May 2012 - Neuro-All - University of Manitoba Mailing Lists

CANCELLED - Dr. Sheena Josselyn talk - Friday June 1
by Winnipeg Chapter Society for Neuroscience 30 May '12

30 May '12

CANCELLED St. Boniface Hospital Research Neuroscience Seminar Series Hosted by the Division of Neurodegenerative Disorders Friday, June 1st, 2012 PZ236/238 PsychHealth Bldg. Bannatyne Campus 12:00 Noon Dr. Sheena Josselyn Senior Scientist, Neurosciences & Mental Health Canada Research Chair <http://www.chairs.gc.ca> , Molecular and Cellular Cognition Associate Professor, Department of Physiology University of Toronto Hospital for Sick Children, Toronto, ON Topic: Making and Breaking Memories A fundamental goal of neuroscience is to understand how memories are encoded and stored in the brain. Indeed, identifying the physical basis of memory within the brain (the memory trace) has been a long-standing challenge for scientists since Karl Lashley's "search for the engram" in the 1950's. Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased CREB are preferentially activated by fear memory expression, suggesting they are selectively recruited into the memory trace. Here we used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning blocked expression of that fear memory. The resulting memory loss was robust and persistent, suggesting that the memory was permanently erased. These results establish a causal link between a specific neuronal subpopulation and memory expression, thereby identifying critical neurons within the memory trace. Short bio: The research in Dr. Josselyn's lab is dedicated to understanding the neural basis of cognitive function and dysfunction. To unravel the molecular, cellular and circuit processes that underlie learning and memory, her lab uses a multidisciplinary approach include the use of genetically-engineered mice, viral vectors, cellular imaging, electrophysiology and detailed behavioral analysis. Her program of research focuses on two main elements 1) examining the brain regions and molecules responsible for normal memory formation and 2) using this knowledge to intervene in conditions in which memory is impaired (for instance in neurodegenerative diseases such as Alzheimer's disease). She has published extensively in the top scientific journals on these subjects and has shown that fear memories in mice can be "erased" and is currently examining novel treatments for the memory disorders that characterize Alzheimer's disease. Kelly Jorundson Administrative Manager Division of Neurodegenerative Disorders St. Boniface Hospital Research Department of Pharmacology & Therapeutics University of Manitoba Tel: 204.235.3939 Fax: 204.237.4092 Email: kjorund(a)sbrc.ca OR kjorund(a)yahoo.ca Website: www.sbrc.ca/dnd OR www.umanitoba.ca/medicine/units/pharmacology

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MAY 31 Registration deadline for Manitoba Neuroscience Network Meeting June 4
by Winnipeg Chapter Society for Neuroscience 28 May '12

28 May '12

Dear Manitoba Neuroscientists, Please register by MAY 31 for the MNN annual meeting this Monday June 4 at the Hilton Suites Winnipeg Airport. The program committee is pleased to bring you a day filled with talks and posters from YOUR local Manitoba neuroscience research community, along with plenty of opportunities for informal discussion with your peers. Highlights of the day include 2 keynote presentations by top Canadian neuroscientists, Drs. Quentin Pittman (Hotchkiss Brain Research Institute, Calgary) and Keith Murai (McGill University, Montreal). Don't miss these excellent visiting speakers. For the entire PROGRAM, please visit: http://www.cvent.com/events/manitoba-neuroscience-network-3rd-annual-mee ting/agenda-12348237e5b847648c27a499d8e7f015.aspx REGISTER at: http://www.cvent.com/events/manitoba-neuroscience-network-3rd-annual-mee ting/custom-20-12348237e5b847648c27a499d8e7f015.aspx See you Monday! ------------------------------------------------------------------------ --------------- Chris M. Anderson, Ph.D. President, Winnipeg Chapter, Society for Neuroscience Director, Manitoba Neuroscience Network 204.235.3939 wcsn(a)sbrc.ca

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Reminder: Dr. Sheena Josselyn talk - Friday June 1
by Winnipeg Chapter Society for Neuroscience 28 May '12

