Current motor and cognitive regions of interest include the basal ganglia, cerebellum, limbic system and cerebral cortex. We have previously demonstrated alterations in the GABAergic system in multiple brain regions, and our studies are now revealing atypical expression of specific types of GABAergic, cholinergic, serotonergic, dopaminergic and glutamatergic receptors. By characterizing abnormalities in the key neurotransmitter systems involved in early brain development, the experiments are designed to better understand the formation of aberrant circuitry and developmental timing of the neuropathology of autism. The aim is to quantify novel biomarkers and to identify specific targets for the development of pharmacotherapies for this complex condition.

Autism is a developmental neurological condition that is characterized by altered social interaction, difficulties with language and atypical responses to sensory stimuli. While the etiology of autism is largely unknown, the condition is thought to be highly genetic.  Recent findings in the field have pointed to key genes suspected to be involved in developmental and molecular processes. In the Autism Neurocircuitry Laboratory, we investigate the role and significance of specific biomarkers as products of altered genetic expression. Our focus has been to explore the GABAergic and Glutamatergic systems in parallel, investigating the balance of excitation and inhibition in affected areas of the autism brain. We study the neuropathology and neuropharmacology of autism in postmortem human brain tissue utilizing modern methods such as in situ hybridization, immunohistochemistry, and in vitro ligand binding for neurotransmitter receptors and transporters.

Hampson DR & Blatt GJ (2015). Autism spectrum disorders and neuropathology of the cerebellum. Frontiers in Neuroscience, 9:420 doi: 10.3389/fnins.2015.00420

Zhang K., Hill K., Labak S., Blatt G.J. and Soghomonian J.J. (2014) Loss of glutamic acid decarboxylase (Gad67) in Gpr88-expressing neurons induces learning and social behavior deficits in mice. Neuroscience. 275:238-47.

Oblak A., Gibbs T.T. and Blatt G.J. (2013) Reduced serotonin receptor subtypes in a limbic and a neocortical region in autism.  Autism Res. 6(6):571-83.

Lanoue A.C., Blatt G.J. and Soghomonian J.J. (2013) Decreased parvalbumin mRNA expression in dorsolateral prefrontal cortex in Parkinson’s disease. Brain Res. 1531:37-47.

Fatemi S.H., Aldinger K.A., Ashwood P. Bauman M.L., Blaha C.D., Blatt G.J., Chauhan A., Chauhan V., Dager S.R., Dickson P.E., Estes A.M., Goldowitz D., Heck D.H., Kemper T.L., King B.H., Martin L.A., Millen K.J., Mittleman G., Mosconi M.W., Persico A.M., Sweeney J.A., Webb S.J., and Welsh J.P. (2012) Consensus paper: pathological role of the cerebellum in autism. Cerebellum. 11(3):777-807.

Blatt G.J. (2012) The Neuropathology of autism. Scientifica. 2012:703675

Lister J.P., Blatt G.J., Kemper T.L., Tonkiss J., DeBassio W.A., Galler J.R. and Rosene D.L. (2011) Prenatal protein malnutrition alters the proportion but not numbers of parvalbumin-immunoreactive interneurons in the hippocampus of the adult Sprague-Dawley rat. Nutr Neurosci. 14(4):165-78.

Blatt GJ, Fatemi SH. (2011) Alterations in GABAergic biomarkers in the autism brain: research findings and clinical implications. Anat Rec. 294(10):1646-52.

Oblak, A., Gibbs T.T. and Blatt,G.J. (2011) Reduced GABA_A receptors and benzodiazepine binding sites in the posterior cingulate cortex and fusiform gyrus in autism. Brain Res. 1380:218-228.

Oblak, A., Kemper, T.L., Bauman, M.L. and Blatt, G.J. (2011) Altered posterior cingulate cortical cytoarchitecture, but normal density of neurons and interneurons in the posterior cingulate cortex and fusiform gyrus in autism. Autism Res. 4(3):200-211.

Blatt, G.J., ed., (2010) The Neurochemical Basis of Autism: Molecules to Minicolumns, Springer Publishers, N.Y., Berlin.

Lawrence, Y.L., Kemper, T.L., Bauman, M.L., and Blatt, G.J.  (2010) Parvalbumin, Calbindin, and Calretinin Immunoreactive Interneuron Density in Autism.  Acta Neurol. Scan. 121(2):99-108.

Oblak, A., Gibbs, T.T., and Blatt, G.J.  (2010) Decreased GABA_B receptors in the cingulate cortex and fusiform gyrus in autism. J. Neurochem. 114(5):1414-1423.

Oblak, A, Gibbs, T.T., and Blatt, G.J.  (2009) Decreased GABA_A receptors and benzodiazepine binding sites in the anterior cingulate cortex in autism.  Autism Res. 2:205-219.

Yip, J., Soghomonian, J-J. and Blatt, G.J. (2009) Decreased GAD65 mRNA levels in select subpopulations of neurons in the cerebellar dentate nuclei in autism: an in situ hybridization study. Autism Res. 2:50-59.

Yip, J., Soghomonian, J-J. and Blatt, G.J. (2008) Increased GAD67 mRNA expression in cerebellar interneurons in autism:implications for Purkinje cell dysfunction. J. Neurosci. Res. 86:525-530.

Yip, J., Soghomonian, J-J. and Blatt, G.J. (2007)  Decreased GAD67 mRNA levels in cerebellar Purkinje cells in autism: pathophysiological implications. Acta Neuropath. 113:559-568.