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Antibodies to Glutathione: Production, Characterization, and Immunocytochemical Application to the Central Nervous System
Published in Christopher A. Shaw, Glutathione in the Nervous System, 2018
Ole P. Hjelle, E. Rinvik, D. Huster, W. Reichelt, Ole P. Ottersen
Gold particles signaling glutathione immunoreactivity occured in glial well as in neuronal elements (Fig. 4). The highest labeling intensities were found in glial processes, particularly in perivascular glia, and in subpopulations of myelinated axons (Fig. 4 C). All neuronal populations exhibited significant immunolabeling. The labeling intensity of Purkinje-cell somata was relatively high (Fig. 4 D) and comparable to that of the adjacent glial cell bodies (Golgi epithelial cells). Mossy fiber terminals [putatively glutamatergic; (Ji et al. 1991)] also displayed relatively strong glutathione immunoreactivity (Fig. 4 A), whereas basket-cell axons (GABAergic) were weakly labeled.
Histamine as Neurotransmitter
Published in Divya Vohora, The Third Histamine Receptor, 2008
Oliver Selbach, Helmut L. Haas
The histamine effects on PKA signaling, ion channel function, and neuronal excitability have been analyzed in synaptic isolation (low Ca2+, high Mg2+) [175]. Histamine has bidirectional effects on pyramidal cell firing in the CA1 region, an initial and short-lasting depression (H1R) followed by a long-lasting (>2 h) excitation (H2R). This excitation was less effective than a coincident activation of both H1R and H2R [164,175,189]. In addition, histamine causes a long-lasting enhancement of synaptically evoked population spikes in the CA1 and CA3 regions through H2R activation [304] (Figure 3.7). A postsynaptic effect of H2R in CA3 enhances the response to glutamate released at the mossy fiber synapse [305]. CA3 pyramidal cells synchronize themselves and discharge in bursts (Figure 3.10), which can be recorded as sharp waves in the EEG. This is an important effect in light of the decisive role of CA3 synchronization in synaptic plasticity and memory trace formation [306].
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
There are two groups of mossy fibres in the brain. One is the mossy fibres in the HIPPOCAMPUS, which are axons of GRANULE CELLS in the DENTATE GYRUS. They course laterally and terminate in the stratum lucidum of the CA3 region (see CA1- CA3) of the hippocampus. The second group of mossy fibres is in the CEREBELLUM. These mossy fibres represent one class of AFFERENT to the CEREBELLAR CORTEX. Their terminal endings are called rosettes. Rosettes make multiple synaptic contacts with various neuronal elements in the granular layer, in a complex nodular arrangement called a GLOMERULUS.
Lactation in large litters influences anxiety, memory, and spreading depression in adult male rats that were chronically subjected to a non-convulsive pilocarpine dose
Published in Nutritional Neuroscience, 2022
Regina de Deus Lira Benevides, Suênia Marcele Vitor de-Lima, Camila Lima Chagas, Clara Farah de Lima, Ricardo Abadie-Guedes, Rubem Carlos Araujo Guedes
Based on previous literature, we hypothesize that neuronal cell loss via mitogen-activated protein kinases (MAPK) regulation [41] could help in explaining our findings in pilocarpine-treated rats. The MAPKs encompass signaling of important cell events and signal transduction [40]. This pathway has been associated with regulation of synaptic excitability, and cognition [41,42]. These last authors found increased apoptosis in epileptic rats treated with pilocarpine, which presented with deficient performance in the Morris water maze. Thus, we speculated that the pilocarpine-related activation of MAPK pathway could be involved in the neuronal cell loss that led to memory impairment in the present work. In contrast, the involvement of pilocarpine-induced mossy fiber sprouting on the cognitive disturbances is yet to be elucidated because sprouting does not appear to necessarily participate in the epileptogenesis [43,44].
Phoria Adaptation: The Ghost in the Machine
Published in Journal of Binocular Vision and Ocular Motility, 2020
When prisms are placed before one eye of an orthotropic patient, the visual image discordance is interpreted as an error signal. Adaptation and learning to correct motor error signals is modulated at the level of the vestibulocerebellum.10,69 It, therefore, seems likely that phoria adaptation is similarly mediated by both climbing and mossy fibers within the cerebellum, which implement modifiable, adaptive, and “plastic” responses10 (Figure 3).70 The cerebellum receives continuous information via the mossy fiber system. The climbing fiber system originates from the inferior olivary nucleus and provides a powerful timing and error signal to Purkinje cells. The inferior olivary nucleus acts as a comparator of motor commands from the cerebral cortex, brainstem nuclei and receives feedback from receptors via the spinal cord, visual system, or vestibular organs. The inferior olive senses the error and recalibrates the tonic firing of the Purkinje cells. The increased frequency of inferior olivary nucleus discharge and complex spikes in the Purkinje cells triggers long-term depression of the synapse between the parallel fibers and the Purkinje cells, thereby resetting the single spike discharge rate to produce the necessary motor learning and adaptation. The Purkinje cell provides profound inhibition via GABA to the cerebellar nuclei, which provide the output of the cerebellum. It is therefore likely that the neural circuitry subserving phoria adaptation is not localized to a specific area but modulated by cortical, midbrain, and cerebellar circuitry.10,65,66
An update of cyclooxygenase (COX)-inhibitors in epilepsy disorders
Published in Expert Opinion on Investigational Drugs, 2019
In a rat model of lithium–pilocarpine SE, aspirin (acetylsalicylic acid; a nonselective COX-inhibitor with more selectivity toward COX-1) at a dose of 20 mg/kg was administered at 0, 3, or 24 h after the termination of SE and continued until 20 days. The authors found that acetylsalicylic acid reduced the episodes of SRS in these animals. Aspirin, in this animal model, prohibited the neurodegeneration in the hippocampus region [62]. Aspirin also prevented the sprouting of mossy fibers when administered 3 or 24 h after SE [62]. The mossy fiber sprouting is significant in the pathophysiology of epilepsy as it sketches the formation of an aberrant circuit that could promote the generation or spread of spontaneous seizure activity [63]. Additionally, aspirin was found to be useful in PTZ-kindled rats when administered at a dose of 20 mg/kg, IP for a total of 35 days [64]. In the corticohippocampal brain region, aspirin reduced the levels of lipoxin A4 (LXA4), interleukin-1β, and nuclear factor-κB, resulted in reduce damage caused by PTZ compared to the vehicle control group [64]. Diclofenac sodium (5 and 10 mg/kg; a nonselective COX-inhibitor with more selectivity toward COX-1 enzyme) was found to reduce the seizure severity and modify the levels of IL-6 and TNF-α in PTZ-kindled rats. However, the effect in reducing the cytokine levels was not found to be dose-dependent. In addition, diclofenac sodium did not change the levels of IL-1β in the plasma or brain [65].