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ABSTRACT: The valvula cerebelli of the mormyrid electric fish is a useful site for the study of cerebellar function. The valvula forms a part of the electrosensory-electromotor system of this fish, a system that offers many possibilities for the study of sensory-motor integration. The valvula also has a number of histological features not present in mammals which facilitate investigation of cerebellar circuitry and its plasticity. This initial study characterizes the basic physiology and pharmacology of cells in the valvula using an in vitro slice preparation. Intrinsic properties and synaptic responses of Purkinje cells and other cell types were examined. We found that Purkinje cells fire a small narrow Na(+) spike and a large broad Ca(2+) spike, generated in the axon initial segment and dendritic-soma region, respectively. Purkinje cells respond to parallel fiber inputs with graded excitatory postsynaptic potentials (EPSPs) and to climbing fiber inputs with all-or-none EPSPs. Efferent cells, Golgi cells, and deep stellate cells all fire a single type of large narrow spike and respond only to parallel fiber inputs. Both parallel fiber and climbing fiber responses in Purkinje cells appear to be entirely mediated by AMPA-type glutamate receptors, whereas parallel fiber responses in efferent cells and stellate cells include AMPA and NMDA components. In addition, a strong synaptic inhibition was uncovered in both Purkinje cells and efferent cells in response to the focal stimulation of parallel fibers. Dual cell recordings indicate that deep stellate cells contribute at least partially to this inhibition. We conclude that despite its unique histology, the local functional circuitry of the mormyrid valvula cerebelli is largely similar to that of the mammalian cerebellum. Thus, what is learned concerning the functioning of the mormyrid valvula cerebelli may be expected to be informative about cerebellar function in general.
Neuroscience 03/2011; 182:11-31. · 3.38 Impact Factor
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ABSTRACT: Necroptosis is a newly discovered type of cell death characterized with the combined biochemical and ultrastructural features of necrosis and apoptosis. Nec-1 has been reported to exhibit the selective inhibition for necroptosis, which has now been used as an operational definition of necroptosis. The purpose of this study was to evaluate whether necroptosis is involved in the NMDA-induced excitotoxicity and furthermore whether the elevation of intracellular Ca(2+) is involved in the NMDA-induced necroptosis. Our findings showed that Nec-1 (100 micromol/L) inhibited NMDA-induced decrease of cell viability by 26% (p<0.01), suppressed NMDA-induced decrease of living cells by 23% (p<0.01) and attenuated NMDA-induced leakage of LDH by 28% (p<0.01). In addition, Nec-1 also suppressed NMDA-induced elevation of intracellular Ca(2+) by 36% (p<0.05). These findings indicated for the first time that necroptosis contributes to the NMDA-induced excitotoxicity, and the elevation of intracellular Ca(2+) may be one of the potential mechanisms underlying NMDA-induced necroptosis. Although necroptosis may be involved in NMDA-induced excitotoxicity, it may just constitute a small contribution.
Neuroscience Letters 09/2008; 447(2-3):120-3. · 2.11 Impact Factor
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ABSTRACT: Photomicrograph of a Golgi cell from the valvular ridge of the cerebellum of a mormyrid fish (Gnathonemus petersii). The cell was filled with neurobiotin in a transverse slice of the valvular ridges and the neurobiotin was revealed with red fluorescent dye. Nissl counterstaining is shown in green. The cell was photographed in a slice of 200 mum using a confocal laser scanning microscope. The cell body is located in the basal region of the ganglionic layer. Several smooth primary dendrites arise from the molecular side of the soma and give off secondary and tertiary branches irregularly. The dendrites become thinner and smoother as they extend further into the molecular layer. The thick axon arises from the granular layer side of the soma and projects into the granular layer where it branches extensively. En passant synaptic boutons are visible on the axonal branches. The large ball-like ending of the main axon is probably a cut branch of the axon at the edge of the slice. J. Comp. Neurol. 509:449-473, 2008. (c) 2008 Wiley-Liss, Inc.
The Journal of Comparative Neurology 09/2008; 509(6):spc1. · 3.81 Impact Factor
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ABSTRACT: Necroptosis is a newly discovered type of cell death characterized with the combined biochemical and ultrastructural features of necrosis and apoptosis. Nec-1 has been reported to exhibit the selective inhibition for necroptosis, which has now been used as an operational definition of necroptosis. The purpose of this study was to evaluate whether necroptosis is involved in the NMDA-induced excitotoxicity and furthermore whether the elevation of intracellular Ca2+ is involved in the NMDA-induced necroptosis. Our findings showed that Nec-1 (100 μmol/L) inhibited NMDA-induced decrease of cell viability by 26% (p < 0.01), suppressed NMDA-induced decrease of living cells by 23% (p < 0.01) and attenuated NMDA-induced leakage of LDH by 28% (p < 0.01). In addition, Nec-1 also suppressed NMDA-induced elevation of intracellular Ca2+ by 36% (p < 0.05). These findings indicated for the first time that necroptosis contributes to the NMDA-induced excitotoxicity, and the elevation of intracellular Ca2+ may be one of the potential mechanisms underlying NMDA-induced necroptosis. Although necroptosis may be involved in NMDA-induced excitotoxicity, it may just constitute a small contribution.
Neuroscience Letters.
