Cost of auditory sharpness: Model-Based estimate of energy use by auditory brainstem "octopus" neurons.

Octopus cells (OCs) of the mammalian auditory brainstem precisely encode timing of fast transient sounds and tone onsets. Sharp temporal fidelity of OCs relies on low resting membrane resistance, which suggests high energy expenditure on maintaining ion gradients across plasma membrane. We provide a model-based estimate of energy consumption in resting and spiking OCs. Our results predict that a resting OC consumes up to 2.6 × 109 ATP molecules (ATPs) per second which remarkably exceeds energy consumption of other CNS neurons. Glucose usage by all OCs in the rat is nevertheless low due to their low number. Major part of the OCs energy use results from the ion mechanisms providing for the low membrane resistance: hyperpolarization-activated mixed cation conductance and low-voltage activated K+-conductance. Spatially ordered synapses-a feature of the OCs allowing them to compensate for asynchrony of the synaptic input-brings only a 12% energy saving to OCs excitability cost. Only 13% of total OC energy used for an AP generation (1.5 × 107 ATPs) is associated with the AP generation in the axon initial segment, 64%-with synaptic currents processing and 23%-with keeping resting potential.

Imbalance in the blood antioxidant system in growth hormone-deficient children before and after 1 year of recombinant growth hormone therapy.

The aim of our study was to examine the effects of 12-month therapy with recombinant growth hormone (rGH) on the blood antioxidant system in children with growth hormone deficiency (GHD). Total antioxidant capacity (TAC) of plasma was measured by FRAP (ferric reducing antioxidant power or ferric reducing ability of plasma); activities of superoxide dismutase (SOD) and catalase (CAT) in erythrocytes were assessed; non-protein thiols (NT) and ceruloplasmin (CP) levels were also measured. These parameters were determined before and after 12 month of rGH treatment. Eleven treatment-naive prepubertal children with growth hormone deficiency were included in the study. Another 11 prepubertal children comprised a control group. Before rGH treatment, TAC of plasma and NT level in the control group were significantly lower (726 ± 196 vs. 525 ± 166 µmol/L, P = 0.0182 and 0.92 ± 0.18 vs. 0.70 ± 0.22 µmol/ml, P = 0.0319, before and after the therapy, respectively). The only parameter that significantly (19.6 ± 4.7 vs. 14.5 ± 3.4 Units/g Hb, P = 0.0396) exceeded the same in the control group after rGH therapy was SOD activity. However, none of the measured parameters of antioxidant system in GHD children, except for TAC (525 ± 166 vs. 658 ± 115 µmol/L, P = 0.0205), exhibited significant improvement toward the end of the 12-month treatment period, although non-significant changes in CAT activity and CP level were also observed. This work has demonstrated that some parameters of the blood antioxidant system are out of balance and even impaired in GHD children. A 12-month treatment with rGH resulted in a partial improvement of the antioxidant system.