1. PHARMACOLOGICAL HYPERPROLACTINEMIA PROTECTS AGAINST DIABETIC RETINOPATHY IN RATS

Background: The white matter of the cerebellum has a population of GFAP+ cells with neurogenic potential restricted to early postnatal development (P2-P12), these astrocytes are the precursors of stellate cells and basket cells in the molecular layer. On the other hand, GABA is known to serve as a feedback regulator of neural production and migration through tonic activation of GABA-A receptors. Aim: To investigate the functional expression of GABA-A receptors in the cerebellar white matter astrocytes at P7-9 and P18-20. Methods: Immunofluorescence for α1, α2, β1 subunits & GAD67 enzyme in GFAP-EGFP mice (n=10 P8; n= 8 P18). Calcium Imaging: horizontal acute slices were incubated with Fluo4 AM in order to measure the effect of GABA-A or GATs antagonist bicuculline or nipecotic acid on spontaneous calcium oscillations, as well as on GABA application evoked responses. Results: Our results showed that α1 (3.18%), α2 (10.4%) and β1 (not detected) subunits were not predominantly expressed in astrocytes of white matter at P8. However, GAD67 co-localized with 54% of GFAP+ cells, suggesting that a fraction of astrocytes could synthesize GABA. Moreover, calcium imaging experiments showed that white matter cells responded to GABA. This response was antagonized by bicuculline suggesting functional expression of GABA-A receptors. Conclusions: Together these results suggest that GABA is synthesized by half astrocytes in white matter at P8 and that GABA could be released locally to activate GABA-A receptors that are also expressed in cells of the white matter of the cerebellum, during early postnatal development. (D) Acknowledgements: We thank the technical support of E. N. Hernández-Ríos, A, Castilla, L. Casanova, A. E. Espino & M. García-Servín. F.E. Labrada-Moncada is a CONACyT (640190) scholarship holder. This work was supported by PAPIIT-UNAM grants (IN201913 e IN201915) to A. Martínez-Torres and D. Reyes-Haro. 48. PROLACTIN PROTECTS AGAINST JOINT INFLAMMATION AND BONE LOSS IN ARTHRITIS Ledesma-Colunga MG, Adán N, Ortiz G, Solis-Gutierrez M, López-Barrera F, Martínez de la Escalera G, y Clapp C. Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, UNAM Campus Juriquilla, Querétaro, México. Prolactin (PRL) reduces joint inflammation, pannus formation, and bone destruction in rats with polyarticular adjuvant-induced arthritis (AIA). Here, we investigate the mechanism of PRL protection against bone loss in AIA and in monoarticular AIA (MAIA). Joint inflammation and osteoclastogenesis were evaluated in rats with AIA treated with PRL (via osmotic minipumps) and in mice with MAIA that were null (Prlr-/-) or not (Prlr+/+) for the PRL receptor. To help define target cells, synovial fibroblasts isolated from healthy Prlr+/+ mice were treated or not with T-cell-derived cytokines (Cyt: TNFa, IL-1b, and IFNg) with or without PRL. In AIA, PRL treatment reduced joint swelling, lowered joint histochemical accumulation of the osteoclast marker, tartrateresistant acid phosphatase (TRAP), and decreased joint mRNA levels of osteoclasts-associated genes (Trap, Cathepsin K, Mmp9, Rank) and of cytokines with osteoclastogenic activity (Tnfa, Il-1b, Il-6, Rankl). Prlr-/mice with MAIA showed enhanced joint swelling, increased TRAP activity, and elevated expression of Trap, Rankl, and Rank. The expression of the long PRL receptor form increased in arthritic joints, and in joints and cultured synovial fibroblasts treated with Cyt. PRL induced the phosphorylation/activation of Jornadas Académicas, 2016 Martes 27 de Septiembre, Cartel 35 al 67 signal transducer and activator of transcription-3 (STAT3) and inhibited the Cyt-induced expression of Il-1b, Il-6, and Rankl in synovial cultures. The STAT3 inhibitor S31-201 blocked inhibition of Rankl by PRL. PRL protects against bone loss in inflammatory arthritis by inhibiting cytokine-induced activation of RANKL in joints and synoviocytes via its canonical STAT3 signaling pathway. Hyperprolactinemia-inducing drugs are promising therapeutics for preventing bone loss in rheumatoid arthritis. We thank Gabriel Nava, Daniel Mondragón, Antonio Prado, Martín García, and Alejandra Castilla for technical assistance. Research Support: UNAM-PAPIIT Grant IN201315. M.G.L.C is a doctoral student from Programa de Doctorado en Ciencias Biomédicas, Universidad Nacional Autónoma de México (UNAM) receiving fellowship 245828 from CONACYT. (D) 49. ADC MEASUREMENT IN LATERALY MEDULLARY INFARCTION (WALLENBERG SYNDROME) León-Castro LR1, Fourzán-Martínez M1, Rivas-Sánchez LA1, García-Zamudio E1, Nigoche J2, Ortíz-Retana J1, Barragán-Campos HM1. 