Dynorphin A: Difference between revisions

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Latest revision as of 20:28, 16 March 2025

Dynorphin A is a neuropeptide that belongs to the dynorphin family. It is an endogenous opioid that is found in neurons in many different parts of the brain, including the hypothalamus, hippocampus, and spinal cord. Dynorphin A is known for its role in modulating pain and maintaining the body's response to stress.

Structure and Function[edit]

Dynorphin A is a peptide that consists of 17 amino acids. It is derived from the precursor protein prodynorphin, which is cleaved to produce dynorphin A, along with other dynorphins.

Dynorphin A functions by binding to and activating the kappa opioid receptor (KOR). This receptor is a type of G protein-coupled receptor that is found in the nervous system. When dynorphin A binds to KOR, it triggers a series of events inside the cell that ultimately lead to the inhibition of adenylate cyclase, a decrease in the production of cAMP, and a reduction in neuronal excitability.

Role in Pain and Stress[edit]

Dynorphin A is best known for its role in modulating pain. It is released in response to painful stimuli and acts to inhibit the transmission of pain signals in the spinal cord. This makes dynorphin A a key player in the body's natural pain relief system.

In addition to its role in pain, dynorphin A is also involved in the body's response to stress. It is released in response to stressors and acts to inhibit the release of corticotropin-releasing hormone (CRH) from the hypothalamus. This helps to dampen the body's stress response and prevent overactivation of the hypothalamic-pituitary-adrenal axis (HPA axis).

Clinical Significance[edit]

Due to its role in pain and stress, dynorphin A is a potential target for the development of new drugs for the treatment of chronic pain and stress-related disorders. However, the development of drugs that target the kappa opioid system has been challenging due to the complex pharmacology of this system and the potential for side effects.

See Also[edit]

References[edit]

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