Dopamine receptor D1
Dopamine receptor D1 (also known as DRD1) is one of the five main dopamine receptors in the human body. It is a G protein-coupled receptor that is primarily located in the striatum, a component of the basal ganglia in the brain. The receptor is activated by the neurotransmitter dopamine, which is a key player in the brain's reward system and is involved in the regulation of mood, motivation, and attention.
Structure[edit | edit source]
The structure of the DRD1 receptor is similar to that of other G protein-coupled receptors. It consists of seven transmembrane domains, an extracellular N-terminus, and an intracellular C-terminus. The receptor's binding site for dopamine is located within the transmembrane domains.
Function[edit | edit source]
Upon activation by dopamine, the DRD1 receptor stimulates the production of cyclic AMP (cAMP) via the activation of an enzyme called adenylyl cyclase. This leads to a series of intracellular events that ultimately result in changes in neuronal activity. The DRD1 receptor is particularly important in the regulation of motor control, cognition, and reward.
Clinical significance[edit | edit source]
Alterations in the function or expression of the DRD1 receptor have been implicated in a number of neurological and psychiatric disorders, including Parkinson's disease, schizophrenia, and drug addiction. For example, in Parkinson's disease, the loss of dopamine-producing neurons leads to a decrease in the activation of DRD1 receptors, contributing to the motor symptoms of the disease. In schizophrenia, it is thought that an overactivity of DRD1 receptors may contribute to the positive symptoms of the disease, such as hallucinations and delusions.
Pharmacology[edit | edit source]
Several drugs have been developed that target the DRD1 receptor. These include agonists, which activate the receptor, and antagonists, which block the receptor. Agonists are used in the treatment of Parkinson's disease to increase the activation of DRD1 receptors, while antagonists are used in the treatment of schizophrenia to decrease the overactivity of the receptors.
See also[edit | edit source]
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Contributors: Prab R. Tumpati, MD