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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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Bulbotomy results in a decreased number of DCX (+) neuroblasts. (a) Whisker plot of the total number of DCX (+) cells in the piriform cortex in sham versus lesioned animals 3 and 7 days after bulbotomy. At 3 days, the number of DCX (+) cells was comparable in sham (1450±165) and lesioned animals (1533±815). By 7 days, the number of DCX (+) cells in lesioned animals decreased markedly (490±546), resulting in a significant difference in the number of DCX (+) cells between groups by 7 days (P=0.04). (b–g) Expression of DCX-DsRed in the canonical neurogenic regions, dentate gyrus (b), and subventricular zone (c, red: DsRed, green: DCX immunostain), as well as basal expression pattern in normal piriform cortex (d). (e) Expression of DCX in sham animals is largely confined to layer II (compact layer) of the piriform cortex. (f) Three days after bulbotomy, DCX expression is more diffuse and DCX (+) cells are observed in superficial cortical layers in addition to layer II. (g) By 7 days after bulbotomy, DCX expression is largely reduced. DCX, doublecortin.
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Figure 3: Bulbotomy results in a decreased number of DCX (+) neuroblasts. (a) Whisker plot of the total number of DCX (+) cells in the piriform cortex in sham versus lesioned animals 3 and 7 days after bulbotomy. At 3 days, the number of DCX (+) cells was comparable in sham (1450±165) and lesioned animals (1533±815). By 7 days, the number of DCX (+) cells in lesioned animals decreased markedly (490±546), resulting in a significant difference in the number of DCX (+) cells between groups by 7 days (P=0.04). (b–g) Expression of DCX-DsRed in the canonical neurogenic regions, dentate gyrus (b), and subventricular zone (c, red: DsRed, green: DCX immunostain), as well as basal expression pattern in normal piriform cortex (d). (e) Expression of DCX in sham animals is largely confined to layer II (compact layer) of the piriform cortex. (f) Three days after bulbotomy, DCX expression is more diffuse and DCX (+) cells are observed in superficial cortical layers in addition to layer II. (g) By 7 days after bulbotomy, DCX expression is largely reduced. DCX, doublecortin.

Mentions: We further investigated conditional neurogenesis in response to bulbotomy using DCX-DsRed transgenic mice. Bulbotomized and sham animals were allowed to survive for 3 or 7 days postlesion and brain tissue was processed for fluorescence microscopy after perfusion fixation. DsRed expression and colocalization with DCX was confirmed in uninjured adult mice in the canonical neurogenic regions of the dentate gyrus (DG) (Fig. 3b) and SVZ (Fig. 3c). Interestingly, DCX expression was also observed extending from the external capsule/lateral ventricle through the dorsal endopiriform cortex to the superficial layers of the piriform cortex (Fig. 3d).


Remodeling of the piriform cortex after lesion in adult rodents.

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

Bulbotomy results in a decreased number of DCX (+) neuroblasts. (a) Whisker plot of the total number of DCX (+) cells in the piriform cortex in sham versus lesioned animals 3 and 7 days after bulbotomy. At 3 days, the number of DCX (+) cells was comparable in sham (1450±165) and lesioned animals (1533±815). By 7 days, the number of DCX (+) cells in lesioned animals decreased markedly (490±546), resulting in a significant difference in the number of DCX (+) cells between groups by 7 days (P=0.04). (b–g) Expression of DCX-DsRed in the canonical neurogenic regions, dentate gyrus (b), and subventricular zone (c, red: DsRed, green: DCX immunostain), as well as basal expression pattern in normal piriform cortex (d). (e) Expression of DCX in sham animals is largely confined to layer II (compact layer) of the piriform cortex. (f) Three days after bulbotomy, DCX expression is more diffuse and DCX (+) cells are observed in superficial cortical layers in addition to layer II. (g) By 7 days after bulbotomy, DCX expression is largely reduced. DCX, doublecortin.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 3: Bulbotomy results in a decreased number of DCX (+) neuroblasts. (a) Whisker plot of the total number of DCX (+) cells in the piriform cortex in sham versus lesioned animals 3 and 7 days after bulbotomy. At 3 days, the number of DCX (+) cells was comparable in sham (1450±165) and lesioned animals (1533±815). By 7 days, the number of DCX (+) cells in lesioned animals decreased markedly (490±546), resulting in a significant difference in the number of DCX (+) cells between groups by 7 days (P=0.04). (b–g) Expression of DCX-DsRed in the canonical neurogenic regions, dentate gyrus (b), and subventricular zone (c, red: DsRed, green: DCX immunostain), as well as basal expression pattern in normal piriform cortex (d). (e) Expression of DCX in sham animals is largely confined to layer II (compact layer) of the piriform cortex. (f) Three days after bulbotomy, DCX expression is more diffuse and DCX (+) cells are observed in superficial cortical layers in addition to layer II. (g) By 7 days after bulbotomy, DCX expression is largely reduced. DCX, doublecortin.
Mentions: We further investigated conditional neurogenesis in response to bulbotomy using DCX-DsRed transgenic mice. Bulbotomized and sham animals were allowed to survive for 3 or 7 days postlesion and brain tissue was processed for fluorescence microscopy after perfusion fixation. DsRed expression and colocalization with DCX was confirmed in uninjured adult mice in the canonical neurogenic regions of the dentate gyrus (DG) (Fig. 3b) and SVZ (Fig. 3c). Interestingly, DCX expression was also observed extending from the external capsule/lateral ventricle through the dorsal endopiriform cortex to the superficial layers of the piriform cortex (Fig. 3d).

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