The decrease in serum zinc is linked to the hypothalamic-pituitary-adrenal (HPA) axis activation that increases the serum glucocorticoid level, indicating the importance of zinc homeostasis in physiological function. Zinc homeostasis in the brain is maintained through the blood-brain and blood-cerebrospinal fluid barriers. At young age, however, the increase in zinc concentration in the brain extracellular fluid along with brain development is suppressed under chronic zinc deficiency, followed by suppression of the increase in zinc in the synaptic vesicles that serves as the Zn(2+) signal. Zn(2+) is released from glutamatergic (zincergic) neuron terminals and serves as the Zn(2+) signal in the intracellular (cytosol) compartment through calcium-permeable channels in addition to the extracellular compartment. Synaptic Zn(2+) signals may participate in synaptic plasticity such as long-term potentiation (LTP) and cognitive function. Both the lack and excess of synaptic Zn(2+) signals may affect them. Because there is limited evidence for the significance of Zn(2+) signaling, the exact relationship between synaptic Zn(2+) function and cognitive activity remains to be solved. Synaptic Zn(2+) homeostasis seems to be controlled by the two major pools of Zn(2+), i.e., the synaptic vesicle and the extracellular compartment, in the brain. Synaptic Zn(2+) homeostasis is affected by the enhanced glutamatergic (zincergic) neuron activity. This paper summarizes the significance of synaptic Zn(2+) homeostasis in zincergic neuron activity.

No abstract

We examined an idea that short-term cognition is transiently affected by a state of confusion in Zn2+ transport system due to a local increase in amyloid-β (Aβ) concentration. A single injection of Aβ (25 pmol) into the dentate gyrus affected dentate gyrus long-term potentiation (LTP) 1 h after the injection, but not 4 h after the injection. Simultaneously, 1-h memory of object recognition was affected when the training was performed 1 h after the injection, but not 4 h after the injection. Aβ-mediated impairments of LTP and memory were rescued in the presence of zinc chelators, suggesting that Zn2+ is involved in Aβ action. When Aβ was injected into the dentate gyrus, intracellular Zn2+ levels were increased only in the injected area in the dentate gyrus, suggesting that Aβ induces the influx of Zn2+ into cells in the injected area. When Aβ was added to hippocampal slices, Aβ did not increase intracellular Zn2+ levels in the dentate granule cell layer in ACSF without Zn2+, but in ACSF containing Zn2+. The increase in intracellular Zn2+ levels was inhibited in the presence of CaEDTA, an extracellular zinc chelator, but not in the presence of CNQX, an AMPA receptor antagonist. The present study indicates that Aβ-mediated Zn2+ influx into dentate granule cells, which may occur without AMPA receptor activation, transiently induces a short-term cognitive deficit. Extracellular Zn2+ may play a key role for transiently Aβ-induced cognition deficits.

The purpose of this study is to analyze the performance of a lugged wheel for a lunar micro rover on sloped terrain by a 2D discrete element method (DEM), which was initially developed for horizontal terrain. To confirm the applicability of DEM for sloped terrain locomotion, the relationships of slope angle with slip, wheel sinkage and wheel torque obtained by DEM, were compared with experimental results measured using a slope test bed consisting of a soil bin filled with lunar regolith simulant. Among the lug parameters investigated, a lugged wheel with rim diameter of 250 mm, width of 100 mm, lug height of 10 mm, lug thickness of 5 mm, and total lug number of 18 was found, on average, to perform excellently in terms of metrics, such as slope angle for 20% slip, power number for self-propelled point, power number for 15-degree-slope and power number for 20% slip. The estimation of wheel performance over sloped lunar terrain showed an increase in wheel slip, and the possibility exists that the selected lugged wheel will not be able to move up a slope steeper than 20 degrees.

The role of perforant pathway-dentate granule cell synapses in cognitive behavior was examined focusing on synaptic Zn(2+) signaling in the dentate gyrus. Object recognition memory was transiently impaired when extracellular Zn(2+) levels were decreased by injection of clioquinol and N,N,N',N'-tetrakis-(2-pyridylmethyl) ethylendediamine. To pursue the effect of the loss and/or blockade of Zn(2+) signaling in dentate granule cells, ZnAF-2DA (100 pmol, 0.1 mM/1 µl), an intracellular Zn(2+) chelator, was locally injected into the dentate molecular layer of rats. ZnAF-2DA injection, which was estimated to chelate intracellular Zn(2+) signaling only in the dentate gyrus, affected object recognition memory 1 h after training without affecting intracellular Ca(2+) signaling in the dentate molecular layer. In vivo dentate gyrus long-term potentiation (LTP) was affected under the local perfusion of the recording region (the dentate granule cell layer) with 0.1 mM ZnAF-2DA, but not with 1-10 mM CaEDTA, an extracellular Zn(2+) chelator, suggesting that the blockade of intracellular Zn(2+) signaling in dentate granule cells affects dentate gyrus LTP. The present study demonstrates that intracellular Zn(2+) signaling in the dentate gyrus is required for object recognition memory, probably via dentate gyrus LTP expression.