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Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex.

Ueno H, Suemitsu S, Matsumoto Y, Okamoto M - Neural Plast. (2015)

Bottom Line: We determined the effects of sensory deprivation from birth to postnatal day 28 (P28) or P58 on the density of parvalbumin (PV), calbindin (CB), and calretinin (CR) neurons in the prelimbic, infralimbic, and dorsal anterior cingulate cortices.The density of PV and CB neurons was significantly increased in layer 5/6 (L5/6).These results suggest that long-term sensory deprivation causes the changes of intracortical inhibitory networks in the PFC and the changes of inhibitory networks in the PFC may contribute to cross-modal plasticity.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558, Japan ; Department of Medical Technology, Kawasaki College of Allied Health Professions, Okayama 701-0194, Japan.

ABSTRACT
Early loss of one sensory system can cause improved function of other sensory systems. However, both the time course and neuronal mechanism of cross-modal plasticity remain elusive. Recent study using functional MRI in humans suggests a role of the prefrontal cortex (PFC) in cross-modal plasticity. Since this phenomenon is assumed to be associated with altered GABAergic inhibition in the PFC, we have tested the hypothesis that early postnatal sensory deprivation causes the changes of inhibitory neuronal circuit in different regions of the PFC of the mice. We determined the effects of sensory deprivation from birth to postnatal day 28 (P28) or P58 on the density of parvalbumin (PV), calbindin (CB), and calretinin (CR) neurons in the prelimbic, infralimbic, and dorsal anterior cingulate cortices. The density of PV and CB neurons was significantly increased in layer 5/6 (L5/6). Moreover, the density of CR neurons was higher in L2/3 in sensory deprived mice compared to intact mice. These changes were more prominent at P56 than at P28. These results suggest that long-term sensory deprivation causes the changes of intracortical inhibitory networks in the PFC and the changes of inhibitory networks in the PFC may contribute to cross-modal plasticity.

No MeSH data available.


Sensory deprivation changes CR neuron density in the PFC. The density of CR neurons in the PL (a, b), IL (c, d), and dAC (e, f). CR neuron density at P28 (a, c, e) and P58 (b, d, f) in each area are shown. (a)-(b) There was no effect of sensory deprivation on the density of CR neurons in the PFC at P28. The density of CR neurons in L2/3 was increased by sensory deprivation at P56. (c)-(d) At P56 the density of CR neurons in L2/3 was increased by whisker trimming and dark rearing. (e)-(f) The density of CR neurons in L2/3 was increased by sensory deprivation at P56. Data are expressed as mean density S.E.M. (n = 6 per group). Abbreviations are the same as in Figure 4. ∗P < 0.05 compared with intact mice.
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fig7: Sensory deprivation changes CR neuron density in the PFC. The density of CR neurons in the PL (a, b), IL (c, d), and dAC (e, f). CR neuron density at P28 (a, c, e) and P58 (b, d, f) in each area are shown. (a)-(b) There was no effect of sensory deprivation on the density of CR neurons in the PFC at P28. The density of CR neurons in L2/3 was increased by sensory deprivation at P56. (c)-(d) At P56 the density of CR neurons in L2/3 was increased by whisker trimming and dark rearing. (e)-(f) The density of CR neurons in L2/3 was increased by sensory deprivation at P56. Data are expressed as mean density S.E.M. (n = 6 per group). Abbreviations are the same as in Figure 4. ∗P < 0.05 compared with intact mice.

Mentions: There was no significant difference in CR neuron density between sensory deprived mice and intact mice in the PFC at P28 (Figures 7(a), 7(c), and 7(e)).


Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex.

Ueno H, Suemitsu S, Matsumoto Y, Okamoto M - Neural Plast. (2015)

Sensory deprivation changes CR neuron density in the PFC. The density of CR neurons in the PL (a, b), IL (c, d), and dAC (e, f). CR neuron density at P28 (a, c, e) and P58 (b, d, f) in each area are shown. (a)-(b) There was no effect of sensory deprivation on the density of CR neurons in the PFC at P28. The density of CR neurons in L2/3 was increased by sensory deprivation at P56. (c)-(d) At P56 the density of CR neurons in L2/3 was increased by whisker trimming and dark rearing. (e)-(f) The density of CR neurons in L2/3 was increased by sensory deprivation at P56. Data are expressed as mean density S.E.M. (n = 6 per group). Abbreviations are the same as in Figure 4. ∗P < 0.05 compared with intact mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig7: Sensory deprivation changes CR neuron density in the PFC. The density of CR neurons in the PL (a, b), IL (c, d), and dAC (e, f). CR neuron density at P28 (a, c, e) and P58 (b, d, f) in each area are shown. (a)-(b) There was no effect of sensory deprivation on the density of CR neurons in the PFC at P28. The density of CR neurons in L2/3 was increased by sensory deprivation at P56. (c)-(d) At P56 the density of CR neurons in L2/3 was increased by whisker trimming and dark rearing. (e)-(f) The density of CR neurons in L2/3 was increased by sensory deprivation at P56. Data are expressed as mean density S.E.M. (n = 6 per group). Abbreviations are the same as in Figure 4. ∗P < 0.05 compared with intact mice.
Mentions: There was no significant difference in CR neuron density between sensory deprived mice and intact mice in the PFC at P28 (Figures 7(a), 7(c), and 7(e)).

Bottom Line: We determined the effects of sensory deprivation from birth to postnatal day 28 (P28) or P58 on the density of parvalbumin (PV), calbindin (CB), and calretinin (CR) neurons in the prelimbic, infralimbic, and dorsal anterior cingulate cortices.The density of PV and CB neurons was significantly increased in layer 5/6 (L5/6).These results suggest that long-term sensory deprivation causes the changes of intracortical inhibitory networks in the PFC and the changes of inhibitory networks in the PFC may contribute to cross-modal plasticity.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558, Japan ; Department of Medical Technology, Kawasaki College of Allied Health Professions, Okayama 701-0194, Japan.

ABSTRACT
Early loss of one sensory system can cause improved function of other sensory systems. However, both the time course and neuronal mechanism of cross-modal plasticity remain elusive. Recent study using functional MRI in humans suggests a role of the prefrontal cortex (PFC) in cross-modal plasticity. Since this phenomenon is assumed to be associated with altered GABAergic inhibition in the PFC, we have tested the hypothesis that early postnatal sensory deprivation causes the changes of inhibitory neuronal circuit in different regions of the PFC of the mice. We determined the effects of sensory deprivation from birth to postnatal day 28 (P28) or P58 on the density of parvalbumin (PV), calbindin (CB), and calretinin (CR) neurons in the prelimbic, infralimbic, and dorsal anterior cingulate cortices. The density of PV and CB neurons was significantly increased in layer 5/6 (L5/6). Moreover, the density of CR neurons was higher in L2/3 in sensory deprived mice compared to intact mice. These changes were more prominent at P56 than at P28. These results suggest that long-term sensory deprivation causes the changes of intracortical inhibitory networks in the PFC and the changes of inhibitory networks in the PFC may contribute to cross-modal plasticity.

No MeSH data available.