The ever-changing brain: Cellular and molecular mechanisms for the effects of stressful experiences

Authors


  • The Ira Black and the McEwen laboratories collaborated on two studies of hormone actions and 3 papers related to catecholamine neural development:

    • Luine VN, McEwen BS, Black IB. 1977. Effect of 17β-estradiol on hypothalamic tyrosine hydroxylase activity. Brain Res 120: 188–192.

    • Bohn CM, McEwen BS, Luine VN, Black IB. 1984. Development and characterization of glucocorticoid receptors in rat superior cervical ganglion. Dev Brain Res 14: 211–218.

    • Friedman W, Dreyfus C, McEwen BS, Black I. 1988. Presynaptic transmitters and depolarizing influences regulate development of the substantia nigra in culture. J Neurosci 8: 3616–3623.

    • Friedman WJ, Dreyfus CF, McEwen B, Black IB. 1988. Substance K (NKA) increases tyrosine hydroxylase mRNA in cultured substantia nigra. Brain Res 427: 203–205.

    • Friedman W, Dreyfus C, McEwen BS, Black I. 1989. Developmental regulation of tyrosine hydroxylase in the mediobasal hypothalamus. Dev Brain Res 48: 177–185.

  • This article has been written in memory of Ira Black.

Abstract

The adult brain is capable of considerable structural and functional plasticity and the study of hormone actions in brain has contributed to our understanding of this important phenomenon. In particular, stress and stress-related hormones such as glucocorticoids and mineralocorticoids play a key role in the ability of acute and chronic stress to cause reversible remodeling of neuronal connections in the hippocampus, prefrontal cortex, and amygdala. To produce this plasticity, these hormones act by both genomic and non-genomic mechanisms together with ongoing, experience-driven neural activity mediated by excitatory amino acid neurotransmitters, neurotrophic factors such as brain derived neurotrophic factor, extracellular molecules such as neural cell adhesion molecule, neuropeptides such as corticotrophin releasing factor, and endocannabinoids. The result is a dynamic brain architecture that can be modified by experience. Under this view, the role of pharmaceutical agents, such as antidepressants, is to facilitate such plasticity that must also be guided by experiences. © 2011 Wiley Periodicals, Inc. Develop Neurobiol 72: 878–890, 2012

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