Browsing by Subject "Visual cortex"

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    Adaptive changes in the visual cortex after photoreceptor degeneration in retinitis pigmentosa
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Martinez Galan, Juan R.; Caminos, Elena; Biología Celular e Histología
    Retinitis pigmentosa (RP) is a group of hereditary disorders that cause progressive retinal degeneration, affecting the rods and, subsequently, the cones, which results in progressive vision loss. RP is genetically heterogeneous and is inherited in an autosomal dominant, autosomal recessive, X-linked, or sporadic non-Mendelian manner. The recent advance-ments in repairing damaged retinas highlight the necessity of understanding the impact of photoreceptor degeneration on the visual cortex. This is because functional vision may not be adequately restored if this region is significantly impaired prior to treatment. In the present review, we have analyzed the rodent models of RP that have been most frequently used and the physiological and morphological changes occurring in both humans and rodents with this disorder. Following visually evoked stimulation, the processing of visual information in the primary visual cortex (V1) of individuals with RP is altered due to modifications in the transduction of the signal originating in the degenerated retina. Moreover, alterations in the intrinsic electro-physiological properties of cortical neurons and neural circuits have also been documented. Finally, several neurochemical and/or morphological changes are observed in synaptic structures associated with pyramidal neurons and in select inhibitory interneurons. Nevertheless, despite the physiological and morphologi-cal changes that have been described, the impact of RP on the visual cortex does not inevitably result in irreversible damage, as the alterations do not appear to be particularly severe. Brain plasticity is more restricted in adults; however, remodeling of the visual cortex in mice and humans is possible, which encourages further work on therapies capable of partially restoring the lost visual function.
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    Immunocytochemical localization of the calcium-binding proteins calbindin D28K, calretinin and parvalbumin in bat visual cortex
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Kim, Hang-Gu; Gu, Ya-Nan; Lee, Kyoung-Pil; Lee, Ji-Gun; Kim, Chan-Wook; Lee, Ji-Won; Jeong, Tae-Hee; Jeong, Young-Wun; Jeon, Chang-Jin
    It is a common misconception that bats are blind, and various studies have suggested that bats have visual abilities. The purpose of this study was to investigate the cytoarchitecture of calbindin D28K (CB)-, calretinin (CR)-, and parvalbumin (PV)-immunoreactive (IR) neurons in the bat visual cortex using immunocytochemistry. The highest density of CB- and PV-IR neurons was located in layer IV of the visual cortex. The majority of CB- and PV-IR neurons were characterized by a stellate or round/oval shape. CR-IR neurons were predominantly located in layers II/III, and the cells were principally round/oval in shape. Two-color immunofluorescence revealed that 65.96%, 24.24%, and 77.00% of the CB-, CR-, and PV-IR neurons, respectively, contained gamma-aminobutyric acid (GABA). We observed calcium-binding protein (CBP)- IR neurons in specific layers of the bat visual cortex and in specific cell types. Many of the CBP-IR neurons were GABAergic interneurons. These data provide useful clues to aid in understanding the functional aspects of the bat visual system.
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    The axon initial segment of corticocollicular neurons in the rabbit visual cortex, an electron-microscope study with HRP
    (Murcia : F. Hernández, 1987) Matute, C.; Contamina, P.; Martínez Millán, L.
    The synaptic connections of the axon initial segment (IS) of retrogradely labeled corticocollicular neurons in the rabbit visual cortex were studied using the HRP-EM method. Identified IS showed relatively few synaptic boutons unevenly distributed along their surface. All these axo-axonic terminals contained pleomorphic vesicles and formed symmetrical synaptic junctions with the IS. The possible origin and chemical nature of these synaptic boutons are discussed.