Thursday, June 23, 2016
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
Figure 1: Sleep apnea occurs slightly more often in men
and causes substantial daytime sleepiness and can
impair cognitive function. (Source: geralt)
Monday, April 18, 2016
Figure 1: A California mouse that is OMG cute.
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
|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
Figure 1: X chromosome with mutations in the FMR1
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.