28 May '12

St. Boniface Hospital Research Neuroscience Seminar Series Hosted by the Division of Neurodegenerative Disorders Friday, June 1st, 2012 PZ236/238 PsychHealth Bldg. Bannatyne Campus 12:00 Noon Dr. Sheena Josselyn Senior Scientist, Neurosciences & Mental Health Canada Research Chair <http://www.chairs.gc.ca> , Molecular and Cellular Cognition Associate Professor, Department of Physiology University of Toronto Hospital for Sick Children, Toronto, ON Topic: Making and Breaking Memories A fundamental goal of neuroscience is to understand how memories are encoded and stored in the brain. Indeed, identifying the physical basis of memory within the brain (the memory trace) has been a long-standing challenge for scientists since Karl Lashley's "search for the engram" in the 1950's. Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased CREB are preferentially activated by fear memory expression, suggesting they are selectively recruited into the memory trace. Here we used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning blocked expression of that fear memory. The resulting memory loss was robust and persistent, suggesting that the memory was permanently erased. These results establish a causal link between a specific neuronal subpopulation and memory expression, thereby identifying critical neurons within the memory trace. Short bio: The research in Dr. Josselyn's lab is dedicated to understanding the neural basis of cognitive function and dysfunction. To unravel the molecular, cellular and circuit processes that underlie learning and memory, her lab uses a multidisciplinary approach include the use of genetically-engineered mice, viral vectors, cellular imaging, electrophysiology and detailed behavioral analysis. Her program of research focuses on two main elements 1) examining the brain regions and molecules responsible for normal memory formation and 2) using this knowledge to intervene in conditions in which memory is impaired (for instance in neurodegenerative diseases such as Alzheimer's disease). She has published extensively in the top scientific journals on these subjects and has shown that fear memories in mice can be "erased" and is currently examining novel treatments for the memory disorders that characterize Alzheimer's disease. Everyone is invited to attend! For more information contact DND Office: (T) 235.3939 or (E) dnd(a)sbrc.ca Kelly Jorundson Administrative Manager Division of Neurodegenerative Disorders St. Boniface Hospital Research Department of Pharmacology & Therapeutics University of Manitoba Tel: 204.235.3939 Fax: 204.237.4092 Email: kjorund(a)sbrc.ca OR kjorund(a)yahoo.ca Website: www.sbrc.ca/dnd OR www.umanitoba.ca/medicine/units/pharmacology

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Neuroscience Seminar: Dr. Sheena Josselyn
by Winnipeg Chapter Society for Neuroscience 24 May '12

24 May '12

Please circulate/post: St. Boniface Hospital Research Neuroscience Seminar Series (Hosted by the Division of Neurodegenerative Disorders) Friday, June 1st, 2012 PX236/238 PsychHealth Bldg., Bannatyne Campus 12:00 Noon Dr. Sheena Josselyn Senior Scientist, Neurosciences & Mental Health Canada Research Chair, Molecular and Cellular Cognition Associate Professor, Department of Physiology University of Toronto Hospital for Sick Children, Toronto, ON Topic: Making and Breaking Memories Abstract: A fundamental goal of neuroscience is to understand how memories are encoded and stored in the brain. Indeed, identifying the physical basis of memory within the brain (the memory trace) has been a long-standing challenge for scientists since Karl Lashley's "search for the engram" in the 1950's. Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased CREB are preferentially activated by fear memory expression, suggesting they are selectively recruited into the memory trace. Here we used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning blocked expression of that fear memory. The resulting memory loss was robust and persistent, suggesting that the memory was permanently erased. These results establish a causal link between a specific neuronal subpopulation and memory expression, thereby identifying critical neurons within the memory trace. Short bio: The research in Dr. Josselyn's lab is dedicated to understanding the neural basis of cognitive function and dysfunction. To unravel the molecular, cellular and circuit processes that underlie learning and memory, her lab uses a multidisciplinary approach include the use of genetically-engineered mice, viral vectors, cellular imaging, electrophysiology and detailed behavioral analysis. Her program of research focuses on two main elements 1) examining the brain regions and molecules responsible for normal memory formation and 2) using this knowledge to intervene in conditions in which memory is impaired (for instance in neurodegenerative diseases such as Alzheimer's disease). She has published extensively in the top scientific journals on these subjects and has shown that fear memories in mice can be "erased" and is currently examining novel treatments for the memory disorders that characterize Alzheimer's disease. Kelly Jorundson Administrative Manager Division of Neurodegenerative Disorders St. Boniface Hospital Research Department of Pharmacology & Therapeutics University of Manitoba Tel: 204.235.3939 Fax: 204.237.4092 Email: kjorund(a)sbrc.ca OR kjorund(a)yahoo.ca Website: www.sbrc.ca/dnd OR www.umanitoba.ca/medicine/units/pharmacology

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MNN Seminar this Friday - CANCELLED
by Winnipeg Chapter Society for Neuroscience 24 May '12

24 May '12

Dear Neuro-all, The MNN Seminar scheduled for Friday, May 25, 2012 at 9am has been CANCELLED. /send on behalf of Chris Anderson Kelly Jorundson Winnipeg Chapter Society for Neuroscience R4046 - 351 Tache Avenue Winnipeg, MB R2H 2A6 Tel: 204.235.3939 Fax: 204.237.4092 Email: kjorund(a)sbrc.ca OR kjorund(a)yahoo.ca

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Visiting Speraker - Dr. Subrata Chakrabarti May 18th
by Winnipeg Chapter Society for Neuroscience 15 May '12

