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Binocular pattern deprivation interferes with the expression of proteins involved in primary visual cortex maturation in the cat.

Laskowska-Macios K, Nys J, Hu TT, Zapasnik M, Van der Perren A, Kossut M, Burnat K, Arckens L - Mol Brain (2015)

Bottom Line: Consistent with the maturation delay, distinct developmental protein expression changes observed for normal kittens were postponed by BD, especially in the peripheral region.Verification of the expression of proteins from each of the biological processes via Western analysis disclosed that some of the transient proteomic changes correlate to the distinct behavioral outcome in adult life, depending on timing and duration of the BD period [Neuroscience 2013;255:99-109].Taken together, the plasticity potential to recover from BD, in relation to ensuing restoration of normal visual input, appears to rely on specific protein expression changes and cellular processes induced by the loss of pattern vision in early life.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Neuroplasticity, Nencki Institute of Experimental Biology, 02-093, Warsaw, Poland. karolina.laskowska.macios@gmail.com.

ABSTRACT

Background: Binocular pattern deprivation from eye opening (early BD) delays the maturation of the primary visual cortex. This delay is more pronounced for the peripheral than the central visual field representation within area 17, particularly between the age of 2 and 4 months [Laskowska-Macios, Cereb Cortex, 2014].

Results: In this study, we probed for related dynamic changes in the cortical proteome. We introduced age, cortical region and BD as principal variables in a 2-D DIGE screen of area 17. In this way we explored the potential of BD-related protein expression changes between central and peripheral area 17 of 2- and 4-month-old BD (2BD, 4BD) kittens as a valid parameter towards the identification of brain maturation-related molecular processes. Consistent with the maturation delay, distinct developmental protein expression changes observed for normal kittens were postponed by BD, especially in the peripheral region. These BD-induced proteomic changes suggest a negative regulation of neurite outgrowth, synaptic transmission and clathrin-mediated endocytosis, thereby implicating these processes in normal experience-induced visual cortex maturation. Verification of the expression of proteins from each of the biological processes via Western analysis disclosed that some of the transient proteomic changes correlate to the distinct behavioral outcome in adult life, depending on timing and duration of the BD period [Neuroscience 2013;255:99-109].

Conclusions: Taken together, the plasticity potential to recover from BD, in relation to ensuing restoration of normal visual input, appears to rely on specific protein expression changes and cellular processes induced by the loss of pattern vision in early life.

No MeSH data available.


Related in: MedlinePlus

Semi-quantitative Western blotting for proteins involved in GABA synthesis: GAD67 (a) and GAD65 (b). GAD67 expression increased with age and was not different in BD animals as compared to age-matched normal controls. Nevertheless, the increase between month 4 and 6 observed in BD animals was not present in normal animals. GAD65 expression also increased with age, with a significantly slower rate in BD as compared to normal animals in both regions of area 17, achieving the highest level at 6 instead of 4 months. Additionally, in the central region of 4BD kittens GAD65 did not show a developmental increase, maintaining a lower level as compared to the 4N group. Together all observations are indicative for a delay in the development of normal cortical inhibition levels. Asterisks above bars denote significant differences (P < 0.05) for a given region between age groups of a given condition (normal or BD). Numbers above BD-related bars denote the % statistical difference between BD and age-matched normal control groups (P < 0.05). Results are means with ± SD
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Fig4: Semi-quantitative Western blotting for proteins involved in GABA synthesis: GAD67 (a) and GAD65 (b). GAD67 expression increased with age and was not different in BD animals as compared to age-matched normal controls. Nevertheless, the increase between month 4 and 6 observed in BD animals was not present in normal animals. GAD65 expression also increased with age, with a significantly slower rate in BD as compared to normal animals in both regions of area 17, achieving the highest level at 6 instead of 4 months. Additionally, in the central region of 4BD kittens GAD65 did not show a developmental increase, maintaining a lower level as compared to the 4N group. Together all observations are indicative for a delay in the development of normal cortical inhibition levels. Asterisks above bars denote significant differences (P < 0.05) for a given region between age groups of a given condition (normal or BD). Numbers above BD-related bars denote the % statistical difference between BD and age-matched normal control groups (P < 0.05). Results are means with ± SD

Mentions: GAD67 produces the main cellular pool of GABA, whereas GAD65 produces GABA that is preferentially packed into vesicles for fast neurotransmitter use [22–29]. The expression of GAD65 and GAD67 increased during normal cortical development achieving mature levels at 6 months of age for GAD67 and at 4 months for GAD65 for both central and peripheral area 17 (Fig. 4a, b). In early and late onset BD animals GAD67 expression levels did not differ from age-matched normal controls or across regions (Fig. 4a). The only difference we detected relates to the lack of a significant increase in GAD67 levels between month 4 and 6. The developmental increase of GAD65 expression was slower in BD compared to normal animals in both regions of area 17, achieving the highest level only in 6BD kittens (Fig. 4b). Additionally, in the central region of 4BD kittens GAD65 did not show a developmental increase, maintaining a lower level as compared to the 4N group (Fig. 4b). As such, the GAD65 expression level in 4BD was similar to that in 2N kittens (Fig. 4b). In 2N2BD, GAD65 expression did not differ from age-matched 4N controls or younger 2N animals. However, similar to 4BD, 2N2BD showed a lower GAD65 level than 6BD in both regions, indicating that both late onset and short early onset BD arrests the developmental increase in GAD65 levels (Fig. 4b).Fig. 4


Binocular pattern deprivation interferes with the expression of proteins involved in primary visual cortex maturation in the cat.

