**6. Acetylcholine**

Chemical and histochemical studies in the brains of individuals with ASD has shown loss of nicotinic receptors, in addition to that basal forebrain cholinergic neurons have been reported to be abnormally large and surplus [102]. A postmortem investigation of parietal neocortex showed reduced number of neuronal α-4 and β-2 nicotinic acetylcholine receptor (nAChR) subunit [103]. A while decreased cerebellar α-3/α-4 / β-2 nAChR ligand binding was detected, α-7 receptor subunit was exhibited compensatory increase [104].

Another study showed reduction in the expression of α-4 nAChR subunit in the frontal cortex whereas expression of α-4 nAChR subunit was found to increase in the cerebel‐ lum [105]. In another study, the α-7 nAChR subunit was determined to decreas especial‐ ly in paraventricular nucleus and nucleus reuniens [106]. Postmortem samples taken from ASD individuals demonstrated significantly decreased α-7 receptor mRNA levels in frontal cortex [107]

Brain samples of cerebral cortex and basal forebrain choline acetyltransferase and acetylcho‐ linesterase enzyme activity was measured, but no significant relationship was found with ASD. However, increased BDNF levels were detected which has affect on development and functions of cholinergic neurons in the basal forebrain [103]. Evidence of relation‐ ship between ASD and cholinergic circuits is still weak. Therefore extensive research in this area are needed.
