A retrograde cell degeneration study of the cortical projection field of the pulvinar in the monkey

1950 ◽  
Vol 93 (3) ◽  
pp. 313-340 ◽  
Author(s):  
Kao Liang Chow
Keyword(s):  
Cell Degeneration ◽  
Cortical Projection ◽  
Degeneration Study ◽  
Projection Field

The projection of the lateral geniculate nucleus upon the cortex in the cat

1967 ◽  
Vol 169 (1014) ◽  
pp. 107-126 ◽  
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Small Cells ◽  
Lateral Part ◽  
Area 17 ◽  
Medial Part ◽  
Cell Degeneration ◽  
Cortical Projection ◽  
Area 18 ◽  
Lateral Geniculate ◽  
Areas 17 And 18

The retrograde cell degeneration in the lateral geniculate nucleus of the cat has been studied after lesions of the visual and adjoining areas of the cortex. Following lesions which are limited to area 17, the medium and small cells of the main laminae of the nucleus degenerate; damage restricted to area 18 does not result in any localized, severe degeneration, but com­bined destruction of areas 17 and 18 causes all the cells—large, medium and small—of the main laminae and the central interlaminar nucleus to degenerate. Cellular change in the medial interlaminar nucleus is only found after involvement of area 19. When the cortex of the middle suprasylvian gyrus is removed in addition to these areas the degeneration in the lateral geniculate nucleus is much more severe, and there is loss of the laminar pattern due to severe gliosis in the central interlaminar nucleus. There is a well-defined topical organiza­tion in the geniculo-cortical projection, and in the antero-posterior dimension it is the same to all areas of the visual cortex, anterior parts of the nucleus projecting anteriorly and posterior parts posteriorly. Medial parts of the main laminae are related to the lateral part of area 17 and to the medial part of area 18, and lateral parts of the laminae project to the medial part of area 17 and to the lateral part of area 18. After partial lesions which involve both areas 17 and 18 the cellular degeneration affects the laminae differentially along their antero-posterior extent, that in lamina A being the most anterior and that in lamina B the most posterior; in sagittal sections such a band, or column, of degeneration passes from antero-superior to postero-inferior at right angles to the plane of the laminae.

Author response for "Laminar distribution of cortical projection neurons to the pulvinar: A comparative study in cats and mice"

2020 ◽  
Author(s):  
Bruno Oliveira Ferreira de Souza ◽  
Éve‐Marie Frigon ◽  
Robert Tremblay‐Laliberté ◽  
Christian Casanova ◽  
Denis Boire
Keyword(s):  
Comparative Study ◽  
Author Response ◽  
Projection Neurons ◽  
Cortical Projection ◽  
Laminar Distribution

Restraint stress exacerbates cell degeneration induced by acute binge ethanol in the adolescent, but not in the adult or middle-aged, brain

2019 ◽  
Vol 364 ◽  
pp. 317-327 ◽  
Author(s):  
Macarena Soledad Fernández ◽  
Soledad de Olmos ◽  
Michael E. Nizhnikov ◽  
Ricardo Marcos Pautassi
Keyword(s):  
Restraint Stress ◽  
Middle Aged ◽  
Cell Degeneration ◽  
Aged Brain ◽  
Binge Ethanol

scholarly journals Neuroplastin expression is essential for hearing and hair cell PMCA expression

2021 ◽  
Author(s):  
Xiao Lin ◽  
Michael G. K. Brunk ◽  
Pingan Yuanxiang ◽  
Andrew W. Curran ◽  
Enqi Zhang ◽  
...  
Keyword(s):  
Hair Cell ◽  
White Noise ◽  
Hair Cells ◽  
Normal Development ◽  
Single Photon ◽  
Photon Emission ◽  
Auditory Brainstem ◽  
Outer Hair Cells ◽  
Emission Computed Tomography ◽  
Cell Degeneration

