Brain Camp
Brain Camp is a residential summer experience for high school students interested in
the inner-workings of the brain. Students at Brain Camp live in on campus at
Muhlenberg College. The Camp features hands-on workshops that explore brain
anatomy, physiology, and development; and pioneer research projects in faculty
laboratories.
Each day at Brain Camp each year includes:
Morning sessions that demonstrate hot topics in neuroscience through hands-on
activities. Past activities have included: da Vinci and Brain Anatomy, What's Really
Happening on Fear Factor?, and This is Your Brain on Drugs.
Afternoon research projects that let students design their own experiments. Projects
are directed by faculty from the biology, neuroscience, and psychology departments at
Muhlenberg College.
Evening social activities including Dorney Park, outdoor movies, and more!
Brain Camp is a residential summer experience for high school students interested in
the inner-workings of the brain. Students at Brain Camp live in on campus at
Muhlenberg College. The Camp features hands-on workshops that explore brain
anatomy, physiology, and development; and pioneer research projects in faculty
laboratories.
Each day at Brain Camp each year includes:
Morning sessions that demonstrate hot topics in neuroscience through hands-on
activities. Past activities have included: da Vinci and Brain Anatomy, What's Really
Happening on Fear Factor?, and This is Your Brain on Drugs.
Afternoon research projects that let students design their own experiments. Projects
are directed by faculty from the biology, neuroscience, and psychology departments at
Muhlenberg College.
Evening social activities including Dorney Park, outdoor movies, and more!
Our Focus
News
Sentience Foundation Makes Two Campaign Gifts to Muhlenberg
to Support Undergraduate Research and Brain Camp:
http://www.muhlenberg.edu/talentscampaign/sentience.html
Sentience Foundation Makes Two Campaign Gifts to Muhlenberg
to Support Undergraduate Research and Brain Camp:
http://www.muhlenberg.edu/talentscampaign/sentience.html
Research
MUHLENBERG SUMMER STUDIES, 2011
-Amnesia Studies
"Consolidation theory" has long held as the foremost explanation for
many forms of amnesia. This theory proposed that old memories (i.e.,
those previously consolidated) were safe from the effects of an
amnesic agent, while newer memories (i.e., those presumably still
undergoing consolidation) were vulnerable. Work by neuroscientists
(Misanin et al. 968) challenged "consolidation theory" by showing that
old memories could be made vulnerable again simply by making them
“active” via a reactivation treatment (e.g., re-exposure to aspects of
the testing apparatus or context). , a small number of recent studies
have shown that protein synthesis is not required during
reconsolidation, unless the memory is being “updated” in some way
(i.e., new information is being integrated into the existing memory)
(e.g., Rossato et al., 2007; Winters et al., 2009; Robinson et al.,
2011; Lee, 2009). Particularly which novel elements play a role in
updating a memory, and therefore, make it vulnerable to a protein
synthesis inhibitor, are unclear. Muhlenberg summer neuroscience
students will systematically examine methods of “updating
consolidation."
-The Declining Bee Population
In 2010, a Muhlenberg student began examining the effects of pollution
on neurological responses to plant odors in Bombus impatiens.
Influenced by a recent marked decline in bumblebee populations in
North America and Europe, For 2011, Muhlenberg continued the hypothese
that agricultural products, such as fungicides, may have a deleterious
on bumblebee odor receptors. Certain pollutants that block receptors
on bee antennae used to locate plants. Theoretically, the bees then
have difficulty finding plant sources that they generally pollinate
and gain nutrients from. Thus, both a decline in bee and certain plant
populations would ensue. The student neuroscientist anesthetizes a bee
and performs a dissection of the antennal nerve. Once exposed, the bee
is placed on the rig and a pulled glass electrode is positioned just
outside of nerve using a micromanipulator. Extracellular recordings
are collected using the DataWave Sciworks computer program. Throughout
the recording, the bee is exposed to various conditions using an air
delivery system which is calibrated to release different combinations
of air, odorant, and pollutant. 2011 is devoted to continuing
expansion of the types of exposure the bees receive. the student will
records of just odorant, just pollutant, and a combination of both.
Additionally, he/she will now learning how to properly analyze my
recordings using a “cutting” technique to isolate the neurological
responses from motor responses and background noise. Once a larger
sample of successful recordings is available, formal statistical
analyses will be performed on this data in the hopes of finding a
trend in the neurological detection of pure odorants compared to
odorants masked by fertilizer pollutants.