Laskowska-Macios K, Nys J, Hu TT, Zapasnik M, Van der Perren A, Kossut M, Burnat K, Arckens L - Mol Brain (2015)

Semi-quantitative Western blotting for proteins involved in GABA synthesis: GAD67 (a) and GAD65 (b). GAD67 expression increased with age and was not different in BD animals as compared to age-matched normal controls. Nevertheless, the increase between month 4 and 6 observed in BD animals was not present in normal animals. GAD65 expression also increased with age, with a significantly slower rate in BD as compared to normal animals in both regions of area 17, achieving the highest level at 6 instead of 4 months. Additionally, in the central region of 4BD kittens GAD65 did not show a developmental increase, maintaining a lower level as compared to the 4N group. Together all observations are indicative for a delay in the development of normal cortical inhibition levels. Asterisks above bars denote significant differences (P < 0.05) for a given region between age groups of a given condition (normal or BD). Numbers above BD-related bars denote the % statistical difference between BD and age-matched normal control groups (P < 0.05). Results are means with ± SD
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Related In: Results  -  Collection

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Fig4: Semi-quantitative Western blotting for proteins involved in GABA synthesis: GAD67 (a) and GAD65 (b). GAD67 expression increased with age and was not different in BD animals as compared to age-matched normal controls. Nevertheless, the increase between month 4 and 6 observed in BD animals was not present in normal animals. GAD65 expression also increased with age, with a significantly slower rate in BD as compared to normal animals in both regions of area 17, achieving the highest level at 6 instead of 4 months. Additionally, in the central region of 4BD kittens GAD65 did not show a developmental increase, maintaining a lower level as compared to the 4N group. Together all observations are indicative for a delay in the development of normal cortical inhibition levels. Asterisks above bars denote significant differences (P < 0.05) for a given region between age groups of a given condition (normal or BD). Numbers above BD-related bars denote the % statistical difference between BD and age-matched normal control groups (P < 0.05). Results are means with ± SD
Mentions: GAD67 produces the main cellular pool of GABA, whereas GAD65 produces GABA that is preferentially packed into vesicles for fast neurotransmitter use [22–29]. The expression of GAD65 and GAD67 increased during normal cortical development achieving mature levels at 6 months of age for GAD67 and at 4 months for GAD65 for both central and peripheral area 17 (Fig. 4a, b). In early and late onset BD animals GAD67 expression levels did not differ from age-matched normal controls or across regions (Fig. 4a). The only difference we detected relates to the lack of a significant increase in GAD67 levels between month 4 and 6. The developmental increase of GAD65 expression was slower in BD compared to normal animals in both regions of area 17, achieving the highest level only in 6BD kittens (Fig. 4b). Additionally, in the central region of 4BD kittens GAD65 did not show a developmental increase, maintaining a lower level as compared to the 4N group (Fig. 4b). As such, the GAD65 expression level in 4BD was similar to that in 2N kittens (Fig. 4b). In 2N2BD, GAD65 expression did not differ from age-matched 4N controls or younger 2N animals. However, similar to 4BD, 2N2BD showed a lower GAD65 level than 6BD in both regions, indicating that both late onset and short early onset BD arrests the developmental increase in GAD65 levels (Fig. 4b).Fig. 4

Bottom Line: Consistent with the maturation delay, distinct developmental protein expression changes observed for normal kittens were postponed by BD, especially in the peripheral region.Verification of the expression of proteins from each of the biological processes via Western analysis disclosed that some of the transient proteomic changes correlate to the distinct behavioral outcome in adult life, depending on timing and duration of the BD period [Neuroscience 2013;255:99-109].Taken together, the plasticity potential to recover from BD, in relation to ensuing restoration of normal visual input, appears to rely on specific protein expression changes and cellular processes induced by the loss of pattern vision in early life.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Neuroplasticity, Nencki Institute of Experimental Biology, 02-093, Warsaw, Poland. karolina.laskowska.macios@gmail.com.

ABSTRACT

Background: Binocular pattern deprivation from eye opening (early BD) delays the maturation of the primary visual cortex. This delay is more pronounced for the peripheral than the central visual field representation within area 17, particularly between the age of 2 and 4 months [Laskowska-Macios, Cereb Cortex, 2014].

Results: In this study, we probed for related dynamic changes in the cortical proteome. We introduced age, cortical region and BD as principal variables in a 2-D DIGE screen of area 17. In this way we explored the potential of BD-related protein expression changes between central and peripheral area 17 of 2- and 4-month-old BD (2BD, 4BD) kittens as a valid parameter towards the identification of brain maturation-related molecular processes. Consistent with the maturation delay, distinct developmental protein expression changes observed for normal kittens were postponed by BD, especially in the peripheral region. These BD-induced proteomic changes suggest a negative regulation of neurite outgrowth, synaptic transmission and clathrin-mediated endocytosis, thereby implicating these processes in normal experience-induced visual cortex maturation. Verification of the expression of proteins from each of the biological processes via Western analysis disclosed that some of the transient proteomic changes correlate to the distinct behavioral outcome in adult life, depending on timing and duration of the BD period [Neuroscience 2013;255:99-109].

Conclusions: Taken together, the plasticity potential to recover from BD, in relation to ensuing restoration of normal visual input, appears to rely on specific protein expression changes and cellular processes induced by the loss of pattern vision in early life.

No MeSH data available.


Related in: MedlinePlus