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Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
Vascularización cerebral (parte ii)
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Vascularización cerebral (parte ii)

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  • 1. Angiogénesis yneurogénesis Dos caminos paralelosmartes 15 de noviembre de 2011
  • 2. “De humani corporis fabrica”martes 15 de noviembre de 2011
  • 3. Carmeliet and Tessier-Lavigne, Nature. 2005martes 15 de noviembre de 2011
  • 4. Zacchigna et al., Nature Reviews Neuroscience. 2008martes 15 de noviembre de 2011
  • 5. Desarrollo cortical Predeterminado genéticamente Mediado por experienciamartes 15 de noviembre de 2011
  • 6. Desarrollo cortical Predeterminado genéticamente Mediado por experiencia PERIODO CRÍTICO 3ª - 5ª semanasmartes 15 de noviembre de 2011
  • 7. Neurogenesis Angiogenesis ?martes 15 de noviembre de 2011
  • 8. Neurogenesis Angiogenesis ?martes 15 de noviembre de 2011
  • 9. Neurogenesis Angiogenesis ?martes 15 de noviembre de 2011
  • 10. Neurogenesis Angiogenesis Nicho vascular (neurogenesis). Palmer 2000. Incremento demanda. Black 1987. Coordinados. Carmeliet 2005.martes 15 de noviembre de 2011
  • 11. Desarrollo neurovascular Evento coordinado Respuesta común a señales comunes VEGF Neurotrofinas (NGF, BDNF, NTs) Neuropilinas (Nrp1, Nrp2) Semaforinas (Sema3A) Efrinas/Ephs (EphB-ephrinB) Angiopoyetinas (Ang2)martes 15 de noviembre de 2011
  • 12. Neuroscience 171 (2010) 214 –226 ANGIOGENESIS BUT NOT NEUROGENESIS IS CRITICAL et al. / Neuroscience 171 (2010) 214 –226 A. L. Kerr FOR NORMAL LEARNING AND MEMORY ACQUISITION A. L. KERR,1 E. L. STEUER, V. POCHTAREV AND cognitive performance on a variety of tasks including the R. A. SWAIN* Morris water maze (MWM), contextual fear conditioning, University of Wisconsin-Milwaukee, Milwaukee, WI, USA extinction of contextual fear, and radial arm maze (Ander- son et al., 2000; Baruch et al., 2004; Fordyce and Wehner, 1993; Gobbo and O’Mara, 2004; Pietropaolo et al., 2006; Abstract—Aerobic exercise has been well established to pro- mote enhanced learning and memory in both human and Powell, 2005; Vaynman et al., 2004). In humans, exercise non-human animals. Exercise regimens enhance blood per- has been associated with improved cognitive performance in fusion, neo-vascularization, and neurogenesis in nervous young adult, aging adult, and brain-injured populations system structures associated with learning and memory. The (Churchill et al., 2002; Grealy et al., 1999; Kramer and Erick- impact of specific plastic changes to learning and memory son, 2007; Kramer et al., 2006; Winter et al., 2007) and has performance in exercising animals are not well understood. been shown to protect against the onset of various demen- The current experiment was designed to investigate the con- tias, including Alzheimer’s disease (Laurin et al., 2001). tributions of angiogenesis and neurogenesis to learning and memory performance by pharmacologically blocking each The means by which experience facilitates learning process in separate groups of exercising animals prior to and memory are not fully understood. However, the sur- visual spatial memory assessment. Results from our experi- vival of new neurons may contribute to learning and mem- ment indicate that angiogenesis is an important component ory changes following exercise. It has been consistently of learning as animals receiving an angiogenesis inhibitor shown that both enriched environments and exercise (vol- exhibit retarded Morris water maze (MWM) acquisition. Inter- untary and forced) promote neurogenesis in the adult hip- estingly, our results also revealed that neurogenesis inhibi- pocampus, specifically in the dentate gyrus (DG) (Christie tion improves learning and memory performance in the MWM. Animals that received the neurogenesis inhibitor dis- et al., 2008; Kempermannn et al., 1997, 1998; Kim et al., played the best overall MWM performance. These results 2002; Olson et al., 2006; Uysal et al., 2005; Van