http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
Effects Of Cortisol On The Development Of The Chick Brain
Many hormones appear to affect the development of the embryonic central nervous system (CNS), causing either gross morphological defects or subtle changes in the functional maturation of neurons which are manifested as post-natal behavioral aberrations. To cite examples, certain glucocorticoids, especially cortisol, have been shown to induce morphological defects such as in myelination development and brain maturation, and biochemical changes such as altering enzyme levels in the brain, oxygen consumption of the brain, and amino acid metabolism during development of the CNS. The primary role of these hormones in developing neurons is, however, not understood. Evidence also suggests that experimental alterations of neurotransmitter synthesis may lead to degeneration of both postsynaptic and presynaptic neurons, and may inhibit functional maturation of neurons. The interactions between hormones and neurotransmitter synthesis in the embryonic brain remains to be elucidated. But, recent findings indicate that hormones may directly or indirectly influence neurotransmitter synthesis. For example, hypothyroidism in embryos leads to reduced synaptogenesis and transmitter synthesis, and thyroxin treatment restores normal development. It has also been discovered that application of thyroid hormones greatly increases the branching of neuronal processes. The intracellular effects of many hormones are mediated either directly or indirectly by the cyclic adenosine monophosphate (cAMP) as a second messenger. The central role of cAMP and the cAMP dependent protein kinases (A-PK) in neurotransmitter synthesis and/or transduction of neurotransmitter action suggests that some of the hormonal effects may be controlled via the cAMP - A-PK system. cAMP itself binds to specific receptor proteins which are generally subunits of a class of enzymes, the cyclic adenosine monophosphate dependent protein kinases (A-PK) which catalyze the phosphorolation, via adenosine triphosphate (ATP), of various substrate proteins in certain cell types. The activation of A-PK by cAMP leads to phosphorolation of specific proteins which may alter membrane permeability, neurotransmitter synthesis, and growths and differentiation of neurons. The exact mechanism of how glucocorticoids work has been under much discussion lately. One prevalent theory is that they bind to a receptor on the cell membrane, are transported into the cytoplasm, picked up by a cytoplasmic receptor, and taken to the nucleus of the cell. Their effect then is somewhat unclear, but the hormone is thought to bind to the chromosomes and affect gene transcription in some manner. In the chick embryo, as in other embryonic systems, the brain is the first part to mature. At day four of development, the major features of the brain are clearly delineated, except for any major differentiation between the metencephalon and myencephalon. By day seven, normal receptors have been shown to have started development. By day twelve, all portions of the brain are fairly well developed, and growth and differentiation continues until hatching at day twenty one.
Undergraduate thesis written for Program year: 1981/1982
Digitized from print version held at Pickle Center High Density Storage, barcode 24829681
University Undergraduate Fellows, sponsored by Biochemistry Department.
adenosine monophosphate dependent protein kinases