Thursday, June 23, 2016
Keeping a Lab Notebook
Here's an example lab notebook page I made for my undergrads. It's the general format I use for experiments and thought it might be handy for some of you too.
Tuesday, April 26, 2016
#expbio APS Program: Chronic intermittent hypoxia suppresses adult neurogenesis and disrupts synaptic plasticity in the dentate gyrus of the hippocampus through a pro-oxidant state
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Figure 1: Sleep apnea occurs slightly more often in men
and causes substantial daytime sleepiness and can
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Monday, April 18, 2016
#expbio ASPET Blogging: Social defeat stress in males and females: Role of kappa opioid receptors
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Figure 1: A California mouse that is OMG cute.
(Sarah Laredo)
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Most currently prescribed anti-depressants
are neurotransmitter reuptake inhibitors. That means they work by keeping more
of certain molecules, called neurotransmitters, in the spaces between brain cells.
One-third to one-half of people with major depression find relief from symptoms
by taking one or more anti-depressants of this type. Women tend to respond
better to those of the serotonin selective reuptake inhibitor (SSRI) class,
which suggests there could be differences in how depression occurs in women and
men. Women are twice as likely to be diagnosed with major depression and yet
most scientific research on depression is done using male rodents. Dr. Brian
Trainor at the University of California, Davis uses both male and female
animals to better understand how depression and the response to
anti-depressants is different between the sexes. He is studying a different
type of anti-depressant treatment that works through the opioid system in the
brain.
Wednesday, April 13, 2016
#expbio ASPET Blogging: Chronic Antagonism of p38α MAPK Normalizes Serotonin Clearance, Serotonin Receptor Hypersensitivity and Social Behavior Deficits in a Genetic Murine Model of Autism Spectrum Disorder
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Figure 1: Serotonin synapse. (Source) |
Autism is a disorder with a high level of
heritability, meaning it is passed down through families genetically. There are
hundreds of gene mutations associated with autism. Some of these affect the
chemical and neurotransmitter serotonin. Previous work from the Blakely lab has
found five genetic variants in the serotonin transporter (SERT) associated with
autism. In about 30 percent of autism cases, there is an increase in serotonin
in blood platelets. This effect stems from SERT activity on the surface of
platelets. Neurons in the brain also contain these transporters and the gene
mutations associated with autism pull more serotonin into the cell, similar to
the transporters on platelets in the blood. In the brain, this leaves less
serotonin in the gap between neurons, called the synapse. Dr. Matthew Robson, a
postdoc in Dr. Randy Blakely’s lab at Vanderbilt University, is studying one
gene mutation implicated in autism. He is also using a drug that may help
relieve some of the symptoms of autism, such as impaired sociability, that are
untreatable with current medications.
Tuesday, April 12, 2016
#expbio ASPET Blogging: Correcting memory deficits in fragile X syndrome in targeting Rac1/PAK1 signaling
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Figure 1: X chromosome with mutations in the FMR1
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Fragile X Syndrome is the leading cause of
inherited intellectual disability. It is also the largest known genetic cause
of autism, though not the only genetic cause. The gene containing a mutation leading
to Fragile X Syndrome in humans is called FMR1 for Fragile X mental retardation
1. The protein made from the gene is involved in learning and memory so a
mutation in it leads to learning deficits. Previous research showed that FMR1
interacts with another protein implicated in intellectual disability called
Rac1. Rac1 is increased
in post-mortem brain tissue from patients with Fragile X Syndrome. Rac1 is one
protein that Luis Martinez is studying as an early graduate student in Dr. Maria
Tejada-Simon’s lab at the University of Houston College of Pharmacy. He is working
to find out how Rac1 signaling may be involved in the memory problems in
Fragile X Syndrome.
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