It is increasingly recognized that maternal exposure to metabolic (nutritional) stimuli, infections, illicit or prescription drugs and environmental stressors during pregnancy can predispose affected offspring to developing devastating postnatal illnesses. If detrimental maternal stimuli coincide with critical periods of tissue production and organogenesis then they can permanently derail key cellular differentiation programs. Maternal programming can thus either provoke developmental failure directly (‘direct hit’) or introduce latent developmental errors that enable otherwise sub-threshold secondary stressors to manifest as disease (‘double hit’) postnatally. Accumulating evidence suggests that nervous system development is tightly controlled by maternal metabolic stimuli, and whose synaptic wiring and integrative capacity are adversely affected by dietary and hormonal challenges, infections or episodes of illicit drug use. Endocannabinoids, a family of signal lipids derived from polyunsaturated fatty acids, have been implicated in neuronal fate determination, the control of axonal growth, synaptogenesis and synaptic neurotransmission. Therefore the continuum and interdependence of endocannabinoid actions during the formation and function of synapses together with dynamic changes in focal and circulating endocannabinoid levels upon maternal nutritional imbalance suggest that endocannabinoids can execute the ‘reprogramming’ of specific neuronal networks. In the present paper, we review molecular evidence suggesting that maternal nutrition and metabolism during pregnancy can affect the formation and function of the hippocampus and hypothalamus by altering endocannabinoid signalling such that neuropsychiatric diseases and obesity respectively ensue in affected offspring. Moreover, we propose that the placenta, fetal adipose and nervous tissues interact via endocannabinoid signals. Thus endocannabinoids are hypothesized to act as a molecular substrate of maternal programming.
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Conference Article|
November 20 2013
Endocannabinoid signals in the developmental programming of delayed-onset neuropsychiatric and metabolic illnesses
Erik Keimpema;
Erik Keimpema
1
*Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Scheeles väg 1:A1, Karolinska Institutet, SE-17177 Stockholm, Sweden
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Daniela Calvigioni;
Daniela Calvigioni
*Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Scheeles väg 1:A1, Karolinska Institutet, SE-17177 Stockholm, Sweden
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Tibor Harkany
Tibor Harkany
2
*Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Scheeles väg 1:A1, Karolinska Institutet, SE-17177 Stockholm, Sweden
†Department of Molecular Neuroscience, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria
‡European Neuroscience Institute at Aberdeen, University of Aberdeen, Aberdeen AB25 2ZD, U.K.
2To whom correspondence should be addressed (emailtibor.harkany@ki.se).
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Publisher: Portland Press Ltd
Received:
August 07 2013
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2013 Biochemical Society
2013
Biochem Soc Trans (2013) 41 (6): 1569–1576.
Article history
Received:
August 07 2013
Citation
Erik Keimpema, Daniela Calvigioni, Tibor Harkany; Endocannabinoid signals in the developmental programming of delayed-onset neuropsychiatric and metabolic illnesses. Biochem Soc Trans 1 December 2013; 41 (6): 1569–1576. doi: https://doi.org/10.1042/BST20130117
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