The A-B-C (Allocortex-Brainstem-Core) circuitry of endocrine-autonomic integration and regulation: a proposed hypothesis on the anatomical-functional relationships between estradiol sites of action and peptidergic-aminergic neuronal systems.
A sex steroid hormone sensitive brainstem-allocortex axis of neuronal cell groups and projections is recognized with convergent pathways of aminergic-peptidergic messenger systems, which subserves the adjustment for varying reproductive and environmental conditions and the coordination of endocrine-autonomic functions. Main stations in the A-B-C (Allocortex-Brainstem-Core) periventricular axis include the substantia gelatinosa, nucleus (n.) tractus solitarii-dorsal vagal nucleus-area postrema complex, locus ceruleus, n. parabrachialis, central gray and associated raphe nuclei, ventral tegmental area, lateral and periventricular hypothalamus, n. paraventricularis, bed nucleus of the stria terminalis, preoptic-septal nuclei and n. centralis amygdalae with associated amygdaloid nuclei, as well as the ventral and dorsal allocortex. All of these stations and their periventricular and medial forebrain bundle projections contain estradiol sites of action and represent elements of earlier defined periventricular estradiol-target neuron systems. Results from colocalization of 3H estradiol by thaw-mount autoradiography and aminergic and peptidergic messengers by immunohistochemistry or other histochemical techniques indicate direct nuclear effects of estradiol on certain noradrenalin, dopamine, gamma aminobutyric acid, somatostatin, and neurophysin neurons. Additional data about correspondence of estradiol-target neuron accumulations with neuronal sites of peptide messenger production suggest direct effects of estradiol on certain enkephalin, endorphin, corticotropin releasing hormone, adrenalin, serotonin, cholecystokinin, pancreatic polypeptide and gonadotropin releasing hormone neurons--and probably others. As documented for the pituitary, and as an approach to understand varying and dual effects, it is postulated that estradiol activation of brain messenger systems parallels the heterogeneous estradiol binding in the A-B-C- system. This is expressed in the concept of differential Multiple Activation of Heterogeneous Systems (MAHS).(ABSTRACT TRUNCATED AT 250 WORDS)
D000588:Amines / Q000502:physiology*; D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D001921:Brain / Q000502:physiology*; D002395:Catecholamines / Q000502:physiology; D003346:Corticotropin-Releasing Hormone / Q000502:physiology; D004702:Endocrine Glands / Q000502:physiology*; D004723:Endorphins / Q000502:physiology; D004958:Estradiol / Q000502:physiology*; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism; D008954:Models, Biological; D009474:Neurons / Q000502:physiology; D009496:Neurotensin / Q000502:physiology; D010191:Pancreatic Polypeptide / Q000502:physiology; D010455:Peptides / Q000502:physiology*; D010903:Pituitary Gland, Anterior / Q000502:physiology; D010908:Pituitary Hormones, Anterior / Q000378:metabolism; D012701:Serotonin / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D000588:Amines; D002395:Catecholamines; D004723:Endorphins; D010455:Peptides; D010908:Pituitary Hormones, Anterior; D012701:Serotonin; D007987:Gonadotropin-Releasing Hormone; D009496:Neurotensin; D004958:Estradiol; D005680:gamma-Aminobutyric Acid; D010191:Pancreatic Polypeptide; D003346:Corticotropin-Releasing Hormone