Studies of hormone action in the hippocampal formation: possible relevance to depression and diabetes.
OBJECTIVE
The goal is to review the plasticity and vulnerability of the hippocampus, a brain structure involved in episodic, declarative, contextual and spatial learning and memory, as well as its being a component in the control of autonomic and vegetative functions such as ACTH secretion. It discusses its possible role in the regulation of glucose homeostasis, and the need of hippocampal neurons for glucose because of their high metabolic activity. The hippocampus is also vulnerable to damage by stroke and head trauma and susceptible to damage during aging and repeated stress, and is sensitive to the effects of diabetes.


METHODS
A summary of recent work in the author's laboratory and related work in the field using citations of literature based, in part, on Medline searches.


CONCLUSIONS
In addition to its vulnerability, the hippocampus is also a plastic and adaptable brain region that is capable of considerable structural reorganization, including remodeling of dendrites and neurogenesis of dentate gyrus granule neurons in response to repeated stress. Animal models of Type 1 diabetes show accelerated remodeling of dendrites, and Type 2 diabetes remains to be studied in this regard. This is relevant to major depressive illness, in which a progressive atrophy of the hippocampal formation is reported and is accompanied by impairment of cognitive function in those subjects with hippocampal shrinkage. Therefore, hippocampal atrophy in depression, as well as in diabetes, may reflect either damage or plasticity involving structural reorganization that is potentially treatable.
McEwen
Bruce S
BS
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, Box 165, 1230 York Avenue, New York, NY 10021, USA. mcewen@mail.rockfeller.edu
Magariños
Ana María
AM
Reagan
Lawrence P
LP
D000375:Aging; D000818:Animals; D001284:Atrophy / Q000473:pathology; D002455:Cell Division; D018891:Dentate Gyrus / Q000502:physiology; D003866:Depressive Disorder / Q000503:physiopathology*; D003920:Diabetes Mellitus / Q000503:physiopathology*; D005947:Glucose / Q000378:metabolism; D051275:Glucose Transporter Type 4; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006728:Hormones / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000378:metabolism; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D009124:Muscle Proteins; D009473:Neuronal Plasticity / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology
D051275:Glucose Transporter Type 4; D006728:Hormones; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495692:SLC2A4 protein, human; D005947:Glucose