GABA and glycine: fast inhibition through chloride channels
GABA and glycine are the main inhibitory neurotransmitters (they make a neuron less likely to fire); their fast receptors are chloride channels, which usually make the cell more negative inside.
Remember
GABA is the main inhibitory neurotransmitter in the brain and glycine in the brainstem and spinal cord, and their fast receptors are chloride channels that usually hyperpolarise the neuron, making the inside of the cell more negative.
Memory aid
GABA is for the brain, glycine is for the brainstem and spinal cord below it, and both open a chloride gate that quietens the neuron.
GABA in the brain and glycine below it both open a chloride gate, which helps you remember that they quieten the neuron.
GABA is the brain's main inhibitory transmitter, and glycine does the same job in the brainstem and spinal cord. In the spinal cord, GABA and glycine are the two main fast inhibitory transmitters. Inhibitory neurotransmitters usually make a neuron less likely to fire. Excitatory neurotransmitters do the opposite: they make a neuron more likely to fire.
Their fast receptors are ionotropic: the receptor is itself an ion channel, opening when the transmitter binds. The GABA-A and glycine receptors let chloride through, so opening them usually makes the inside of the cell more negative. That is called hyperpolarisation, and it makes the neuron less likely to fire.
Firing is commonly inhibited through hyperpolarisation or through shunting. In shunting, current leaks away through the open channels, so excitatory inputs have less effect. The exact voltage change also depends on the chloride gradient and the membrane potential, so it is not invariably hyperpolarising.
GABA-B receptors are different. They are metabotropic, which means they work through messengers inside the cell, and their inhibition is slower.
Benzodiazepines and barbiturates, which are classes of medication, act on GABA receptors in the brain and increase their effects. They therefore have anti-anxiety and sedative effects, but they carry a risk of tolerance, dependence and misuse.
Key facts
- Brain
- GABA is the main inhibitory neurotransmitter.
- Brainstem and spinal cord
- Glycine is the main inhibitory neurotransmitter.
- Fast receptors
- The GABA-A and glycine receptors are ligand-gated chloride channels, which are opened when the transmitter binds.
- Usual effect
- Opening the channels usually hyperpolarises the neuron, so it is less likely to fire.
- Voltage change
- The exact change depends on the chloride gradient and the membrane potential, so it is not invariably hyperpolarising.
- GABA-B
- These receptors are metabotropic and give slower inhibition.
- Medications
- Benzodiazepines and barbiturates increase the effects of GABA receptors, with a risk of tolerance, dependence and misuse.
Exam traps
- GABA-B receptors are metabotropic, which means they act through messengers inside the cell, and they give slower inhibition; GABA-A receptors are not of that type, because they are ion channels themselves.
- GABA and glycine are not excitatory transmitters that depolarise a cell through sodium entry; they are inhibitory amino acid transmitters, and the main excitatory amino acid is glutamate.
- Potassium leaving a cell also hyperpolarises it, but the fast GABA and glycine receptors are chloride channels, not potassium channels.
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