der Borght point to the importance of vascular plasticity in learning and et al., 2006; van Praag et al., 2005), and exercise-induced memory function and provide empirical evidence to support neurogenesis is correlated with improved learning and mem- the use of manipulations that enhance vascular plasticity to ory performance (Uysal et al., 2005; van Praag et al., 2005). improve cognitive function and protect against natural cog- However, there are also reports that manipulation of neuro- nitive decline. © 2010 IBRO. Published by Elsevier Ltd. All genesis does not impact learning and memory function in the rights reserved. MWM (Meshi et al., 2006; Shors et al., 2002) or contextual Key words: vascular plasticity, exercise-induced facilitation, fear conditioning (Clark et al., 2008; Shors et al., 2002), Morris water maze. indicating that neurogenesis may not be the sole supporter of enhanced cognitive performance following exercise. The contribution of neurogenesis to learning and mem- Aerobic exercise promotes enhanced learning and mem- ory function is further complicated by recent evidence sug- ory in both human and non-human animals. At the cellular gesting that newly proliferated neurons are not immedi- level, exercise is associated with increased angiogenesis ately and functionally incorporated into existing learning (the sprouting of new capillaries from preexisting blood networks. While it is clear that new neurons do become vessels) and/or neurogenesis in various areas of the brain functionally integrated into the existing circuitry eventually, including the hippocampus, motor cortex and cerebellum several recent reports indicate that this integration is a (Black et al., 1991; Clark et al., 2009; Isaacs et al., 1992; somewhat delayed process taking between 3 and 4 weeks Kim et al., 2002; Sikorski et al., 2008; Swain et al., 2003; to complete (Kee et al., 2007; Overstreet et al., 2004; van van Praag et al., 2005). Aerobic exercise in rodents is also Praag et al., 2002). These data are supported by behav- associated with improved recovery following ischemic in- ioral studies indicating that impaired neurogenesis does sult (Lee et al., 2003a,b; Sim et al., 2004) and improved not affect visual spatial memory in the MWM immediately 1 Present address: University of Texas, Austin, TX, USA. following treatment but impairs performance when memory *Corresponding author. Tel: 1-414-229-5883; fax: 1-414-229-5219. is tested 28 days later (Hu et al., 2008).martes 15 deABC, avidin-biotin complex;Swain). 4.AZT-injected vol- E-mail address: rswain@uwm.edu (R. A. Abbreviations: noviembre de 2011 Fig. The current experiment investigated the relative con- AZT-VX, BrdU quantification and NeuN colabel. Tissue was treated with immunohistochemical antibodies targeting BrdU to label dividing cells (indi
  • 13. Neuroscience 171 (2010) 214 –226 ANGIOGENESIS BUT NOT NEUROGENESIS IS CRITICAL FOR NORMAL LEARNING AND MEMORY ACQUISITION A. L. KERR,1 E. L. STEUER, V. POCHTAREV AND cognitive performance on a variety of tasks including the R. A. SWAIN* Morris water maze (MWM), contextual fear conditioning, University of Wisconsin-Milwaukee, Milwaukee, WI, USA extinction of contextual fear, and radial arm maze (Ander- son et al., 2000; Baruch et al., 2004; Fordyce and Wehner, 1993; Gobbo and O’Mara, 2004; Pietropaolo et al., 2006; Abstract—Aerobic exercise has been well established to pro- mote enhanced learning and memory in both human and Powell, 2005; Vaynman et al., 2004). In humans, exercise non-human animals. Exercise regimens enhance blood per- has been associated with improved cognitive performance in fusion, neo-vascularization, and neurogenesis in nervous young adult, aging adult, and brain-injured populations system structures associated with learning and memory. The (Churchill et al., 2002; Grealy et al., 1999; Kramer and Erick- impact of specific plastic changes to learning and memory son, 2007; Kramer et al., 2006; Winter et al., 2007) and has performance in exercising animals are not well understood. been