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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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Injury-induced neurogenesis after lesion of the piriform cortex. BrdU induction was observed in the piriform cortex of bulbotomized animals (b) but not sham animals (a) by 4 days postlesion. BrdU (+) cells were colocalized with the immature neuronal markers DCX (c) and PSA-NCAM (d) (confocal representations in C′ and D′, respectively). (e) By 2 weeks postlesion, BrdU (+) cells colocalized with the mature neuronal marker, NeuN. (f) Schematic representation of the inward pattern of shifting in BrdU labeling. DCX, doublecortin. Arrows denote positively double-labeled cells.
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Figure 2: Injury-induced neurogenesis after lesion of the piriform cortex. BrdU induction was observed in the piriform cortex of bulbotomized animals (b) but not sham animals (a) by 4 days postlesion. BrdU (+) cells were colocalized with the immature neuronal markers DCX (c) and PSA-NCAM (d) (confocal representations in C′ and D′, respectively). (e) By 2 weeks postlesion, BrdU (+) cells colocalized with the mature neuronal marker, NeuN. (f) Schematic representation of the inward pattern of shifting in BrdU labeling. DCX, doublecortin. Arrows denote positively double-labeled cells.

Mentions: To directly address the possibility that the piriform cortex undergoes neurogenesis, we administered BrdU to rats for 3 days before or after bulbotomy. In animals injected before bulbotomy, there were no significant differences in the numbers of BrdU (+) cells between bulbotomy and sham procedures. In animals injected following bulbotomy, there was a marked difference in the density of BrdU (+) cells in the piriform cortex and olfactory tract lesion sites as early as 1 day and as late as 10 days following the final BrdU administration, which corresponds to 4 and 14 days after bulbotomy (Fig. 2). Cells dually labeled for BrdU and the migrating neuroblast marker DCX were found interspersed among fibers in the olfactory tract and in superficial layer I immediately next to the olfactory tract 4 days after bulbotomy. At 14 days after bulbotomy, BrdU and DCX (+) cells appeared in the superficial outer layer II of the piriform cortex (Fig. 2c). In addition, immunoreactivity for PSA-NCAM, a marker of migrating neuroblasts and immature neurons, was markedly increased in the olfactory tract and layer I 4 days after bulbotomy and continued to be present at 14 days postlesion. At 14 days, dually labeled cells for PSA-NCAM and BrdU were identified in layer IIα (Fig. 2d). Colocalization of BrdU and NeuN, a marker for mature neurons, was not present in layer II neurons at day 4, but was present by day 14 following bulbotomy (Fig. 2e). BrdU (+) cells colocalized with glial-fibrillary acidic protein in layer I were rare, but were observed at 4 days after lesion formation. Iba-1 (+) macrophages were also BrdU (+), but infrequently and these cells did not cross the pial level into the parenchyma of the piriform cortex.


Remodeling of the piriform cortex after lesion in adult rodents.

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

Injury-induced neurogenesis after lesion of the piriform cortex. BrdU induction was observed in the piriform cortex of bulbotomized animals (b) but not sham animals (a) by 4 days postlesion. BrdU (+) cells were colocalized with the immature neuronal markers DCX (c) and PSA-NCAM (d) (confocal representations in C′ and D′, respectively). (e) By 2 weeks postlesion, BrdU (+) cells colocalized with the mature neuronal marker, NeuN. (f) Schematic representation of the inward pattern of shifting in BrdU labeling. DCX, doublecortin. Arrows denote positively double-labeled cells.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4126869&req=5

Figure 2: Injury-induced neurogenesis after lesion of the piriform cortex. BrdU induction was observed in the piriform cortex of bulbotomized animals (b) but not sham animals (a) by 4 days postlesion. BrdU (+) cells were colocalized with the immature neuronal markers DCX (c) and PSA-NCAM (d) (confocal representations in C′ and D′, respectively). (e) By 2 weeks postlesion, BrdU (+) cells colocalized with the mature neuronal marker, NeuN. (f) Schematic representation of the inward pattern of shifting in BrdU labeling. DCX, doublecortin. Arrows denote positively double-labeled cells.
Mentions: To directly address the possibility that the piriform cortex undergoes neurogenesis, we administered BrdU to rats for 3 days before or after bulbotomy. In animals injected before bulbotomy, there were no significant differences in the numbers of BrdU (+) cells between bulbotomy and sham procedures. In animals injected following bulbotomy, there was a marked difference in the density of BrdU (+) cells in the piriform cortex and olfactory tract lesion sites as early as 1 day and as late as 10 days following the final BrdU administration, which corresponds to 4 and 14 days after bulbotomy (Fig. 2). Cells dually labeled for BrdU and the migrating neuroblast marker DCX were found interspersed among fibers in the olfactory tract and in superficial layer I immediately next to the olfactory tract 4 days after bulbotomy. At 14 days after bulbotomy, BrdU and DCX (+) cells appeared in the superficial outer layer II of the piriform cortex (Fig. 2c). In addition, immunoreactivity for PSA-NCAM, a marker of migrating neuroblasts and immature neurons, was markedly increased in the olfactory tract and layer I 4 days after bulbotomy and continued to be present at 14 days postlesion. At 14 days, dually labeled cells for PSA-NCAM and BrdU were identified in layer IIα (Fig. 2d). Colocalization of BrdU and NeuN, a marker for mature neurons, was not present in layer II neurons at day 4, but was present by day 14 following bulbotomy (Fig. 2e). BrdU (+) cells colocalized with glial-fibrillary acidic protein in layer I were rare, but were observed at 4 days after lesion formation. Iba-1 (+) macrophages were also BrdU (+), but infrequently and these cells did not cross the pial level into the parenchyma of the piriform cortex.

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