significant swine diseases worldwide. Despite its relevance, serum biomarkers associated with early-onset viral infection, when clinical signs are not detectable and the disease is characterized by a weak anti-viral response and persistent infection, have not yet been identified. Surface-enhanced laser desorption ionization time of flight mass spectrometry (SELDI-TOF MS) is a reproducible, accurate, and simple method for the identification of biomarker proteins related to disease in serum. This work describes the SELDI-TOF MS analyses of sera of 60 PRRSV-positive and 60 PRRSV-negative, as measured by PCR, asymptomatic Large White piglets at weaning. Sera with comparable and low content of hemoglobin (< 4.52 μg/mL) were fractionated in 6 different fractions by anion-exchange chromatography and protein profiles in the mass range 1–200 kDa were obtained with the CM10, IMAC30, and H50 surfaces. RESULTS: A total of 200 significant peaks (p < 0.05) were identified in the initial discovery phase of the study and 47 of them were confirmed in the validation phase. The majority of peaks (42) were up-regulated in PRRSV-positive piglets, while 5 were down-regulated. A panel of 14 discriminatory peaks identified in fraction 1 (pH = 9), on the surface CM10, and acquired at low focus mass provided a serum protein profile diagnostic pattern that enabled to discriminate between PRRSV-positive and -negative piglets with a sensitivity and specificity of 77% and 73%, respectively. CONCLUSIONS: SELDI-TOF MS profiling of sera from PRRSV-positive and PRRSV-negative asymptomatic piglets provided a proteomic signature with large scale diagnostic potential for early identification of PRRSV infection in weaning piglets. Furthermore, SELDI-TOF protein markers represent a refined phenotype of PRRSV infection that might be useful for whole genome association studies. Porcine reproductive and respiratory syndrome (PRRS) is one of the most important infectious swine diseases throughout the world [1] [2] [3] and is still having, more than two decades after its emergence, major impacts on pig health and welfare (reviewed by [4] ). The responsible agent is an enveloped, ca. 15 kb long positive-stranded RNA virus (PRRSV) that belongs to the Arteriviridae family [5] and that can cause late-term abortions in sows and respiratory symptoms and mortality in young or growing pigs. Once this virus has entered a herd it tends to remain present and active indefinitely causing severe economic losses and marketing problems due to high direct medication costs and considerable animal health costs needed to control secondary pathogens [6, 7] .