shown to protect against the onset of various demen- The current experiment was designed to investigate the con- tias, including Alzheimer’s disease (Laurin et al., 2001). tributions of angiogenesis and neurogenesis to learning and memory performance by pharmacologically blocking each The means by which experience facilitates learning process in separate groups of exercising animals prior to and memory are not fully understood. However, the sur- visual spatial memory assessment. Results from our experi- vival of new neurons may contribute to learning and mem- ment indicate that angiogenesis is an important component ory changes following exercise. It has been consistently of learning as animals receiving an angiogenesis inhibitor shown that both enriched environments and exercise (vol- exhibit retarded Morris water maze (MWM) acquisition. Inter- untary and forced) promote neurogenesis in the adult hip- estingly, our results also revealed that neurogenesis inhibi- pocampus, specifically in the dentate gyrus (DG) (Christie tion improves learning and memory performance in the MWM. Animals that received the neurogenesis inhibitor dis- et al., 2008; Kempermannn et al., 1997, 1998; Kim et al., played the best overall MWM performance. These results 2002; Olson et al., 2006; Uysal et al., 2005; Van der Borght point to the importance of vascular plasticity in learning and et al., 2006; van Praag et al., 2005), and exercise-induced memory function and provide empirical evidence to support neurogenesis is correlated with improved learning and mem- the use of manipulations that enhance vascular plasticity to ory performance (Uysal et al., 2005; van Praag et al., 2005). improve cognitive function and protect against natural cog- However, there are also reports that manipulation of neuro- nitive decline. © 2010 IBRO. Published by Elsevier Ltd. All genesis does not impact learning and memory function in the rights reserved. MWM (Meshi et al., 2006; Shors et al., 2002) or contextual Key words: vascular plasticity, exercise-induced facilitation, fear conditioning (Clark et al., 2008; Shors et al., 2002), Morris water maze. indicating that neurogenesis may not be the sole supporter of enhanced cognitive performance following exercise. The contribution of neurogenesis to learning and mem- Aerobic exercise promotes enhanced learning and mem- ory function is further complicated by recent evidence sug- ory in both human and non-human animals. At the cellular gesting that newly proliferated neurons are not immedi- level, exercise is associated with increased angiogenesis ately and functionally incorporated into existing learning (the sprouting of new capillaries from preexisting blood networks. While it is clear that new neurons do become vessels) and/or neurogenesis in various areas of the brain functionally integrated into the existing circuitry eventually, including the hippocampus, motor cortex and cerebellum several recent reports indicate that this integration is a (Black et al., 1991; Clark et al., 2009; Isaacs et al., 1992; somewhat delayed process taking between 3 and 4 weeks Kim et al., 2002; Sikorski et al., 2008; Swain et al., 2003; to complete (Kee et al., 2007; Overstreet et al., 2004; van van Praag et al., 2005). Aerobic exercise in rodents is also Praag et al., 2002). These data are supported by behav-WM one probe trials. (A) All animals ischemic equivalentstudies indicating time in the correct quadrant during the first probe trial. (B) All animals associated with improved recovery following spent in- ioral amounts of that impaired neurogenesis does sult (Lee et al., 2003a,b; Sim et al., 2004) and improved not affect visual spatial memory in the MWM immediatelyilar amounts of time in the SW quadrant, which is directlytreatment but impairs performance when memory represents the greatest distance from the plat 1 Present address: University of Texas, Austin, TX, USA. following opposite the target quadrant andals can search.author. Tel: 1-414-229-5883; fax: 1-414-229-5219. trial, SU5416-VX later (Hu et al., 2008). *Corresponding (C) During the remote probe is tested 28 days and VEH-IC animals spent significantly less time in the correct quadrant martes 15 de noviembre de 2011 E-mail address: rswain@uwm.edu (R. A. Swain). The current experiment investigated the relative con-
