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
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
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
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
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
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
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