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Studies on Anoxic Depolarization
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
It is well known that not all areas of the central nervous system are equally prone to both SD and AD.10 For example, in the spinal cord AD is seen only under special conditions,15,16 while cerebral and hippocampal cortices are quite prone to both of them,2 as is the striatum (G. G. Somjen, personal communication). In the transverse rat hippocampal slice, both AD11 and SD6 can be provoked earlier and more easily in CA1 than in the dentate gyrus (DG). All personal research reported in this chapter has been conducted, unless otherwise specified, in the cell body layer of rat hippocampal CA1.
The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
Patients who sustain severe diffuse brain damage after cardiac arrest often die within a few days. The brain may appear normal macroscopically, but, if the patient has survived for more than 12 hours, microscopy shows widespread and severe neuronal necrosis with a distinctive pattern of selective vulnerability. Worst affected are the neocortex and hippocampus, with the greatest involvement of the CA1 sector. There is diffuse necrosis of the Purkinje cells of the cerebellum and loss of the sensory nuclei of the brainstem. In postmortem cases, brain damage is generally more severe in young children than adults. A similar pattern of damage may be seen in carbon monoxide intoxication, status epilepticus, and severe hypoglycaemia, although a slightly different pattern and distribution of pathology may be seen in the latter.
Neuropsychology of Cognitive Aging in Rodents
Published in David R. Riddle, Brain Aging, 2007
Joshua S. Rodefer, Mark G. Baxter
Brightwell and colleagues [39] investigated the effectiveness of signal transduction in aged rats with impaired spatial performance. Individual proteins from the CREB family can function as either enhancers (e.g., CREB1) or repressors (e.g., CREB2) and influence the short-term to long-term memory transitions. Aged animals that were impaired in the Morris water maze were found to have lower levels of CREB1 in the hippocampus compared to both younger animals and aged non-impaired animals, suggesting dysregulation of CREB1 levels may lead to some aspects of spatial learning deficits in aged subjects. Aged rats with impaired spatial memory, compared to young rats, demonstrated increased protein kinase C (PKC)-gamma immunoreactivity in the CA1 region of the hippocampus, but not in the dentate gyrus [40]. Furthermore, this increased PKC-gamma activity in CA1 was significantly correlated with spatial memory deficits. These data are consistent with a report that demonstrated a significant relationship between choice accuracy and PKC-gamma immunogenicity in the hippocampal CA1 region, but not amygdala, of aged animals [41].
Administration of cyclic glycine-proline during infancy improves adult spatial memory, astrocyte plasticity, vascularization and GluR-1 expression in rats
Published in Nutritional Neuroscience, 2022
Gagandeep Singh-Mallah, Maryam Ardalan, Dali Kang, Kuljeet Singh, Christopher D. McMahon, Carina Mallard, Jian Guan
Figure 3(A) shows a representative image of GFAP positive astrocytes. The area of the CA1 SR sub-region of the hippocampus examined is delineated. Figure 3(B) shows representative image of a 3D reconstructed astrocyte. Stereological analysis showed that the total length (p < 0.0001, Figure 3(C)) and total numbers (p < 0.0001, Figure 3(D)) of processes of astrocytes were significantly increased in cGP-treated group (n = 6) compared with saline-treated group (n = 6). The volume of convex hull of astrocytes of cGP-treated group (n = 6) was significantly greater (10,195.39 ± 1264.74 µm3) compared with that of saline-treated group (6674.61 ± 812.20 µm3, p < 0.0001, n = 6, Figure 3(E)). Sholl analysis showed a greater number of branching intersections from the cell soma at distances of 10, 20, 30 and 40 µm in cGP-treated group compared to saline-treated group (p < 0.05–0.001, n = 6, Figure 3(F)). The results of Cohen’s d calculation showed that the effects of cGP on the total length, number and convex hull volume of astrocytes processes were large (d = 1.84; d = 1.74; d = 1.67; respectively).
Neurotensin agonist PD 149163 modulates the neuroinflammation induced by bacterial endotoxin lipopolysaccharide in mice model
Published in Immunopharmacology and Immunotoxicology, 2022
Previous studies have reported that the LPS inhibited neurogenesis and accelerated the neuronal loss in the hippocampus, a key area of the brain responsible for cognitive and memory function and acting as a hotspot of neurogenesis [51]. The pyramidal cell loss in the hippocampus causes cognitive dysfunction and ultimately is modified into a neurodegenerative disorder. The hippocampus is vulnerable to inflammatory cytokines and oxidative stress. Some studies recently showed that the pro-inflammatory cytokines and ROS are responsible for neuronal death in the hippocampal area [60,61]. The CA1 and CA3 are two important sub-regions of the hippocampus made up of pyramidal cells; they act as a connecting link or neuronal circuit between the dentate gyrus and other brain areas, coordinating memory and cognitive function [26]. Therefore, in this study, we target the CA1 and CA3 regions to assess LPS-induced hippocampus deformities. We found that the LPS significantly altered the cytoarchitecture of the CA1 and CA3 region, as reported by others also [69]. CA1 and CA3 regions are marked with disorganization and pyramidal cell loss in the hippocampus, showing pale and darkened nuclei and shrinkage and vacuolization. This hippocampal atrophy might be corroborated with the reduced pyramidal cell layer thickness, pyramidal number and size of CA1 and CA3 regions. This evidence showed that the inflammatory cytokines, oxidative stress, and HPA axis activation were responsible for neuronal loss and thinning of pyramidal layers in the hippocampus.
Antidepressant-like effects of paeoniflorin on post-stroke depression in a rat model
Published in Neurological Research, 2019
Ming-zhe Hu, An-rong Wang, Ze-yu Zhao, Xiang-yan Chen, Yan-bin Li, Bin Liu
The mainstream physiopathologic mechanism of PSD is believed to be multi-factorial, composed of psycho-social and biological factors including location of ischemia, inflammation, genetic susceptibility, neurogenesis, neurotrophic factors, and activation of the HPA axis [4,5]. Hippocampus plays a key role in many major neuropsychiatric disorders [6,7] and axons in the CA1 region of the hippocampus are main pathways contacted with the entorhinal cortex [8]. CA1 region is vulnerable to stress or injury especially because volume and function can be affected by the level of brain-derived neurotrophic factor (BDNF). BDNF is critical for the maintenance of neuronal functions and mood control which is closely associated with depression [7,9]. Growing evidence demonstrates the importance of BDNF in the pathogenesis of mood disorders and the mechanism of therapeutic agents [10,11]. Phosphorylated Cyclic-AMP responsive element binding protein(p-CREB) is a nuclear transcription factor related to the expression of BDNF directly and is involved in the regulation of depression [12,13],but little is known about changes of BNF and p-CREB in PSD models or patients.