  • 14. Sistema visual Sistema Visualmartes 15 de noviembre de 2011
  • 15. Periodo crítico 4ª semana Cambios mediados por experiencia 1º-3ª semanas 4ª-6ª semanas 7ª y 8ª semanas Periodo precritico Periodo crítico Periodo postcrítico Agemartes 15 de noviembre de 2011
  • 16. Empobrecimiento ambiental Descenso densidades neuronal, glial y vascular Retraso maduración Anulación cierre periodo críticomartes 15 de noviembre de 2011
  • 17. Empobrecimiento ambientalmartes 15 de noviembre de 2011
  • 18. Cortical parametersmartes 15 de noviembre de 2011
  • 19. Cortical parametersmartes 15 de noviembre de 2011
  • 20. Cortical parametersmartes 15 de noviembre de 2011
  • 21. Vascular densitymartes 15 de noviembre de 2011
  • 22. Vascular densitymartes 15 de noviembre de 2011
  • 23. Results 120 25 100 20 80 15 Oscuridad 60 Controles 10 40 5 20 0 0 0 DPN 7 DPN 14 DPN 21 DPN 60 DPN 0 DPN 7 DPN 14 DPN 21 DPN 60 DPN Number of Vascular Density perpendicular vesselsmartes 15 de noviembre de 2011
  • 24. Enriquecimiento ambiental Donald Hebb (1949) Kresh, Bennett, Rosenzweig, Diamond (60s) Combinación de complejidad de objetos inanimados y estimulación social.martes 15 de noviembre de 2011
  • 25. Enriquecimiento ambiental Cambios anatómicos Plasticidad neuronal Sinaptogénesis Morfología sináptica Neurogénesis Neurotrofinas (BDNF, NGF, NT-3,VEGF) Gliogénesismartes 15 de noviembre de 2011
  • 26. Enriquecimiento ambiental Reduce el deficit de memoria tras ictus (Dahlqvist, 2004) Mejora la recuperiación funcional tras lesión estriatal (Dobrossy 2004) Induce neurogenesis en hipocampo (Kempermann 1997) Reduce los efectos del Hungtington (Spires 2004) Madura y consolida la corteza visual en ratas privadas de luz (Bertoletti 2004) Revierte los efectos del stress prenatal (Morley-Fletcher 2003) Acelera el desarrollo de la corteza visual (Cancedda 2004)martes 15 de noviembre de 2011
  • 27. Enriquecimiento ambientalmartes 15 de noviembre de 2011
  • 28. Enriquecimiento ambientalmartes 15 de noviembre de 2011
  • 29. Enriquecimiento ambientalmartes 15 de noviembre de 2011
  • 30. Enriquecimiento ambiental Edades : . 14 dpn, 21 dpn Pre-critical . 28 dpn, 35 dpn, 42 dpn Critical period . 49 dpn, 56 dpn, 63 dpn Postcriticalmartes 15 de noviembre de 2011
  • 31. martes 15 de noviembre de 2011
  • 32. Estudio cualitativomartes 15 de noviembre de 2011 Inmunohistoquimia Histoquimia LEA EBA GluT-1
  • 33. LEA EBA Estudio cualitativomartes 15 de noviembre de 2011
  • 34. Estudio cualitativo EBA GluT-1 EBA + GluT-1martes 15 de noviembre de 2011
  • 35. Enriquecimiento ambiental Angiogénesismartes 15 de noviembre de 2011
  • 36. Estudio cuantitativomartes 15 de noviembre de 2011
  • 37. VEGF WESTERN BLOT ELISAmartes 15 de noviembre de 2011
  • 38. martes 15 de noviembre de 2011
  • 39. ELISAmartes 15 de noviembre de 2011
  • 40. VEGF levels 6,0 CE Control DR DR-CE 4,5 3,0 1,5 0 14 dpn 21 dpn 28 dpn 35 dpn 42 dpn 49 dpn 56 dpn 63 dpnmartes 15 de noviembre de 2011
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  • 42. martes 15 de noviembre de 2011
  • 43. Patología SNC TCE Ictus Tumores Patologías neurodegenerativasmartes 15 de noviembre de 2011
  • 44. Patología SNC TCE Ictus Tumores Patologías neurodegenerativas Vascularizaciónmartes 15 de noviembre de 2011
  • 45. Neuroprotección mediante enriquecimiento ambiental Patologías neurodegenerativas Parkinson Alzheimer Hungtinton Ictus TCEmartes 15 de noviembre de 2011
  • 46. Objetivos terapeúticos Neuroprotección/neurorescate Incremento vascularizaciónmartes 15 de noviembre de 2011
  • 47. TCE en Desarrollo Mayor capacidad de plasticidad Interferencia en los mecanismos fisiológicos Apoptosis Plasticidad sináptica (NMDA)martes 15 de noviembre de 2011

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