University of Illinois at Chicago     Jesse Brown VA Medical Center
Research and Development Section
820 South Damen Avenue
Chicago, IL 60612

Office Phone: (312) 569-8684
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M. Guizzetti, P. Costa, J. Peters, L. G. Costa. Acetylcholine as a mitogen: muscarinic receptor mediated proliferation of rat astrocytes and human astrocytoma cells. Eur. J. Pharmacol, 1996; 297: 265-273.

M. Guizzetti and L. G. Costa. Inhibition of muscarinic receptor-stimulated glial cell proliferation by ethanol. J. Neurochem. 1996; 67: 2236-2245. 

K. Yagle, H. Lu, M. Guizzetti, T. Möller, L. G. Costa. Activation of mitogen-activated protein kinase by muscarinic receptors in astroglial cells: role in DNA synthesis and effect of ethanol. Glia, 2001; 35: 111-120. 

M. Guizzetti, L. G. Costa. Effect of ethanol on protein kinase C and p70S6 kinase activation by carbachol: a possible mechanism for ethanol-induced inhibition of glial cell proliferation. J. Neurochem. 2002, 82: 38-46

M. Guizzetti, F. Bordi,  F. J. Dieguez-Acuña, A. Vitalone, F. Madia, J. S. Woods, L. G. Costa.  Nuclear factor kB activation by muscarinic receptors in astroglial cells: effect of ethanol. Neuroscience (2003) 120: 941-950.

M. Guizzetti, B.D. Thompson, Y. Kim, K. VanDeMark, and L. G. Costa. Role of phospholipase D signaling in ethanol-induced inhibition of carbachol-stimulated DNA synthesis of 1321N1 astrocytoma cells. (2004) J. Neurochem. 90: 646-653.

M. Guizzetti, J. Chen, J. F. Oram, K. Dao, T. Möller, L. G. Costa. Ethanol induces ATP-binding cassette A1 and cholesterol efflux in fetal astrocytes. (2007) J. Biol. Chem. 282: 18740-18749.
M. Guizzetti, G. Giordano, N. Moore, L.G. Costa. Modulation of neuritogenesis by astrcyte muscarinic receptors. (2008) J. Biol. Chem. 283: 31884-31897.

N.H. Moore, L.G. Costa, S.A. Shaffer, D.R. Goodlett, M. Guizzetti. Identification by shotgun proteomics of astrocyte-released proteins involved in neuronal development. (2009) J. Neurochem. 108: 891-908.

M. Guizzetti, N. H. Moore, G. Giordano, L. G. Costa. Ethanol inhibits
neuritogenesis  induced by astrocyte muscarinic receptors. (2010) Glia 58: 1395-1406.



Marina Guizzetti, Ph.D.

Associate Professor

Dr. Guizzetti is a recognized expert on basic research in alcohol neurotoxicity. She has been involved in the investigation of mechanisms mediating the neurodevelopmental effects of alcohol since 1994 through her work at the University of Washington in Seattle. She joined the Department of Psychiatry of the University of Illinois at Chicago in 2010 where she continues her research on the neurobiological effects of alcohol.


Dr. Guizzetti’s main research interest is the identification of novel mechanisms of glia-neuron interactions involved in brain development and neuronal plasticity.  Her emphasis is on mechanisms affected by ethanol and implicated in learning and behavioral abnormalities associated with in utero alcohol exposure, as seen in Fetal Alcohol Spectrum Disorders (FASD), as well as in cognitive impairments observed in individuals who abuse alcohol.


International Society for Biomedical Research on Alcoholism (ISBRA) 
Research Society on Alcoholism (RSA)  
American Association for the Advancement of Science (AAAS) 
Association for Women in Science (AWIS)   
Society of Toxicology (SOT)
Member of the Editorial Board of “NeuroToxicology”
Research Affiliate, Center on Human Development and Disability, University of Washington, Seattle, WA.


Dr. Guizzetti is currently involved in three research projects:

The first project investigates the role of astrocyte neurotransmitter receptors in neuronal differentiation and the effects of ethanol.
Astrocytes are able to modulate many neuronal functions, including neurite outgrowth and synaptogenesis, by secreting neuroactive proteins and peptides and by regulating the composition of the extracellular matrix, creating microenvironments that can be permissive or inhibitory of neuronal differentiation.
We have recently identified a new mechanism of glia-neuron communication involved in brain development: activation of muscarinic receptors in astrocytes induces neuritogenesis in neurons through the release of extracellular matrix proteins and modulators of protease activity. Ethanol inhibits the differentiating effect exerted on neurons by muscarinic receptor-activated astrocytes. This represents a new and important mechanism that can contribute to the deleterious effects of alcohol on cognitive functions during development and in the adult.

The second project investigates the effects of ethanol on cholesterol homeostasis in CNS cells.
This research project explores the hypothesis that some of the teratogenic effects of ethanol may be caused by the disruption of cholesterol homeostasis in the developing brain. Cholesterol is essential for fetal development and striking similarities between Fetal Alcohol Syndrome (FAS) and a syndrome caused by a genetic defect in the cholesterol biosynthesis have been reported. Cholesterol is involved in many aspects of brain development, including activation of sonic hedgehog signaling, neurite outgrowth, synaptogenesis, and astrocyte proliferation: all functions inhibited by ethanol.
Our data suggest that ethanol, by upregulating ABCA1 and ABCG1 cholesterol transporters and cholesterol efflux in astrocytes, and by increasing lipoprotein production and secretion from astrocytes, may alter cholesterol levels and homeostasis in the brain.

The third project investigates epigenetic mechanisms involved in astrocyte-mediated neuritogenesis.
Epigenetic events are likely to be involved in the modulation of the release of neurotogenic factors from astrocytes by physiological (i.e. mediated by neurotransmitters) and pathological (i.e. as a consequence of heavy alcohol exposure) stimuli, as well as in the response of neurons to astrocyte-released neurtitogenic factors. The investigation of epigenetic mechanisms (with an emphasis on histone acetylation/deacetylation and DNA methylation) regulating the synthesis of extracellular matrix proteins in astrocytes and the signaling cascade proteins activated by integrins in neurons will be carried out.


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