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Molecular Mechanisms of β-Adrenergic Receptor Desensitization

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Molecular Mechanisms of Neuronal Responsiveness

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 221))

Abstract

Desensitization or adaptation is well known in biological regulation. Also referred to as tachyphylaxis, tolerance or refractoriness, it is most commonly observed as a loss of cellular responsiveness to a neurotransmitter or drug after repeated or prolonged exposure to that agent. Examples of systems in which desensitization is observed include Chemotaxis of bacteria or mammalian polymorphonuclear leukocytes, neurotransmission by various neurotransmitters at synapses, stimulation of diverse physiological processes in eukaryotes by many drugs and hormones, and sensory perception. In the context of clinical therapeutics, desensitization significantly limits the efficacy of numerous pharmacological agents.

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Sibley, D.R., Benovic, J.L., Caron, M.G., Lefkowitz, R.J. (1987). Molecular Mechanisms of β-Adrenergic Receptor Desensitization. In: Ehrlich, Y.H., Lenox, R.H., Kornecki, E., Berry, W.O. (eds) Molecular Mechanisms of Neuronal Responsiveness. Advances in Experimental Medicine and Biology, vol 221. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7618-7_19

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