Neuronal nicotinic acetylcholine receptor subunits in autism: an immunohistochemical investigation in the thalamus

The cholinergic system has been implicated in the development of autism on the basis of neuronal nicotinic acetylcholine receptor (nAChR) losses in cerebral and cerebellar cortex. In the present study, the first to explore nAChRs in the thalamus in autism, α4, α7 and β2 nAChR subunit expression in thalamic nuclei of adult individuals with autism (n = 3) and age-matched control cases (n = 3) was investigated using immunochemical methods. Loss of α7- and β2- (but not α4-) immunoreactive neurons occurred in the paraventricular nucleus (PV) and nucleus reuniens in autism. Preliminary results indicated glutamic acid decarboxylase immunoreactivity occurred at a low level in PV, co-expressed with α7 in normal and autistic cases and was not reduced in autism. This suggested loss of neuronal α7 in autism is not caused by loss of GABAergic neurons. These findings indicate nicotinic abnormalities that occur in the thalamus in autism which may contribute to sensory or attentional deficits.