1.Magnetic Resonance Unit, Institute of Neurobiology, Campus Juriquilla, National Autonomous University of México. Querétaro, Qro., 2.Department of Radiology. Naval Highly Specialized General Hospital, México City, México. BACKGROUND: The stroke of the vertebrobasilar system (VBS) represents 20% of ischemic vascular events. When the territory of the posterior inferior cerebellar artery (PICA) is affected, lateral medullary infarction (LMI) occurs, typically called Wallenberg syndrome; it accounts for 2-7% of strokes of VBS. Given the diversity of symptoms that causes, it is a difficult disease to diagnose. The reference exam to evaluate cerebral blood flow is digital subtraction angiography (DSA); however, it is an invasive method. Magnetic resonance imaging (MRI) is a noninvasive study and the sequence of diffusion (DWI) can detect early ischemic changes, after 20 minutes of ischemia onset, it also allows to locate and determine the extent of the affected parenchyma. Measurement of the apparent diffusion coefficient (ADC) is a semiquantitative parameter that confirms or rule out the presence of infarction, although the diffusion sequence (DWI) has restriction signal. OBJECTIVE: To measure the ADC values in patients with LMI and compare their values with the contralateral healthy tissue. MATERIALS AND METHODS: The database of Unit Magnetic Resonance Unit of studies carried out from January 2010 to July 2016 was revised to include cases diagnosed by MRI with LMI. The images were acquired in two resonators of 3.0 T (Phillips Achieva TX and General Electric Discovery 750 MR). DWI sequence with b value of 1000 was used to look after LMI, then ADC value measurement of the infarcted area and the contralateral area was performed in the same patient. Two groups were identified: a) infarction and b) healthy tissue. Eleven patients, 5 female (45.5%) and 6 males (54.5%), were included. A descriptive statistic was performed and infarction and healthy tissue were analyzed with U-Mann-Whitney test. RESULTS: In the restriction areas observed in DWI, ADC values were measured; the infarction tissue has a median of 0.54X10-3 mm2/s, interquartile range 0.41-1.0X10-3 mm2/seg; the healthy tissue has a median of 0.24X103 mm2/seg, interquartile range 0.19-0.56X10-3 mm2/seg. The U-Mann-Whitney test has a statistical significance of p<0.05. CONCLUSION: ADC measurement allows to confirm or rule out LMI in patients with the clinical suspicion of Wallenberg syndrome. It also serves to eliminate other diseases that showed restriction in DWI; for example, neoplasm, pontine myelinolysis, acute disseminated encephalomyelitis, multiple sclerosis and diffuse axonal injury. (L) Jornadas Académicas, 2016 Martes 27 de Septiembre, Cartel 35 al 67 50. ENDOVASCULAR CAROTID STENTING IN A PATIENT WITH PREVIOUS STROKE, ISCHEMIC HEART DISEASE, AND SEVERE AORTIC VALVE STENOSIS Lona-Pérez OA1, Balderrama-Bañares J2, Martínez-Reséndiz JA3, Yáñez-LedesmaM4, Jiménez-Zarazúa O5, Vargas-Jiménez MA6, Galeana-Juárez C6, Asensio-Lafuente E7, Barinagarrementeria-Aldatz F8, Barragán Campos H.M9,10. 1.2nd year student of the Faculty of Medicine at the University Autonomous of Querétaro, Qro., 2. Endovascular Neurological Therapy Department, Neurology and Neurosurgery National Institute “Dr. Manuel Velasco Suarez”, México City, México., 3. Department of Anesthesiology, Querétaro General Hospital, SESEQ, Querétaro, Qro., 4. Department of Anesthesiology, León Angeles Hospital, Gto., 5. Internal Medicine Department, León General Hospital, Gto., 6. Coordination of Clinical Rotation, Faculty of Medicine at the University Autonomous of Querétaro, Qro., 7. Cardiology-Electrophysiology , Hospital H+, Querétaro, Qro., 8. Neurologist, Permanent Member of National Academy of Medicine of Mexico, Hospital H+, Querétaro, Qro., 9. Magnetic Resonance Unit, Institute of Neurobiology, Campus Juriquilla, National Autonomous University of México, Querétaro, Qro., 10. Radiology Department. Querétaro General Hospital, SESEQ, Querétaro, Qro OBJECTIVE: We present a case report of a 74-year-old feminine patient who suffered from right superior gyrus stroke, ischemic heart disease, and severe valve aortic stenosis, in whom it was needed to identify which problem had to be treated first. Family antecedent of breast, pancreas, and prostate cancer in first order relatives; smoking 5 packages/year during >20 years, occasional alcoholism, right inguinal hernioplasty, hypertension and dyslipidemia of 3 years of evolution, under treatment. She presented angor pectoris at rest, lasted 3 minute long and has spontaneous recovery, 7 days later she had brain stroke at superior right frontal gyrus, developed hemiparesis with left crural predominance. MATERIALS & METHODS: Anamnesis, complete physical examination, laboratory, as well as heart and brain imaging were performed. Severe aortic valvular stenosis diagnosed by echocardiogram with 0.6 cm2 valvular area, average gradient of 38 mmHg and maximum of 66 mmHg; light mitral stenosis with valvular area of 1.8 cm2, without left atrium dilatation, maximum gradient of 8 mmHg; PSAP 30 mmHg, US Carotid Doppler showed atherosclerotic plaques in the proximal posterior wall of the bulb right internal carotid artery (RICA) that determinates a maximum stenosis of 70%. Aggressive management with antihypertensive (Met