Autism is a common developmental disorder associated with structural and inferred neurochemical abnormalities of the brain. Cerebellar abnormalities frequently have been identified, based on neuroimaging or neuropathology. Recently, the cholinergic neurotransmitter system has been implicated on the basis of nicotinic receptor loss in the cerebral cortex. Cerebellar cholinergic activities were therefore investigated in autopsy tissue from a series of autistic individuals. The presynaptic cholinergic enzyme, choline acetyltransferase, together with nicotinic and muscarinic receptor subtypes were compared in the cerebellum from age-matched mentally retarded autistic (eight), normal control (10) and non-autistic mentally retarded individuals (11). The nicotinic receptor binding the agonist epibatidine (the high affinity receptor subtype, consisting primarily of alpha3 and alpha4, together with beta2 receptor subunits) was significantly reduced by 40-50% in the granule cell, Purkinje and molecular layers in the autistic compared with the normal group (P < 0.05). There was an opposite increase (3-fold) in the nicotinic receptor binding alpha-bungarotoxin (to the alpha7 subunit) which reached significance in the granule cell layer (P < 0.05). These receptor changes were paralleled by a significant reduction (P < 0.05) and non-significant increase, respectively, of alpha4 and alpha7 receptor subunit immunoreactivity measured using western blotting. Immunohistochemically loss of alpha(4 )reactivity was apparent from Purkinje and the other cell layers, with increased alpha7 reactivity in the granule cell layer. There were no significant changes in choline acetyltransferase activity, or in muscarinic M1 and M2 receptor subtypes in autism. In the non-autistic mentally retarded group, the only significant abnormality was a reduction in epibatidine binding in the granule cell and Purkinje layers. In two autistic cases examined histologically, Purkinje cell loss was observed in multiple lobules throughout the vermis and hemispheres. This was more severe in one case with epilepsy, which also showed vermis folial malformation. The case with less severe Purkinje cell loss also showed cerebellar white matter thinning and demyelination. These findings indicate a loss of the cerebellar nicotinic alpha4 receptor subunit in autism which may relate to the loss of Purkinje cells, and a compensatory increase in the alpha7 subunit. It remains to be determined how these receptor abnormalities are involved in neurodevelopment in autism and what is the relationship to mental function. Since nicotinic receptor agonists enhance attentional function and also induce an elevation in the high affinity receptor, nicotinic therapy in autism may be worth considering.

Increases in neuronal nicotinic receptors (nAChRs) in response to nicotine exposure have been reported in cell cultures, rodent brains, and in the brains of human smokers. The present study examines alterations in alpha4 and alpha7 nAChR subunit cellular expression in human hippocampus and entorhinal cortex from normal elderly individuals with known smoking history. There were significant increases in the intensity of alpha4 immunoreactive neuropil, but not the number of cell bodies, in many regions of hippocampus and entorhinal cortex in smokers compared to age-matched non-smokers and ex-smokers. There was also an increase in alpha7 immunoreactive perikarya in the granular cell layer of dentate gyrus in smokers but not other regions examined. There was, in contrast, a significant reduction in alpha7 immunoreactive astrocytes in smokers and ex-smokers compared to non-smokers. These findings suggest exposure to tobacco smoke acutely up-regulates alpha4 receptors in axon terminals and dendrites but not perikarya, whereas tobacco smoking induced down-regulation of alpha7 expression on astrocytes is a long-term effect. As the alpha4 subunit decreases with ageing and degenerative diseases such as Alzheimer's disease, whereas alpha7 increases in astrocytes in Alzheimer's disease, the findings further indicate the therapeutic relevance of nicotinic agonists such as nicotine.

The effects of dieldrin (hexachloro-epoxy-octahydro-dimethanonaphthalene) were studied in acute experiments on cats and rabbits. When injected intravenously or intra-arterially, it caused excitation of the central nervous system, which resulted in increased reflex excitability, convulsions, bradycardia, and some vasodepression. Dieldrin potentiated the effects of acetylcholine on the central nervous system and on the circulatory system as well as on intestinal motility. These latter manifestations were abolished by section of the vagus nerves, indicating a central action. Dieldrin had no effect on salivary secretion produced either by stimulation of the chorda tympani or by injections of acetylcholine in the decentralized submaxillary gland. Thus, although dieldrin has a marked parasympathomimetic action, this effect is exerted through stimulation of central mechanisms and not peripherally.

The effects of dieldrin (hexachloro-epoxy-octahydro-dimethanonaphthalene) were studied in acute experiments on cats and rabbits. When injected intravenously or intra-arterially, it caused excitation of the central nervous system, which resulted in increased reflex excitability, convulsions, bradycardia, and some vasodepression. Dieldrin potentiated the effects of acetylcholine on the central nervous system and on the circulatory system as well as on intestinal motility. These latter manifestations were abolished by section of the vagus nerves, indicating a central action. Dieldrin had no effect on salivary secretion produced either by stimulation of the chorda tympani or by injections of acetylcholine in the decentralized submaxillary gland. Thus, although dieldrin has a marked parasympathomimetic action, this effect is exerted through stimulation of central mechanisms and not peripherally.

The soil and plants at a 27.4 ha field site near Kalgoorlie, Western Australia, were surveyed and analysed with multivariate statistics. Cluster analysis identified four distinct plant communities at the study site. These were: Acacia acuminata shrubland Eucalyptus gvfithsii woodland Eucalyptus salrnonophloia woodland 'Ground Covers' - areas characterised by the presence of generalist herbs, low shrubs and weeds, and the absence of dominant upper storey species. Discriminant function analysis identified site elevation and soil exchangeable Ca as the primary environmental discriminants between the plant communities. Using these two variables, sample points were classified into one of the four plant communities. The two methods of classification matched well, with classification based on the two environmental variables providing an indication of which plant community would be most likely to establish in disturbed areas. This type of information can be important to revegetation programs in the region, guiding the use of appropriate plant species under different rehabilitation conditions. Key wcrds: environmental variables, plant communities, multivariate analysis, classification, revegetation