On the molecular mechanism of adrenocorticotrophic hormone in the CNS: neurotransmitters and receptors.
A neural mechanism for the clinical efficacy of adrenocorticotrophic hormone (ACTH) independent of steroid effects in neurological disorders such as infantile spasms, myoclonic seizures in infants, and the opsoclonus-myoclonus syndrome remains controversial. This article reviews evidence that ACTH is a neurotransmitter, neuromodulator, and growth factor. It summarizes studies of anticonvulsant, antimyoclonic, and neurophysiologic effects of ACTH and ACTH fragments, the binding of ACTH in vitro to neurotransmitter receptors in brain, the chronic effects of ACTH on central neurotransmitter receptors and metabolism, effects of neurotransmitters on ACTH secretion, effects of ACTH on growth of cultured neurons, anatomic evidence for interactions of ACTH with neurotransmitters, behavioral effects and interactions of ACTH with neurotransmitter systems in vivo, and other neurochemical properties which may alter neurotransmission.
Pranzatelli
M R
MR
Department of Neurology, George Washington University, Washington, DC 20010.
D000324:Adrenocorticotropic Hormone / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology*; D000595:Amino Acid Sequence; D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology; D001921:Brain / Q000378:metabolism; D002490:Central Nervous System / Q000502:physiology*; D006133:Growth Substances / Q000502:physiology; D006801:Humans; D008969:Molecular Sequence Data; D009207:Myoclonus / Q000188:drug therapy; D018377:Neurotransmitter Agents / Q000378:metabolism / Q000502:physiology*; D010446:Peptide Fragments / Q000494:pharmacology; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*
D000927:Anticonvulsants; D006133:Growth Substances; D018377:Neurotransmitter Agents; D010446:Peptide Fragments; D011956:Receptors, Cell Surface; D000324:Adrenocorticotropic Hormone