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At least 397 records · Page 22Linked to original sources
PubMed1984

Effects of tetraethylammonium-chloride and divalent cations on the afterhyperpolarization following repetitive firing in leech neurons.

In leech Retzius cells, repetitive activity evoked a prolonged Ca2+-dependent after-hyperpolarization (PAH) (30-60 s) accompanied by an increase in input conductance. PAH persisted in Retzius cells, as well as in nociceptive (N) cells, when Sr2+ but not Mg2+ was substituted for Ca2+. In the presence of tetraethylammonium-chloride (TEA) or Ba2+, PAH was replaced by a Ca2+-dependent, Mg2+-blockable depolarization which was present in the order N greater than R. Careful study of the differences in such phenomena in identified cells may improve our understanding of the differential susceptibility of various neurons to hyperexcitability.

Animals↗
PubMed1990

Hypoxic failure of synaptic transmission in the isolated spinal cord, and the effects of divalent cations.

Responses evoked by stimulation of a dorsal root were recorded from ventral and dorsal roots of isolated spinal cords of infant mice. Interstitial potassium, [K+]o, and extracellular DC voltage were recorded from dorsal gray matter in some experiments. When oxygen was withdrawn, synaptically transmitted discharges (dorsal horn response, DHR, and monosynaptic ventral root reflex, VRR) began to be depressed within a minute, and were depressed to less than 30% of control amplitude in 10-15 min. Responses recovered fully if oxygen was readmitted within 45 min, but no recovery was seen after 90 min of hypoxia. The degree of the depression of VRR was as expected from the depression of the electrotonically conducted excitatory postsynaptic potential (VRepsp). Responses failed much more rapidly in spinal cords of 15-16-day-old mice, than of 9-14-day-olds. When the spinal cord was bathed in elevated [Ca2+]o or in reduced [Mg2+]o, synaptic transmission was consistently maintained for a longer period of hypoxia than in bathing fluid of normal cation content. In a sizeable minority of the trials during hypoxia an abrupt increase of [K+]o occurred, accompanied by a sudden negative shift of extracellular potential, closely resembling spreading depression (SD) of forebrain structures. Delayed post-hypoxic spontaneous activity was seen in many spinal cords. The results are compatible with the hypothesis that hypoxic failure of synaptic transmission is due, in part or whole, to blockade of inward Ca2(+)-current in presynaptic terminals. Cells in spinal gray matter can no longer be regarded as 'immune' to SD-like depolarization, but the limited conditions under which SD can occur are not yet clear.

Aging↗
PubMed1993

Modulation by divalent cations of the current generated by vasopressin in facial motoneurons.

Vasopressin generates a voltage-gated, sodium-dependent current in facial motoneurons in brainstem slices. Reducing the extracellular calcium concentration from 2 to 0.01 mM caused a 30 to 120% increase in the amplitude of this current. Lowering extracellular magnesium also enhanced it, but less efficiently. In the physiological solution, the response of facial neurons to vasopressin is thus partially blocked. Increasing extracellular calcium was without effect. Current-voltage curves indicate that the vasopressin current reversed at around 0 mV and suggest that the low-calcium-induced potentiation was due to an attenuation of the region of negative slope conductance.

Animals↗
PubMed1991

NOTPME: a 31P NMR probe for measurement of divalent cations in biological systems.

1,4,7-Triazacyclononane-N,N',N''-tris(methylenephosphonate monoethylester) (NOTPME) has been synthesized, characterized and analyzed for use as a 31P NMR indicator of intracellular Mg2+ and Zn2+ ions. The 31P NMR spectrum of this chelate in the presence of metal ions shows characteristic resonances for the free chelate, Mg(NOTPME)-, Zn(NOTPME)-, and Ca(NOTPME)-. The Kd values indicate that this chelate has a 10-fold higher affinity for Mg2+ than for Ca2+ at physiological pH values. In the presence of Mg2+, NOTPME is readily loaded into red blood cells. A 31P NMR spectrum of red cells taken after several washings shows resonances characteristic of entrapped NOTPME and the Mg(NOTPME)- complex, the relative areas of which report an intracellular free Mg2+ concentration of 0.32 mM. The 31P chemical shifts of the free chelate and its metal complexes are far downfield from the typical phosphorus-containing metabolites observed in biological systems, thus making it possible to monitor intracellular cation concentrations and cell energetics simultaneously.

Cations, Divalent↗
PubMed1992

Alkaline p-nitrophenylphosphate phosphatase activity from Halobacterium halobium. Selective activation by manganese and effect of other divalent cations.

1. Alkaline p-nitrophenylphosphate phosphatase (pNPPase) activity of Halobacterium halobium is selectively stabilized and stimulated by Mn2+ ions. 2. Mn2+ binding to native pNPPase is characterized by a dissociation constant of 0.35 mM at pH 8.5, 37 degrees C, with a Hill coefficient of 0.988. 3. Mn2+ behaves as a mixed type nonessential activator, increasing the Vmax value (beta = 6.09, pH 8.5) and decreasing the Km value for pNPP (alpha = 0.56, pH 8.5). The Ki value for inorganic phosphate (a competitive inhibitor) was also decreased in the presence of Mn2+. 4. Activation of native pNPPase by preincubation with Mn2+ is a slow temperature-dependent process, which can be described by an exponential relationship vs time. However, a weak but immediate activation was also detected. 5. Zn2+, Cu2+ and Ni2+ were found to inhibit both native and Mn(2+)-stimulated pNPPase, whereas Co2+ and Cd2+ inhibited the Mn(2+)-stimulated pNPPase but had no effect on the native enzyme form.

4-Nitrophenylphosphatase↗