A comparative analysis of axospinous synapses was performed in the middle (MML) and inner (IML) molecular layer of the hippocampal dentate gyrus of rats kindled via medial perforant path stimulation and sacrificed 4 weeks after reaching a criterion of 5 generalized seizures. The MML was a directly stimulated structure, while the IML was not. Both are immediately adjacent synaptic fields likely to be equally susceptible to any generalized effects of convulsions and hypoxia. In these two subdivisions of the molecular layer, the so-called perforated and non-perforated synapses, distinguished respectively by a discontinuous or continuous postsynaptic density, were differentially quantified. In the MML, the ratio of perforated to non-perforated synapses was found to be markedly increased in kindled rats relative to controls. In the IML, however, no change in this ratio was detected following kindling. Thus, the shift in the relative preponderance of perforated synapses over non-perforated ones is not a consequence of generalized phenomena accompanying the kindling process.
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http://dx.doi.org/10.1016/0006-8993(90)90291-i | DOI Listing |
Evidence shows that ultra-high dose-rate FLASH-radiotherapy (FLASH-RT) protects against normal tissue complications and functional decrements in the irradiated brain. Past work has shown that radiation-induced cognitive impairment, neuroinflammation and reduced structural complexity of granule cell neurons were not observed to the same extent after FLASH-RT (> MGy/s) compared to conventional dose-rate (CONV, 0.1 Gy/s) delivery.
View Article and Find Full Text PDFPhilos Trans R Soc Lond B Biol Sci
July 2024
UCL Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
Which proportion of the long-term potentiation (LTP) expressed in the bulk of excitatory synapses is postsynaptic and which presynaptic remains debatable. To understand better the possible impact of either LTP form, we explored a realistic model of a CA1 pyramidal cell equipped with known membrane mechanisms and multiple, stochastic excitatory axo-spinous synapses. Our simulations were designed to establish an input-output transfer function, the dependence between the frequency of presynaptic action potentials triggering probabilistic synaptic discharges and the average frequency of postsynaptic spiking.
View Article and Find Full Text PDFHeliyon
March 2024
Department of Pathology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Introduction: The typical functionality of astrocytes was previously shown to be disrupted by Parkinson's disease (PD), which actively regulates synaptic neurotransmission. However, the morphological changes in astrocytes wrapping glutamatergic synapses in the striatum after dopamine (DA) neuronal degeneration is unclear.
Methods: We utilized a range of methodologies, encompassing the 6-hydroxydopamine (6OHDA)-induced PD model, as well as techniques such as immunohistochemistry, Western blotting, immunofluorescence and immunoelectron microscopy (IEM) to delve into the consequences of DA neuronal degeneration on the morphological attributes of perisynaptic astrocytes.
Eur J Neurosci
April 2024
Emory National Primate Research Center, Emory University, Atlanta, Georgia, USA.
DYT1 dystonia is associated with decreased striatal dopamine release. In this study, we examined the possibility that ultrastructural changes of nigrostriatal dopamine terminals could contribute to this neurochemical imbalance using a serial block face/scanning electron microscope (SBF/SEM) and three-dimensional reconstruction to analyse striatal tyrosine hydroxylase-immunoreactive (TH-IR) terminals and their synapses in a DYT1(ΔE) knockin (DYT1-KI) mouse model of DYT1 dystonia. Furthermore, to study possible changes in vesicle packaging capacity of dopamine, we used transmission electron microscopy to assess the synaptic vesicle size in striatal dopamine terminals.
View Article and Find Full Text PDFMov Disord
June 2022
Department of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Background: The network pathophysiology underlying the motor symptoms of Parkinson's disease (PD) is poorly understood. In models of late-stage PD, there is significant cell-specific remodeling of corticostriatal, axospinous glutamatergic synapses on principal spiny projection neurons (SPNs). Neurons in the centrolateral nucleus (CLN) of the thalamus that relay cerebellar activity to the striatum also make axospinous synapses on SPNs, but the extent to which they are affected in PD has not been definitively characterized.
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