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Changes in mouse barrel synapses consequent to sensory deprivation from birth

Journal

JOURNAL OF COMPARATIVE NEUROLOGY
Volume 457, Issue 1, Pages 75-86

Publisher

WILEY-LISS
DOI: 10.1002/cne.10518

Keywords

thalamocortical; plasticity; receptive field; development; cortical representations; numerical density

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Neonatal sensory deprivation induced by whisker trimming affects significantly the functional organization of receptive fields in adult barrel cortex. In this study, the effects of deprivation on thalamocortical synapses and on asymmetrical and symmetrical synapses not of thalamic origin were examined. Thalamocortical synapses were labeled by lesion-induced degeneration in adult (postnatal day 60) mice subjected to whisker trimming from birth, other synaptic types were unlabeled. Brains were processed for electron microscopy, and numerical densities of synapses were evaluated by using stereologic approaches for whisker trimmed vs. control animals. Results demonstrated no change in nonthalamic, asymmetrical synapses; however, a decrease of 52% in the numerical density of symmetrical synapses (46.3 vs. 88.5 million per mm(3); Z = -2.121; P < 0.05) and a decrease of 43% in the numerical density of thalamocortical synapses (57.5 vs. 102.33 million per mm(3); Z = -2.121; P < 0.05) were observed after deprivation. Thus, experience-dependent plasticity of receptive fields in barrel cortex involves directly axons of both extrinsic and intracortical origin. The proportion of thalamocortical axospinous to axodendritic synapses was the same in control vs. deprived animals: in each instance, 80% of the synapses were axospinous (Z = 0.85; P = 0.2). These results suggest that neither excitatory neurons, whose thalamocortical. synapses are primarily axospinous, nor inhibitory neurons, whose thalamocortical synapses are mainly axodendritic (White [1989] Cortical Circuits. Synaptic Organization of the Cerebral Cortex; Structure, Function, and Theory. 1989; Boston: Birkhauser), are affected preferentially by the deprivation-associated decrease in thalamocortical synapses.

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