Calcium-permeable AMPA and kainate receptors of GABAergic neurons.

This Commentary presents a brief discussion of the action of glutamate calcium permeable receptors present with neurons on the release of the neurotransmitter gamma-aminobutyric acid (GABA). In particular, Glutamate sensitive Kainic Acid Receptors (KARs) and α-Amino-3-hydroxy-5-Methyl-4-isoxazole Propionic Acid Receptor (AMPARs) are Na+ channels that typically cause neuronal cells to depolarize and release GABA. Some of these receptors are also permeable to Ca2+ and are hence involved in the calcium-dependent release of GABA neurotransmitters. Calcium-permeable kainate and AMPA receptors (CP-KARs and CP-AMPARs) are predominantly located in GABAergic neurons in the mature brain and their primary role is to regulate GABA release. AMPARs which do not contain the GluA2 subunit are mainly localized in the postsynaptic membrane. CP-KAR receptors are located mainly in the presynapse. GABAergic neurons expressing CP-KARs and CP-AMPARs respond to excitation earlier and faster, suppressing hyperexcitation of other neurons by the advanced GABA release due to an early rapid [Ca2+]i increase. CP-AMPARs have demonstrated a more pronounced impact on plasticity compared to NMDARs because of their capacity to elevate intracellular Ca2+ levels independently of voltage. GABAergic neurons that express CP-AMPARs contribute to the disinhibition of glutamatergic neurons by suppressing GABAergic neurons that express CP-KARs. Hence, the presence of glutamate CP-KARs and CP-AMPARs is crucial in governing hyperexcitation and synaptic plasticity in GABAergic neurons.

Comparative effects of different supplemented dietary doses of chlorophyll on blood parameters of experimental male rats.

Chlorophylls are organic pigments that are a part of our daily diet, particularly in light of the increased popularity of more eco-friendly and healthy practices. Since altering oxidative equilibrium seems to be connected to the emergence of numerous illnesses, the antioxidant capacities of both groups of lipophilic compounds have been studied. The objective was to evaluate adding dietary chlorophyll at two concentrations-30 and 60 mg/ml-would improve blood characteristics in rats. Supplemented dietary chlorophyll showed significantly increased WBCs, RBCs, granulocytes, lymphocytes, HGB, HCT MCHC, and Platelets. it nonsignificant effect on RDW, MPV, and Eosinophil. These findings support a significant rise in critical hematological parameters at two separate time intervals, 14 and 28 days following dietary chlorophyll supplementation, at dosages of 30 and 60 mg/ml. After 30 and 60 mg/ml, platelet count, PCT, lymphocytes, and monocytes substantially (p0.001) rose. In light of these findings, critical hematological indicators markedly rise in response to exogenous dietary chlorophyll. To strengthen blood parameters and enhance blood features and prevent anemia, dietary chlorophyll is advised.

Antitumor activity of ethanol extract from Hippophae rhamnoides L. leaves towards human acute myeloid leukemia cells in vitro.

We studied the effects of ethanol extract from Hippophae rhamnoides L. leaves on the growth and differentiation of human acute myeloid leukemia cells (KG-1a, HL60, and U937). The extract of Hippophae rhamnoides L. leaves inhibited cell growth depending on the cell strain and extract dose. In a high concentration (100 µg/ml), the extract also exhibited a cytotoxic effect on HL60 cells. Hippophae rhamnoides L. leaves extract did not affect cell differentiation and did not modify the differentiating effect of calcitriol, active vitamin D metabolite. Inhibition of cell proliferation was paralleled by paradoxical accumulation of phase S cells (synthetic phase) with a reciprocal decrease in the count of G1 cells (presynthetic phase). The extract in a concentration of 100 µg/ml induced the appearance of cells with a subdiploid DNA content (sub-G1 phase cells), which indicated induction of apoptosis. The antiproliferative effect of Hippophae rhamnoides L. extract on acute myeloid leukemia cells was at least partially determined by activation of the S phase checkpoint, which probably led to deceleration of the cell cycle and apoptosis induction.

Effect of perfluorodecalin on viability of Ehrlich ascites tumor cells under conditions of hypoxia.

Perfluorodecalin increased survival rate of Ehrlich ascites tumor cells under pathological conditions of hypoxia in combination with hyperkalemia. High potassium medium increased the content of lysophospholipids in samples, while in the presence of perfluorodecalin, phosphatidylethanolamine level decreased.