Glutamate is the primary excitatory neurotransmitter of the human nervous system. It is an amino acid neurotransmitter that interacts with both ionotropic and metabotropic receptors. There are 3 identified ionotropic glutamate receptors: NMDA, AMPA, and kainate receptors, and 3 identified metabotropic glutamate receptors. Glutamate is removed from the synaptic cleft by excitatory amino acid transporters, or EAATs. Glutamate that is transported into glial cells is converted to glutamine before being sent back to the neuron to be converted back to glutamate, a process referred to as the glutamate-glutamine cycle.
Welcome to 2 minute neuroscience, where I explain neuroscience topics in 2 minutes or less. In this installment I will discuss glutamate.
Glutamate is an amino acid that also functions as a neurotransmitter. Although glutamate is obtained through the diet, it cannot pass the blood-brain barrier and thus must be synthesized in the brain. It can be synthesized from alpha ketoglutarate, an intermediate product in the citric acid cycle.
Glutamate generally has excitatory actions, meaning that when it interacts with the receptors of a neuron it makes that neuron more likely to fire an action potential. It is, in fact, used at the vast majority of excitatory connections in the brain and at more than half of all synapses in the brain.
Glutamate interacts with several different types of receptors. There are 3 identified ionotropic glutamate receptors, named for substances that activate them: NMDA, AMPA, and kainate receptors. When activated, all 3 allow positively charged sodium ions to flow into a postsynaptic neuron, depolarizing the neuron and making it more likely to fire an action potential. NMDA receptors have unique characteristics that make them well-suited to be involved in synaptic plasticity, or synaptic changes that occur in response to experience, which are an important component of learning and memory.
There are also 3 identified types of metabotropic glutamate receptors. These receptors have more varied effects than ionotropic glutamate receptors, and may be involved with excitatory or inhibitory actions.
Glutamate is removed from the synaptic cleft by a class of transporter proteins called the excitatory amino acid transporters, or EAATs. EAATs carry glutamate into neurons and glial cells. Glutamate taken into glial cells is converted to the amino acid glutamine by the enzyme glutamine synthetase. Glutamine is then transported back into neurons, where it is converted back to glutamate. This process is referred to as the glutamate-glutamine cycle.
Purves D, Augustine GJ, Fitzpatrick D, Hall WC, Lamantia AS, McNamara JO, White LE. Neuroscience. 4th ed. Sunderland, MA. Sinauer Associates; 2008.
In this video I discuss the neurotransmitter gamma-aminobutyric acid, or GABA. GABA is the primary inhibitory neurotransmitter in the human nervous system; its effects generally involve making neurons less likely to fire action potentials or release neurotransmitters. GABA acts at both ionotropic (GABAa) and metabotropic (GABAb) receptors, and its action is terminated by a transporter called the GABA transporter. Several drugs like alcohol and benzodiazepines cause increased GABA activity, which is associated with sedative effects.
Welcome to 2 minute neuroscience, where I simplistically explain neuroscience topics in 2 minutes or less. In this installment I will discuss gamma-aminobutyric acid, or GABA.
Although GABA’s primary functions are as a neurotransmitter, it has the structure of an amino acid and thus is referred to as an amino acid neurotransmitter. It is synthesized from another amino acid neurotransmitter, glutamate, in a reaction catalyzed by the enzyme glutamic acid decarboxylase.
The function of GABA changes over the course of neural development, but in the mature brain it acts primarily as an inhibitory neurotransmitter; in other words when GABA interacts with the receptors of a neuron, it generally makes the neuron less likely to fire an action potential or release neurotransmitters.
There are two types of receptors GABA interacts with, GABAa and GABAb receptors. GABAa receptors are ionotropic receptors. When GABA binds to the GABAa receptor, it causes the opening of an associated ion channel that is permeable to the negatively charged ion chloride. When negative chloride ions flow into the neuron, they hyperpolarize the membrane potential of the neuron and make it less likely the neuron will fire an action potential. GABAb receptors are metabotropic (or g-protein coupled) receptors; when activated they frequently cause the opening of potassium channels. These channels allow positively charged potassium ions to flow out of the neuron, again making the neuron hyperpolarized and less likely to fire an action potential.
The actions of GABA are terminated by proteins called GABA transporters, which transport GABA from the synaptic cleft into neurons or glial cells where it is degraded primarily by mitochondrial enzymes.
Because GABA can reduce neural transmission, increased GABA activity can have sedative effects. Accordingly, a number of drugs that have such effects, like alcohol and benzodiazepines, increase activity at the GABA receptor.