15 May '12

DND Visiting Speaker - Dr. Subrata Chakrabarti <http://www.sbrc.ca/2012/05/05182012-dnd-visiting-speaker-dr-subrata-chakrab…> Posted on: May 15, 2012 Print PDF <http://www.printfriendly.com/print/v2?url=http://www.sbrc.ca/2012/05/051820…> Friday, May 18th, 2012 12:00 Noon - Samuel Cohen Auditorium St. Boniface Hospital Research (Video-linked to Bannatyne Campus, A229 Chown Bldg.) <http://www.sbrc.ca/wp-content/uploads/2012/05/chakrabarti.jpg> Dr. Subrata Chakrabarti Dept. of Pathology, Schulich School of Medicine and Dentistry, Western University and London Health Sciences Center, London, Ontario. Topic: Novel mechanisms in the pathogenesis of diabetic retinopathy. Dysfunction of endothelial cell (ECs) causing increased production of vasoactive factors and extracellular matrix (ECM) proteins are characteristic features of chronic diabetic complications such as diabetic retinopathy. Glucose-induced biochemical alterations in the ECs activate a cascade of signaling pathways leading to such changes. Chronic diabetes leads to the activation of a number of signaling proteins including protein kinase C and advanced glycation end product formation. These signaling cascades are activated in response to hyperglycemia-induced oxidative stress. Such aberrant signaling leads to activation of transcription factors, such as nuclear factor-κB and activating protein-1. Although transcription factors are of importance in the regulation of protein production, they remain ineffective without transcriptional co-activators. In diabetes, transcriptional co-activator p300, with histone acetyl transferase activity, regulates several transcription factors. In addition, microRNA alterations regulate gene expression and the downstream effects eg. increased vasoactive factor and ECM protein production. Blockers of oxidative stress and histone acetylation as well as selected miRNA mimics prevent such alteration. Hence a complex web of pathways including intracellular signaling, epigenetics and miRNA alterations are involved in the pathogenesis of functional and structural changes in chronic diabetic complications. We have identified specific changes in the ECs and in the organs affected by diabetic complications such as retina. We have also identified novel adjunct treatment strategies, targeting epigenetic and transcriptional machinery for chronic diabetic complications such as retinopathy. (Supported by Grants from Canadian Institute of health Research, Canadian Diabetes Association and Heart and Stroke Foundation of Ontario) For more information contact DND Office: (T) 235.3939 or (E) dnd(a)sbrc.ca Kelly Jorundson Administrative Manager Division of Neurodegenerative Disorders St. Boniface Hospital Research Department of Pharmacology & Therapeutics University of Manitoba Tel: 204.235.3939 Fax: 204.237.4092 Email: kjorund(a)sbrc.ca OR kjorund(a)yahoo.ca Website: www.sbrc.ca/dnd OR www.umanitoba.ca/medicine/units/pharmacology

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Visiting Speaker Dr. Subrata Chakrabarti
by Winnipeg Chapter Society for Neuroscience 07 May '12

07 May '12

Neuroscience Seminar Series Hosted by the Division of Neurodegenerative Disorders Friday, May 18th, 2012 Samuel Cohen Auditorium St. Boniface Hospital Research 12:00 Noon (Video-linked to Bannatyne Campus, A229 Chown Bldg.) Dr. Subrata Chakrabarti Dept. of Pathology, Schulich School of Medicine and Dentistry, Western University and London Health Sciences Center, London, Ontario Topic: Novel mechanisms in the pathogenesis of diabetic retinopathy. Dysfunction of endothelial cell (ECs) causing increased production of vasoactive factors and extracellular matrix (ECM) proteins are characteristic features of chronic diabetic complications such as diabetic retinopathy. Glucose-induced biochemical alterations in the ECs activate a cascade of signaling pathways leading to such changes. Chronic diabetes leads to the activation of a number of signaling proteins including protein kinase C and advanced glycation end product formation. These signaling cascades are activated in response to hyperglycemia-induced oxidative stress. Such aberrant signaling leads to activation of transcription factors, such as nuclear factor-κB and activating protein-1. Although transcription factors are of importance in the regulation of protein production, they remain ineffective without transcriptional co-activators. In diabetes, transcriptional co-activator p300, with histone acetyl transferase activity, regulates several transcription factors. In addition, microRNA alterations regulate gene expression and the downstream effects eg. increased vasoactive factor and ECM protein production. Blockers of oxidative stress and histone acetylation as well as selected miRNA mimics prevent such alteration. Hence a complex web of pathways including intracellular signaling, epigenetics and miRNA alterations are involved in the pathogenesis of functional and structural changes in chronic diabetic complications. We have identified specific changes in the ECs and in the organs affected by diabetic complications such as retina. We have also identified novel adjunct treatment strategies, targeting epigenetic and transcriptional machinery for chronic diabetic complications such as retinopathy. (Supported by Grants from Canadian Institute of health Research, Canadian Diabetes Association and Heart and Stroke Foundation of Ontario) For more information contact DND Office: (T) 235.3939 or (E) dnd(a)sbrc.ca Kelly Jorundson Administrative Manager Division of Neurodegenerative Disorders St. Boniface Hospital Research Department of Pharmacology & Therapeutics University of Manitoba Tel: 204.235.3939 Fax: 204.237.4092 Email: kjorund(a)sbrc.ca OR kjorund(a)yahoo.ca Website: www.sbrc.ca/dnd OR www.umanitoba.ca/medicine/units/pharmacology

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