Catecholamines, which include dopamine, epinephrine, and norepinephrine, are neurotransmitters and hormones that are released by the adrenal glands and certain neurons in the brain and nervous system. They play important roles in the body’s fight-or-flight response, as well as in regulating various physiological processes.
What are catecholamines?
Catecholamines are monoamines derived from the amino acid tyrosine. The main catecholamines are:
- Norepinephrine (noradrenaline)
- Epinephrine (adrenaline)
Dopamine acts both as a hormone and a neurotransmitter, and plays important roles in behavior and cognition, voluntary movement, motivation, punishment and reward, inhibition of prolactin production, sleep, mood, attention, working memory, and learning. Dopamine produces feelings of pleasure and satisfaction when released.
Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase and acts as a neurotransmitter. It plays a role in arousal, attention, concentration, memory formation, and executive functioning tasks. Norepinephrine signaling increases heart rate, triggers glucose release, increases blood flow to skeletal muscle, focuses thinking, and mobilizes the body for action.
Epinephrine, also known as adrenaline, acts as a hormone and neurotransmitter. It plays a central role in the short-term stress reaction—the physiological response to threatening, exciting, or environmental stressors. Epinephrine increases heart rate and stroke volume, dilates the pupils, and constricts arterioles in the skin and gastrointestinal tract while dilating arterioles in leg muscles. It elevates blood sugar levels by promoting glycogen and fat metabolism in the liver and skeletal muscle.
Where are catecholamines produced and released?
Catecholamines are primarily produced and released by:
- The adrenal glands – The adrenal medulla produces epinephrine and norepinephrine.
- Postganglionic fibers of the sympathetic nervous system – These neurons release norepinephrine.
- Certain brain regions – Dopamine is produced mainly in the substantia nigra and ventral tegmental area.
The adrenal glands sit atop each kidney and consist of an outer cortex and inner medulla. The medulla synthesizes, stores, and secretes the catecholamines epinephrine and norepinephrine into the bloodstream, especially in response to stress.
The sympathetic division of the autonomic nervous system uses catecholamines for neurotransmission. When a sympathetic nerve is stimulated, norepinephrine is released into the synaptic cleft and binds adrenergic receptors on the target organ, causing effects like increased heart rate and blood pressure.
Dopamine-producing neurons are concentrated in specific areas of the brain like the substantia nigra, ventral tegmental area, and hypothalamus. Dopamine acts as a neurotransmitter when released in these regions and plays major roles in motor control, motivation, and cognitive function.
What stimulates catecholamine release?
Catecholamine release can be stimulated by:
Stressors like fear, anxiety, panic, pain, cold exposure, exercise, and low blood glucose levels can all stimulate catecholamine release, especially epinephrine and norepinephrine.
For example, the sympathetic nerves that innervate the adrenal medulla will activate in response to stresses like hypoglycemia and hemorrhage. This causes increased firing of the nerves and release of acetylcholine, which stimulates medullary cells to secrete epinephrine and norepinephrine into the circulation.
Nerve impulses originating in the sympathetic chain ganglia and traveling along postganglionic sympathetic fibers can stimulate the release of norepinephrine from the fibers’ terminals. The norepinephrine then acts on adrenergic receptors on target organs.
Within the brain, nerve impulses stimulate dopamine release from neurons projecting from the substantia nigra and ventral tegmental area to other brain regions like the striatum and prefrontal cortex.
The release of catecholamines can be influenced by hormonal signals from the hypothalamic-pituitary-adrenal (HPA) axis and hormones like cortisol, angiotensin II, insulin, and leptin.
Cortisol, for example, has complex effects on catecholamine release. Acute stress and high cortisol tend to increase norepinephrine and epinephrine secretion, while chronic stress and sustained high cortisol can blunt catecholamine responses.
Drugs and medications
Many drugs and medications can directly or indirectly stimulate catecholamine release, including:
- Monoamine oxidase inhibitors
For example, caffeine blocks adenosine receptors, resulting in increased firing of neurons and heightened release of dopamine and norepinephrine. Cocaine prevents the reuptake of dopamine from the synaptic cleft, causing dopamine accumulation and amplified signaling.
Eating stimulates catecholamine secretion, especially dopamine and norepinephrine. Neurons in the hypothalamus release norepinephrine in response to glucose ingestion. Dopamine is also secreted before and after meals and plays a role in regulating food intake.
How are catecholamine release and effects terminated?
Once released, catecholamines are rapidly inactivated by:
- Reuptake – Catecholamines are transported back into presynaptic neurons and adrenal chromaffin cells by membrane transporters.
- Enzymatic degradation – Enzymes like catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) metabolize and degrade catecholamines.
Termination of catecholamine signaling prevents excessive stimulation of postsynaptic receptors. Disruptions in catecholamine inactivation can lead to spillover and prolonged signaling, contributing to conditions like hypertension, anxiety disorders, and movement disorders.
- Catecholamines like dopamine, norepinephrine, and epinephrine are critical neurotransmitters and hormones involved in the stress response, cognition, movement, and other processes.
- Major stimuli that induce catecholamine release include stress, nerve impulses, hormones, drugs, and food intake.
- The adrenal glands and sympathetic nerves produce and secrete norepinephrine and epinephrine. Dopamine comes mainly from the substantia nigra, ventral tegmental area, and hypothalamus.
- Once released, catecholamines are rapidly inactivated by reuptake and enzymatic degradation to prevent excessive stimulation of target receptors.