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Excitatory and Inhibitory Effects of Neurotransmitters

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Neurotransmitters released by a presynaptic neuron can be excitatory or inhibitory.

Excitatory neurotransmitters, such as acetylcholine and glutamate increase the chance of generating an action potential in the postsynaptic cell.

The binding of these neurotransmitters on the ion channel receptors of the postsynaptic cell triggers a rapid influx of sodium and a slow efflux of potassium ions. Resulting changes in the electrochemical gradient cause membranes to depolarize, generating an excitatory postsynaptic potential or EPSP. At the axon hillock, the summation of all EPSP then triggers an action potential that travels down the axon.

In contrast, inhibitory neurotransmitters, such as glycine and gamma-aminobutyric acid, decrease the likelihood of an action potential propagation.

The binding of inhibitory neurotransmitters to the postsynaptic cell’s ion channel receptors allows the efflux of potassium ions or influx of chloride ions—in both cases, making the cell cytoplasm more negative. Such hyperpolarizing potential changes are called inhibitory postsynaptic potential or IPSP. It decreases the likelihood of firing or inducing an action potential.

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When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific receptors for the molecule on the postsynaptic cell membrane. Their binding to the target cell or postsynaptic membrane brings an ion influx that allows the cell to fire the impulse, action potential, or not.

For example, when acetylcholine is released at the synapse between a nerve and muscle (called the neuromuscular junction) by a presynaptic neuron, it causes postsynaptic Na⁺channels to open. Na⁺ enters the postsynaptic cell and causes the postsynaptic membrane to depolarize. This depolarization is called an excitatory postsynaptic potential (EPSP) and makes the postsynaptic neuron more likely to fire an action potential. The release of neurotransmitters at inhibitory synapses causes inhibitory postsynaptic potentials (IPSPs) - hyperpolarization of the presynaptic membrane. For example, when the neurotransmitter GABA (gamma-aminobutyric acid) is released from a presynaptic neuron, it binds to and opens chloride channels. As a result, the chloride ions enter the cell and hyperpolarize the membrane, making the neuron less likely to fire an action potential.

Alterations in neurotransmitter levels have been linked to several neurological disorders. For example, Parkinson's disease is a neurodegenerative disorder. Here, the damage or death of the brain cells in the substantia nigra part of the brain, which produces dopamine, results in altered dopamine levels. This causes movement problems associated with the disease like shaking, stiffness, and difficulty in walking, balance, and coordination.

Schizophrenia is a chronic mental disorder that affects a person's ability to think and behave clearly. Here, there is an excess release of the dopamine neurotransmitter, which causes a person to hallucinate, affecting the thought process, perceptions, and emotional responsiveness.

This text is adapted from Openstax, Biology 2e, Section 35.2 How Neurons Communicate.

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Neurotransmitters

Excitatory Postsynaptic Potential

Inhibitory Postsynaptic Potential

Chemical Synapse

Neurological Disorders

Action Potential