AbstractHearing deficits impact on the communication with the external world and severely compromise perception of the surrounding. Deafness can be caused by particular mutations in the neuroplastin (Nptn) gene, which encodes a transmembrane recognition molecule of the immunoglobulin (Ig) superfamily and plasma membrane Calcium ATPase (PMCA) accessory subunit. This study investigates whether the complete absence of neuroplastin or the loss of neuroplastin in the adult after normal development lead to hearing impairment in mice analyzed by behavioral, electrophysiological, and in vivo imaging measurements. Auditory brainstem recordings from adult neuroplastin-deficient mice (Nptn−/−) show that these mice are deaf. With age, hair cells and spiral ganglion cells degenerate in Nptn−/− mice. Adult Nptn−/− mice fail to behaviorally respond to white noise and show reduced baseline blood flow in the auditory cortex (AC) as revealed by single-photon emission computed tomography (SPECT). In adult Nptn−/− mice, tone-evoked cortical activity was not detectable within the primary auditory field (A1) of the AC, although we observed non-persistent tone-like evoked activities in electrophysiological recordings of some young Nptn−/− mice. Conditional ablation of neuroplastin in Nptnlox/loxEmx1Cre mice reveals that behavioral responses to simple tones or white noise do not require neuroplastin expression by central glutamatergic neurons. Loss of neuroplastin from hair cells in adult NptnΔlox/loxPrCreERT mice after normal development is correlated with increased hearing thresholds and only high prepulse intensities result in effective prepulse inhibition (PPI) of the startle response. Furthermore, we show that neuroplastin is required for the expression of PMCA 2 in outer hair cells. This suggests that altered Ca2+ homeostasis underlies the observed hearing impairments and leads to hair cell degeneration. Our results underline the importance of neuroplastin for the development and the maintenance of the auditory system.

scholarly journals Scar Formation and Debris Elimination during Hair Cell Degeneration in the Adult DTR Mouse

Neuroscience ◽  
2021 ◽  
Vol 453 ◽  
pp. 57-68
Author(s):  
Sungsu Lee ◽  
Takaomi Kurioka ◽  
Min Young Lee ◽  
Lisa A. Beyer ◽  
Donald L. Swiderski ◽  
...  
Keyword(s):  
Hair Cell ◽  
Scar Formation ◽  
Cell Degeneration

scholarly journals Retinal Pigment Epithelium Expressed Toll-like Receptors and Their Potential Role in Age-Related Macular Degeneration

2021 ◽  
Vol 22 (16) ◽  
pp. 8387
Author(s):  
Alexa Klettner ◽  
Johann Roider
Keyword(s):  
Retinal Pigment Epithelium ◽  
Inflammatory Response ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Current Status ◽  
Toll Like Receptors ◽  
Cell Degeneration ◽  
Age Related

(1) Background: Inflammation is a major pathomechanism in the development and progression of age-related macular degeneration (AMD). The retinal pigment epithelium (RPE) may contribute to retinal inflammation via activation of its Toll-like receptors (TLR). TLR are pattern recognition receptors that detect the pathogen- or danger-associated molecular pattern. The involvement of TLR activation in AMD is so far not understood. (2) Methods: We performed a systematic literature research, consulting the National Library of Medicine (PubMed). (3) Results: We identified 106 studies, of which 54 were included in this review. Based on these studies, the current status of TLR in AMD, the effects of TLR in RPE activation and of the interaction of TLR activated RPE with monocytic cells are given, and the potential of TLR activation in RPE as part of the AMD development is discussed. (4) Conclusion: The activation of TLR2, -3, and -4 induces a profound pro-inflammatory response in the RPE that may contribute to (long-term) inflammation by induction of pro-inflammatory cytokines, reducing RPE function and causing RPE cell degeneration, thereby potentially constantly providing new TLR ligands, which could perpetuate and, in the long run, exacerbate the inflammatory response, which may contribute to AMD development. Furthermore, the combined activation of RPE and microglia may exacerbate neurotoxic effects.

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