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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.


Localization of interneuron in the mouse PFC. Representative light micrograph showing laminar distribution of PV (a), CB (b), and CR (c) neurons in the PL. (a) PV neurons are located in L2/3 and L5/6. (b) CB neurons are mainly located in L2/3 and L5/6. The principal neurons in L2 are weakly immunopositive to CB. (c) CR neurons are mainly located in L2/3. (A)–(C) Higher magnification images of interneurons in the PL. Scale bars = 200 μm in (c) (applies to (a)–(c)); 50 μm in (C) (applies to (A)–(C)).
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fig2: Localization of interneuron in the mouse PFC. Representative light micrograph showing laminar distribution of PV (a), CB (b), and CR (c) neurons in the PL. (a) PV neurons are located in L2/3 and L5/6. (b) CB neurons are mainly located in L2/3 and L5/6. The principal neurons in L2 are weakly immunopositive to CB. (c) CR neurons are mainly located in L2/3. (A)–(C) Higher magnification images of interneurons in the PL. Scale bars = 200 μm in (c) (applies to (a)–(c)); 50 μm in (C) (applies to (A)–(C)).

Mentions: As shown in Figure 2, all interneuron subtypes were present in the mouse PFC at P28. In the PL, PV neurons were located in both L2/3 and L5/6 (Figure 2(a)). The processes of PV neurons were distributed through all layers. Also CB neurons were present in both L2/3 and 5/6 (Figure 2(b)). Although the principal neurons in L2 are weakly immunopositive to CB [44], CB positive interneurons were darkly stained compared to principal neurons. The majority of CB neurons were multipolar, but bipolar neurons were also observed (Figure 2(B)). CR neurons were more abundant in L2/3 than L5/6 (Figure 2(c)). They displayed bipolar arbor-like morphology (Figure 2(C)). These distribution patterns of calcium-binding proteins were consistent with previous literature [28, 44–47]. In order to evaluate whether specific interneuronal population might be more susceptible to sensory deprivation, we analyzed the density of PV, CB, and CR neurons.


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)

Localization of interneuron in the mouse PFC. Representative light micrograph showing laminar distribution of PV (a), CB (b), and CR (c) neurons in the PL. (a) PV neurons are located in L2/3 and L5/6. (b) CB neurons are mainly located in L2/3 and L5/6. The principal neurons in L2 are weakly immunopositive to CB. (c) CR neurons are mainly located in L2/3. (A)–(C) Higher magnification images of interneurons in the PL. Scale bars = 200 μm in (c) (applies to (a)–(c)); 50 μm in (C) (applies to (A)–(C)).
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig2: Localization of interneuron in the mouse PFC. Representative light micrograph showing laminar distribution of PV (a), CB (b), and CR (c) neurons in the PL. (a) PV neurons are located in L2/3 and L5/6. (b) CB neurons are mainly located in L2/3 and L5/6. The principal neurons in L2 are weakly immunopositive to CB. (c) CR neurons are mainly located in L2/3. (A)–(C) Higher magnification images of interneurons in the PL. Scale bars = 200 μm in (c) (applies to (a)–(c)); 50 μm in (C) (applies to (A)–(C)).
Mentions: As shown in Figure 2, all interneuron subtypes were present in the mouse PFC at P28. In the PL, PV neurons were located in both L2/3 and L5/6 (Figure 2(a)). The processes of PV neurons were distributed through all layers. Also CB neurons were present in both L2/3 and 5/6 (Figure 2(b)). Although the principal neurons in L2 are weakly immunopositive to CB [44], CB positive interneurons were darkly stained compared to principal neurons. The majority of CB neurons were multipolar, but bipolar neurons were also observed (Figure 2(B)). CR neurons were more abundant in L2/3 than L5/6 (Figure 2(c)). They displayed bipolar arbor-like morphology (Figure 2(C)). These distribution patterns of calcium-binding proteins were consistent with previous literature [28, 44–47]. In order to evaluate whether specific interneuronal population might be more susceptible to sensory deprivation, we analyzed the density of PV, CB, and CR neurons.

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.