Structural Abnormalities of Subicular Dendrites in Subjects With Schizophrenia and Mood Disorders

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Abstract
ACONVERGENCE of functional and structural evidence presents elements of cerebral synapses as possible sites of a neuropathological lesion in subjects with schizophrenia. Goldman-Rakic and Selemon,1 citing evidence for decreased cortical volume but normal neuronal number in subjects with schizophrenia,2 state, "Our view is that certain neurons are dystrophic and undergo atrophy of their neuronal processes . . .".1(p442) Olney and Farber3 cite evidence for diminished N-methyl D-aspartate receptor–mediated transmission as a crucial factor in subjects with schizophrenia. Feinberg4 and Keshevan et al5 suggest excessive synaptic pruning as a possible cause of schizophrenia. Each of these hypotheses suggests a loss or alteration of synaptic targets. In the brain, axonal processes may form synapses on neuronal cell bodies, on other axons, or, in most cases, on dendrites. Dendritic synapses may be either on the shaft of the dendrite or on spinous processes that project from these shafts. More than 90% of all excitatory synapses in the central nervous system are on dendritic spines, and the structure of dendritic spines dictates their conductive properties. Thus, loss or alteration of spines would be expected to lead to abnormalities of glutamate transmission, even if presynaptic elements and postsynaptic receptors were maintained.6 Conversely, excitatory neurotransmission influences the size and shape of dendritic spines.