-Post-Traumatic Stress Syndrome
A small number of animal models to examine post-traumatic stress
disorder (PTSD). Much of the work using these models has on reducing
and/or preventing the occurrence of PTSD via amnesia-causing drugs.
Little is known about the memory mechanisms underlying potential
treatments. In particular, given the “connectedness” of memory (i.e.,
the natural formation of schemas in our effective use of memory), it
appears that “erasing” one traumatic memory could cause loss of
similar memories, or their disruption. That "erasing factor" can
render treatment with β-blockers impractical, or even unethical. If a
patient is “reactivating” a traumatic memory using vivid imagery (a
common technique used in the human studies cited above), then it is
likely that any memory related to the trauma may also be reactivated
and made vulnerable to the amnesic agent. Our study aims to examine
the linking of memories: by training rats to discriminate between
sequences of odors pairs, by administering propranolol following
reactivation of a portion of the sequence, and then test rats for
their memory of the entire sequence. If these similar memories are
reactivated simply through exposure to one component of the series,
then we would be able predict that propranolol will cause wide-spread
memory loss and eliminate it from treatment possibilities. In another
experiment manipulating memory. Rats are learning an odor
discrimination task and then one element of the memory will be
changed. Using cycloheximide as a protein synthesis inhibitor, we
will see if our manipulation of the task is enough to reactivate the
memory and “erase” it.
DREW 2011 SUMMER RESEARCH SPONSORED BY SENTIENCE:
(All of Drew University's 2011 Summer Research is dedicated to studying Alzheimer's
Disease)
Student 1 :Recent evidence indicates that Type 2 diabetes is linked with Alzheimer's
disease. Last summer, Drew University's neuroscience laboratory collected
preliminary evidence that a combination of insulin and rosiglitazone could prevent a
loss of neuronal plasticity under Alzheimer's like conditions. However, the
mechanism of this protective effect is unclear. In 2011, Drew students plan to test the
hypothesis that insulin and rosiglitazone treatment maintains neuronal plasticity by
preventing a loss of ATP.
Student 2: There is conflicting evidence that GSK 3Beta inhibitors, such as Lithium,
may be effective in slowing down neuronal degeneration in Alzheimer's disease.
Research in our lab this past year suggests that these Lithium can reduce the
number of neurons that die, but as a consequence, cause neurons to lose plasticity.
We will test the hypothesis that combining a growth factor such as BDNF with lithium
treatment will lead to improved neuronal plasticity under Alzheimer's disease like
conditions.
Student 3: The drug Methylene Blue has had a successful Phase II drug trial in
treating Alzheimer's disease patients, though the mechanism of action is still
unknown. Our research in our lab these past two years points to mitochondria as a
likely site of action of this drug. However, the results of long term exposure to
Methylene Blue on neuronal function is unknown. We will test the hypothesis that
Methylene Blue will prevent a loss of synapses during a long term exposure to
Alzheimer's disease like conditions.
MUHLENBERG SUMMER STUDIES, 2011
-Amnesia Studies
"Consolidation theory" has long held as the foremost explanation for
many forms of amnesia. This theory proposed that old memories (i.e.,
those previously consolidated) were safe from the effects of an
amnesic agent, while newer memories (i.e., those presumably still
undergoing consolidation) were vulnerable. Work by neuroscientists
(Misanin et al. 968) challenged "consolidation theory" by showing that
old memories could be made vulnerable again simply by making them
“active” via a reactivation treatment (e.g., re-exposure to aspects of
the testing apparatus or context). , a small number of recent studies
have shown that protein synthesis is not required during
reconsolidation, unless the memory is being “updated” in some way
(i.e., new information is being integrated into the existing memory)
(e.g., Rossato et al., 2007; Winters et al., 2009; Robinson et al.,
2011; Lee, 2009). Particularly which novel elements play a role in
updating a memory, and therefore, make it vulnerable to a protein
synthesis inhibitor, are unclear. Muhlenberg summer neuroscience
students will systematically examine methods of “updating
consolidation."
-The Declining Bee Population
In 2010, a Muhlenberg student began examining the effects of pollution
on neurological responses to plant odors in Bombus impatiens.
