D2-like receptor
D2-like receptor is a class of G protein-coupled receptors that are prominent in the vertebrate central nervous system (CNS). These receptors are linked to a variety of neurological and psychiatric conditions, including schizophrenia, Parkinson's disease, and drug addiction.
Overview[edit | edit source]
D2-like receptors are a subset of the dopamine receptor family, which also includes D1-like receptors. They are named for their structural and functional similarities to the D2 receptor, the first member of this group to be identified. D2-like receptors include the D2, D3, and D4 receptors.
Structure and Function[edit | edit source]
Like all G protein-coupled receptors, D2-like receptors consist of seven transmembrane domains connected by extracellular and intracellular loops. They are activated by the neurotransmitter dopamine, which binds to a specific site on the receptor and triggers a conformational change that allows the receptor to interact with intracellular signaling proteins.
D2-like receptors are primarily inhibitory, meaning they reduce the activity of the neurons in which they are expressed. They do this by inhibiting the production of cyclic AMP, a second messenger molecule that promotes neuronal activity.
Clinical Significance[edit | edit source]
D2-like receptors are the primary target of many antipsychotic drugs, which are used to treat conditions such as schizophrenia and bipolar disorder. These drugs work by blocking the receptors, thereby reducing the effects of dopamine in the brain.
In Parkinson's disease, the death of dopamine-producing neurons leads to a decrease in D2-like receptor activity, which contributes to the motor symptoms of the disease. Drugs that activate D2-like receptors are therefore used to treat Parkinson's disease.
D2-like receptors are also involved in drug addiction. Drugs of abuse often increase dopamine levels in the brain, leading to overactivation of D2-like receptors. This overactivation is thought to contribute to the development of addiction.
See Also[edit | edit source]
References[edit | edit source]
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