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Remodeling of the piriform cortex after lesion in adult rodents.

Rossi SL, Mahairaki V, Zhou L, Song Y, Koliatsos VE - Neuroreport (2014)

Bottom Line: In this study, we report that following the marked loss of neurons in outer layer II, the piriform cortex is reconstituted by the addition of newly formed neurons that restore the number to a preinjury level within 30 days.We provide evidence that the number of newly divided neuronal progenitors increases after injury and further show that a population of doublecortin-positive cells that resides in the piriform cortex decreases after injury.Taken together, these findings suggest that the piriform cortex has significant neurogenic potential that is activated following sensory denervation and may contribute toward the replacement of neurons in outer layer II.

View Article: PubMed Central - PubMed

Affiliation: aDepartment of Pathology, Division of Neuropathology Departments of bNeurology cPsychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

ABSTRACT
Denervation of the piriform cortex by bulbotomy causes a series of important cellular changes in the inhibitory interneurons of layer I and transsynaptic apoptosis of a large number of pyramidal neurons in outer layer II within 24 h. In this study, we report that following the marked loss of neurons in outer layer II, the piriform cortex is reconstituted by the addition of newly formed neurons that restore the number to a preinjury level within 30 days. We provide evidence that the number of newly divided neuronal progenitors increases after injury and further show that a population of doublecortin-positive cells that resides in the piriform cortex decreases after injury. Taken together, these findings suggest that the piriform cortex has significant neurogenic potential that is activated following sensory denervation and may contribute toward the replacement of neurons in outer layer II.

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The piriform cortex is fully reconstituted by 1 month after bulbotomy. (a) Total cell numbers in layer II were obtained using an optical fractionator-based stereological method. Differences between bulbotomy and sham groups across various survival times were analyzed with ANOVA (P=0.0072), followed by post-hoc Bonferroni testing. At 1 (242 054 sham vs. 183 347 bulbotomy) and 7 (241 741 sham vs. 170 362 bulbotomy) days postlesion, the total number of neurons in layer II was significantly less than that observed in sham-operated animals (P=0.0003 and 0.045, respectively). Data are represented as mean±SD (n=3). (b) The thickness of layer II of piriform cortex, as outlined with black lines, is markedly reduced 7 days after bulbotomy (middle). Reduced thickness was mainly caused by the death of pyramidal neurons in sublayer IIα (top). The piriform cortex in lesioned animals (bottom) recovered to the same size as control sham animals at 30 days after bulbotomy. ANOVA, analysis of variance.
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Figure 1: The piriform cortex is fully reconstituted by 1 month after bulbotomy. (a) Total cell numbers in layer II were obtained using an optical fractionator-based stereological method. Differences between bulbotomy and sham groups across various survival times were analyzed with ANOVA (P=0.0072), followed by post-hoc Bonferroni testing. At 1 (242 054 sham vs. 183 347 bulbotomy) and 7 (241 741 sham vs. 170 362 bulbotomy) days postlesion, the total number of neurons in layer II was significantly less than that observed in sham-operated animals (P=0.0003 and 0.045, respectively). Data are represented as mean±SD (n=3). (b) The thickness of layer II of piriform cortex, as outlined with black lines, is markedly reduced 7 days after bulbotomy (middle). Reduced thickness was mainly caused by the death of pyramidal neurons in sublayer IIα (top). The piriform cortex in lesioned animals (bottom) recovered to the same size as control sham animals at 30 days after bulbotomy. ANOVA, analysis of variance.

Mentions: Variances in cell numbers at time points following bulbotomy or sham procedures were analyzed using ANOVA. The overall variance among groups was significant (Fig. 1, P=0.0072). Bonferroni post-hoc testing showed significant differences between bulbotomy and sham groups at 1 and 7 days postlesion (Fig. 1, P=0.0003). Cell death was greatest at 7 days, with 71 380 neurons dying by transsynaptic apoptosis (P=0.045). By 14 days, however, the number of neurons in bulbotomized animals increased, resulting in no significant differences when compared with sham-treated animals at 14, 30, and 90 days after bulbotomy.