Influenced by a recent marked decline in bumblebee populations in
North America and Europe, For 2011, Muhlenberg continued the hypothese
that agricultural products, such as fungicides, may have a deleterious
on bumblebee odor receptors. Certain pollutants that block receptors
on bee antennae used to locate plants. Theoretically, the bees then
have difficulty finding plant sources that they generally pollinate
and gain nutrients from. Thus, both a decline in bee and certain plant
populations would ensue. The student neuroscientist anesthetizes a bee
and performs a dissection of the antennal nerve. Once exposed, the bee
is placed on the rig and a pulled glass electrode is positioned just
outside of nerve using a micromanipulator. Extracellular recordings
are collected using the DataWave Sciworks computer program. Throughout
the recording, the bee is exposed to various conditions using an air
delivery system which is calibrated to release different combinations
of air, odorant, and pollutant. 2011 is devoted to continuing
expansion of the types of exposure the bees receive. the student will
records of just odorant, just pollutant, and a combination of both.
Additionally, he/she will now learning how to properly analyze my
recordings using a “cutting” technique to isolate the neurological
responses from motor responses and background noise. Once a larger
sample of successful recordings is available, formal statistical
analyses will be performed on this data in the hopes of finding a
trend in the neurological detection of pure odorants compared to
odorants masked by fertilizer pollutants.
-Post-Traumatic Stress Syndrome
A small number of animal models to examine post-traumatic stress
disorder (PTSD). Much of the work using these models has on reducing
and/or preventing the occurrence of PTSD via amnesia-causing drugs.
Little is known about the memory mechanisms underlying potential
treatments. In particular, given the “connectedness” of memory (i.e.,
the natural formation of schemas in our effective use of memory), it
appears that “erasing” one traumatic memory could cause loss of
similar memories, or their disruption. That "erasing factor" can
render treatment with β-blockers impractical, or even unethical. If a
patient is “reactivating” a traumatic memory using vivid imagery (a
common technique used in the human studies cited above), then it is
likely that any memory related to the trauma may also be reactivated
and made vulnerable to the amnesic agent. Our study aims to examine
the linking of memories: by training rats to discriminate between
sequences of odors pairs, by administering propranolol following
reactivation of a portion of the sequence, and then test rats for
their memory of the entire sequence. If these similar memories are
reactivated simply through exposure to one component of the series,
then we would be able predict that propranolol will cause wide-spread
memory loss and eliminate it from treatment possibilities. In another
experiment manipulating memory. Rats are learning an odor
discrimination task and then one element of the memory will be
changed. Using cycloheximide as a protein synthesis inhibitor, we
will see if our manipulation of the task is enough to reactivate the
memory and “erase” it.
DREW 2011 SUMMER RESEARCH SPONSORED BY SENTIENCE:
(All of Drew University's 2011 Summer Research is dedicated to studying Alzheimer's
Disease)
Student 1 :Recent evidence indicates that Type 2 diabetes is linked with Alzheimer's
disease. Last summer, Drew University's neuroscience laboratory collected
preliminary evidence that a combination of insulin and rosiglitazone could prevent a
loss of neuronal plasticity under Alzheimer's like conditions. However, the
mechanism of this protective effect is unclear. In 2011, Drew students plan to test the
hypothesis that insulin and rosiglitazone treatment maintains neuronal plasticity by
preventing a loss of ATP.
Student 2: There is conflicting evidence that GSK 3Beta inhibitors, such as Lithium,
may be effective in slowing down neuronal degeneration in Alzheimer's disease.
Research in our lab this past year suggests that these Lithium can reduce the
number of neurons that die, but as a consequence, cause neurons to lose plasticity.
We will test the hypothesis that combining a growth factor such as BDNF with lithium
treatment will lead to improved neuronal plasticity under Alzheimer's disease like
conditions.
Student 3: The drug Methylene Blue has had a successful Phase II drug trial in
treating Alzheimer's disease patients, though the mechanism of action is still
unknown. Our research in our lab these past two years points to mitochondria as a
likely site of action of this drug. However, the results of long term exposure to
Methylene Blue on neuronal function is unknown. We will test the hypothesis that
Methylene Blue will prevent a loss of synapses during a long term exposure to
Alzheimer's disease like conditions.
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Exploring and challenging the mind through
the sponsorship of brain research at the
university level and through a Sentience
Foundation Distinguished Speakers' Series
the sponsorship of brain research at the
university level and through a Sentience
Foundation Distinguished Speakers' Series
Phone: 732-598-1490
Monmouth Co. Office:
c/o of Milton Straus
100 Spruce St.
Freehold, NJ 07728
Web: www.sentiencefoundation.org
Email Us
Monmouth Co. Office:
c/o of Milton Straus
100 Spruce St.
Freehold, NJ 07728
Web: www.sentiencefoundation.org
Email Us