The Role of Gaba and Nmda in the Epileptic Brain

Topics: Neurotransmitter, Action potential, Neuron Pages: 7 (2302 words) Published: May 8, 2006
Epilepsy is a disorder in which the balance between cerebral excitability and inhibition is tipped toward uncontrolled excitability. It is not a single disorder but rather, a wide spectrum of problems. All types of epilepsy share an uncontrolled electrical discharge from nerve cells in the cerebral cortex. This is the part of the brain that integrates higher mental function, general movement and functions of internal organs in the abdominal cavity, perception and behavioral reactions (Holmes, 15). Epilepsy types are generally classified as partial or generalized seizures. A partial or focal seizure is the more common type that implies that such seizures affect only small or specific locations in the brain. Generalized seizures are caused by nerve cell disturbances that occur in more diffused areas of the brain. Therefore they have more serious effects on the patient (Pierson, 210)

Epilepsy may develop because of an abnormality in brain wiring, an imbalance of nerve signaling chemicals called neurotransmitters, or some combination of these factors. Researchers believe that some people with epilepsy have an abnormally high level of excitatory neurotransmitters that increase neuronal activity, while others have an abnormally low level of inhibitory neurotransmitters that decrease neuronal activity in the brain(Wells, 8015). Either situation can result in too much neuronal activity and cause epilepsy. One of the most-studied neurotransmitters is GABA (gamma-aminobutyric acid) which is an excitatory and inhibitory neurotransmitter. NMDA (n-methyl-d-aspartate) is another extensively researched neurotransmitter that plays a vital role in the development in of an epileptic brain. This paper seeks to further explore the impact that GABA and NMDA have on the development of the epileptic brain. An epileptic seizure occurs when the message delivery system becomes unbalanced. Under normal circumstances, the neurotransmitter GABA does its part to make sure the system stays in synch by triggering signals in the form of charged particles. It causes a large concentration of negatively charged chloride particles (Cl-) to enter the receiving neuron. This prevents the neuron from undergoing an action potential or passing on the message (White, 43). When there is not enough GABA a person can have a seizure because receiving neurons can be flooded with signals that say "pass on this message." In accordance with this there was a study conducted at Johns Hopkins University, in which scientists discovered that the glutamate transporter that was blocked imports glutamate molecules that were used to make new GABA molecules. The rats used in the experiments were unable to make new GABA. Over the course of ten days their GABA levels dropped and the epileptic symptoms developed. It was also noted that as the production of GABA was reduced, the electroencephalography (EEG) recording showed rapid spikes in addition to freezing and starring episodes. These symptoms are consistent with those of epileptic seizures.

In adults, epilepsy is caused by this hyperactivation of the neuronal receptors that is triggered by the neurotransmitter, glutamate. This excess activation unleashes the storm of the uncontrolled nerve cell firing that underlies epilepsy. In adults, GABA acts on its receptors to inhibit neurons. This loss of inhibition is also involved in epilepsy. Evidence now shows that the function of GABA is significantly different in the developing brain than in the adult brain. In adult rats GABAergic inhibition exerts a powerful inhibitory drive of CA3 pyramidal neurons and prevents the spread of excitation. Once the inhibition has been reduced by Bicuculline (BIC), a GABA A antagonist, causes excitatory collaterals to prevail and epileptiform discharges are generated. In contrast in postnatal weeks 5 to 7 in rats, both spontaneous and electrically induced activity of CA3 neurons is characterized by the presence of giant depolarization...
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