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Seung Mook Jo

Publications and source records attributed to Seung Mook Jo.

5 recordsLinked to original sources

Adrenalectomy-induced ZnT3 downregulation in mouse hippocampus is followed by vesicular zinc depletion.

The effects of adrenalectomy (ADX) on the vesicular zinc content of zinc-enriched (ZEN) terminals in mouse hippocampus were investigated at light microscopic levels using zinc transporter-3 immunohistochemistry (ZnT3IHC) and zinc selenium autometallography (ZnSeAMG). ZnT3 resides in the synaptic vesicle membranes of ZEN neurons and is believed to move zinc ions into the vesicles. ZnT3IHC staining closely corresponds to the ZnSeAMG staining, but in the present study we present evidence of a delayed decrease of ZEN zinc, as compared to downregulation of the ZnT3 protein following ADX. Twenty-four hours after adrenalectomy the level of ZnT3IHC was visibly reduced while the ZnSeAMG staining intensity seemed unchanged. After 10 and 30 days, however, downregulation of ZnT3 was paralleled by a distinct reduction in ZnSeAMG staining. The total protein concentration of ZnT3 was reduced by about 53%, and the total zinc concentration in the hippocampus of the same mice was reduced by 43-64%, 30 days after the adrenalectomy. The present results support previous results suggesting that ZnT3 is responsible for transport of zinc ions into a pool of synaptic vesicles in ZEN terminals.

Adrenalectomy↗

Dynamic zinc pools in mouse choroid plexus.

We examined the presence of Zn-transporters (ZnT1, ZnT3, ZnT4, and ZnT6) proteins and zinc ions in rat choroid epithelium with immunohistochemistry and zinc selenide autometallography (ZnSe(AMG)). The four ZnT proteins were all expressed in the choroid epithelial cells. ZnT3 immunostaining was found in vesicle membranes in the apical part of the cells, associated to the microvillus membrane. Correspondingly, the ZnSe(AMG) technique revealed zinc ions in small vesicles, in microvilli, and multivesicular bodies in the epithelial cells. Traceable zinc ions were also found in lysosome-like organelles of fenestrated endothelial cells, but here no corresponding ZnT3 immunostaining was seen. The observations suggests that the choroid plexus is instrumental to regulation of the level of zinc ions in the cerebrospinal fluid.

Animals↗

Immunocytochemical localization of zinc transporter 3 in the ependyma of the mouse spinal cord.

We report, for the first time, the light microscopical and ultrastructural appearance of ZnT3-immunoreactivities in the ependymal cells of the central canal of the mouse spinal cord. Light microscopy revealed the presence of ZnT3-immunoreactive (Ir) ependymal cells in 1 microm thick epon sections stained by the ABC method. The ZnT3-Ir cells were observed at all levels of the spinal cord, but were a little more numerous in lumbosacral segments than in cervicothoracic segments. The ZnT3-Ir cells had large, ovoid nuclei with abundant cytoplasm, and protruded into the lumen of the central canal. Our ultrastructural findings suggest that the ZnT3-Ir ependymal cells possess secretory activity directed towards the central canal. We propose that they may play a role in the trans-ependymal mechanism responsible for zinc homeostasis between cerebrospinal fluid and the central area of the gray matter.

Animals↗

Retrograde tracing of zinc-enriched (ZEN) neuronal somata projecting to the olfactory bulb.

Zinc ions seem to be important to several neurological functions and have been connected to the pathophysiology of epilepsy, neuronal cell death after seizure or stroke, and Alzheimer's disease. Both epilepsy and Alzheimer's disease are clinical conditions believed to involve the olfactory bulb. The mammalian olfactory bulb is densely innervated by zinc-enriched (ZEN) neurons, and the distribution of the ZEN terminals in the mouse olfactory bulb has previously been described. The aim of this study was to describe the origins of ZEN terminals projecting into the main olfactory bulb of the rat. Selective labeling of ZEN terminals was accomplished by intracerebral infusion of sodium selenide, whereby zinc selenium clusters are created in the ZEN terminals. Some of these clusters move by retrograde axonal transport to the somata where they can be silver-enhanced by autometallography (AMG). After infusion of sodium selenide into the main olfactory bulb, retrogradely labeled ZEN somata were found (1) ipsilaterally in all anterior olfactory nuclei, taenia tecta, piriform cortex and lateral entorhinal cortex, and (2) contralaterally in anterior olfactory nuclei except the external division. The ipsilateral anterior olfactory nucleus had the densest population of ZEN somata, and it was found that these somata originated mainly from pyramidal neurons in layers II and III of each area. The olfactory-related centrifugal afferents to the main olfactory bulb are discussed.

Afferent Pathways↗

Inhibitory zinc-enriched terminals in the mouse cerebellum: double-immunohistochemistry for zinc transporter 3 and glutamate decarboxylase.

In the present study, we showed for the first time the presence of inhibitory zinc-enriched neuron terminals in the mouse cerebellar cortex by means of double-immunohistochemistry for zinc transporter 3 (ZnT3) and glutamate decarboxylase (GAD). The co-localization of ZnT3 and GAD in the cerebellar cortex was analyzed by confocal microscopy. Strong, punctuate ZnT3-immunoreactivity (Ir) was predominantly distributed in the granule cell layer, while GAD-Ir was seen throughout the cerebellar cortical layers. All of the ZnT3-immunoreactive structures were also immunopositive to GAD, but not vice versa. Based on size and position, these double-labeled elements were axonal terminals of the Golgi and basket cells, in the granule cell and molecular layers, respectively. Observations by electron microscopy revealed that ZnT3-immunoreactive terminals showed typical characteristics of the inhibitory synapses like the following: (1) presynaptic terminals containing flat vesicles; and (2) symmetrical synaptic contacts with dendritic elements. The present results indicate that a zinc-containing GABAergic system exists in the mouse cerebellar cortex.

Animals↗