Remodeling of the piriform cortex after lesion in adult rodents.

Rossi SL, Mahairaki V, Zhou L, Song Y, Koliatsos VE - Neuroreport (2014)

The piriform cortex is fully reconstituted by 1 month after bulbotomy. (a) Total cell numbers in layer II were obtained using an optical fractionator-based stereological method. Differences between bulbotomy and sham groups across various survival times were analyzed with ANOVA (P=0.0072), followed by post-hoc Bonferroni testing. At 1 (242 054 sham vs. 183 347 bulbotomy) and 7 (241 741 sham vs. 170 362 bulbotomy) days postlesion, the total number of neurons in layer II was significantly less than that observed in sham-operated animals (P=0.0003 and 0.045, respectively). Data are represented as mean±SD (n=3). (b) The thickness of layer II of piriform cortex, as outlined with black lines, is markedly reduced 7 days after bulbotomy (middle). Reduced thickness was mainly caused by the death of pyramidal neurons in sublayer IIα (top). The piriform cortex in lesioned animals (bottom) recovered to the same size as control sham animals at 30 days after bulbotomy. ANOVA, analysis of variance.
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Figure 1: The piriform cortex is fully reconstituted by 1 month after bulbotomy. (a) Total cell numbers in layer II were obtained using an optical fractionator-based stereological method. Differences between bulbotomy and sham groups across various survival times were analyzed with ANOVA (P=0.0072), followed by post-hoc Bonferroni testing. At 1 (242 054 sham vs. 183 347 bulbotomy) and 7 (241 741 sham vs. 170 362 bulbotomy) days postlesion, the total number of neurons in layer II was significantly less than that observed in sham-operated animals (P=0.0003 and 0.045, respectively). Data are represented as mean±SD (n=3). (b) The thickness of layer II of piriform cortex, as outlined with black lines, is markedly reduced 7 days after bulbotomy (middle). Reduced thickness was mainly caused by the death of pyramidal neurons in sublayer IIα (top). The piriform cortex in lesioned animals (bottom) recovered to the same size as control sham animals at 30 days after bulbotomy. ANOVA, analysis of variance.
Mentions: Variances in cell numbers at time points following bulbotomy or sham procedures were analyzed using ANOVA. The overall variance among groups was significant (Fig. 1, P=0.0072). Bonferroni post-hoc testing showed significant differences between bulbotomy and sham groups at 1 and 7 days postlesion (Fig. 1, P=0.0003). Cell death was greatest at 7 days, with 71 380 neurons dying by transsynaptic apoptosis (P=0.045). By 14 days, however, the number of neurons in bulbotomized animals increased, resulting in no significant differences when compared with sham-treated animals at 14, 30, and 90 days after bulbotomy.

Bottom Line: In this study, we report that following the marked loss of neurons in outer layer II, the piriform cortex is reconstituted by the addition of newly formed neurons that restore the number to a preinjury level within 30 days.We provide evidence that the number of newly divided neuronal progenitors increases after injury and further show that a population of doublecortin-positive cells that resides in the piriform cortex decreases after injury.Taken together, these findings suggest that the piriform cortex has significant neurogenic potential that is activated following sensory denervation and may contribute toward the replacement of neurons in outer layer II.

View Article: PubMed Central - PubMed

Affiliation: aDepartment of Pathology, Division of Neuropathology Departments of bNeurology cPsychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

ABSTRACT
Denervation of the piriform cortex by bulbotomy causes a series of important cellular changes in the inhibitory interneurons of layer I and transsynaptic apoptosis of a large number of pyramidal neurons in outer layer II within 24 h. In this study, we report that following the marked loss of neurons in outer layer II, the piriform cortex is reconstituted by the addition of newly formed neurons that restore the number to a preinjury level within 30 days. We provide evidence that the number of newly divided neuronal progenitors increases after injury and further show that a population of doublecortin-positive cells that resides in the piriform cortex decreases after injury. Taken together, these findings suggest that the piriform cortex has significant neurogenic potential that is activated following sensory denervation and may contribute toward the replacement of neurons in outer layer II.

Show MeSH
Related in: MedlinePlus