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Brain study may lead to improved epilepsy treatments
April 15, 2008Using a rodent model of epilepsy, researchers found one of the body's own neurotransmitters released during seizures, glutamate, turns on a signaling pathway in the brain that increases production of a protein that could reduce medication entry into the brain. Researchers say this may explain why approximately 30 percent of patients with epilepsy do not respond to antiepileptic medications. The study, conducted by researchers at the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health, and the University of Minnesota College of Pharmacy and Medical School, in collaboration with Heidrun Potschka's laboratory at Ludwig-Maximilians-University in Munich, Germany, is available online and will appear in the May 2008, issue of Molecular Pharmacology.
"Our work identifies the mechanism by which seizures increase production of a drug transport protein in the blood brain barrier, known as P-glycoprotein, and suggests new therapeutic targets that could reduce resistance," said David Miller, Ph.D., a principal investigator in the NIEHS Laboratory of Pharmacology and co-author on the paper.
The blood-brain barrier (BBB), which resides in brain capillaries, is a limiting factor in treatment of many central nervous system disorders. It is altered in epilepsy so that it no longer permits free passage of administered antiepileptic drugs into the brain. Miller explained that P-glycoprotein forms a functional barrier in the BBB that protects the brain by limiting access of foreign chemicals.
"The problem is that the protein does not distinguish well between neurotoxicants and therapeutic drugs, so it can often be an obstacle to the treatment of a number of diseases, including brain cancer," Miller said. Increased levels of P-glycoprotein in the BBB has been suggested as one probable cause of drug resistance in epilepsy.
Using isolated brain capillaries from mice and rats and an animal model of epilepsy, the researchers found that glutamate, a neurotransmitter released when neurons fire during seizures, turns on a signaling pathway that activates cyclooxygenase-2 (COX-2), causing increased synthesis of P-glycoprotein in these experiments. Increased transporter expression was abolished in COX-2 knockout mice or by COX-2 inhibitors. It has yet to be shown in animals or patients that targeting COX-2 will reduce seizure frequency or increase the effectiveness of anti-epileptic drugs.
"These findings provide insight into one mechanism that underlies drug resistance in epilepsy and possibly other central nervous system disorders," said Bjoern Bauer, Ph.D., lead author on the publication. "Targeting blood-brain barrier signals that increase P-glycoprotein expression rather than the transporter itself suggests a promising way to improve the effectiveness of drugs that are used to treat epilepsy, though more research is needed before new therapies can be developed."
NIH/National Institute of Environmental Health Sciences
"The problem is that the protein does not distinguish well between neurotoxicants and therapeutic drugs, so it can often be an obstacle to the treatment of a number of diseases, including brain cancer," Miller said. Increased levels of P-glycoprotein in the BBB has been suggested as one probable cause of drug resistance in epilepsy.
Using isolated brain capillaries from mice and rats and an animal model of epilepsy, the researchers found that glutamate, a neurotransmitter released when neurons fire during seizures, turns on a signaling pathway that activates cyclooxygenase-2 (COX-2), causing increased synthesis of P-glycoprotein in these experiments. Increased transporter expression was abolished in COX-2 knockout mice or by COX-2 inhibitors. It has yet to be shown in animals or patients that targeting COX-2 will reduce seizure frequency or increase the effectiveness of anti-epileptic drugs.
"These findings provide insight into one mechanism that underlies drug resistance in epilepsy and possibly other central nervous system disorders," said Bjoern Bauer, Ph.D., lead author on the publication. "Targeting blood-brain barrier signals that increase P-glycoprotein expression rather than the transporter itself suggests a promising way to improve the effectiveness of drugs that are used to treat epilepsy, though more research is needed before new therapies can be developed."
NIH/National Institute of Environmental Health Sciences
Epilepsy Current Events and Epilepsy News RSSGreater certainty in monitoring 3 therapeutic medications is facilitated by new CRMs
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Theory about long and short-term memory questioned by UCL scientists
The long-held theory that our brains use different mechanisms for forming long-term and short-term memories has been challenged by new research from UCL, published today in PNAS.
Developmental delay could stem from nicotinic receptor deletion
The loss of a gene through deletion of genetic material on chromosome 15 is associated with significant abnormalities in learning and behavior, said a consortium of researchers led by Baylor College of Medicine (www.bcm.edu) in a report that appears online today in the journal Nature Genetics.
Protein critical for insulin secretion may be contributor to diabetes
A cellular protein from a family involved in several human diseases is crucial for the proper production and release of insulin, new research has found, suggesting that the protein might play a role in diabetes.
Packages of care for epilepsy in low- and middle-income countries
In the second in a six part series on treating mental health problems in resource-poor settings, Caroline Mbuba and Charles Newton (Centre for Geographic Medicine Research, Kenya Medical Research Institute, Kilifi, Kenya) discuss "packages of care" for treating epilepsy.
Study pinpoints key mechanism in brain development, raising question about use of antiseizure drug
Researchers at the Stanford University School of Medicine have identified a key molecular player in guiding the formation of synapses - the all-important connections between nerve cells - in the brain.
tudy: The new buzz on detecting tinnitus
It's a ringing, a buzzing, a hissing or a clicking - and the patient is the only one who can hear it. Complicating matters, physicians can rarely pinpoint the source of tinnitus, a chronic ringing of the head or ears that can be as quiet as a whisper or as loud as a jackhammer.
Researchers find a key mechanism in the development of nerve cells
Chaos brews in the brains of newborns: the nerve cells are still bound only loosely to each other.
How mitochondrial gene defects impair respiration, other major life functions
Researchers are delving into abnormal gene function in mitochondria, structures within cells that power our lives. Mitochondria are the place where energy is generated from the most basic molecules of food. Because this function is essential to life, defects in mitochondria may affect a wide range of organ systems in humans and animals.
Pancreatic fat levels may help predict diabetes, UT Southwestern researchers say
Researchers have long suspected that overweight people tend to have large fat deposits in their pancreases, but they've been unable to confirm or calculate how much fat resides there because of the organ's location. Until now.
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