Head mounted telemetry system for seizures monitoring and sleep scoring on non-human primate.

Radio telemetry systems are a useful way to continuously monitor broad electrical neuronal activity in behaving animals. It can also be used to study sleep disturbances or monitor seizure activity. Many different telemeter styles are available, but the more versatile and cost-efficient ones are the head mounted systems. They permit long-term recordings and allow more flexibility in the recordings. However, there are currently no such system available for non-human primate (NHP). In fact, the choices for NHP telemetry solutions are very limited. Here, we present a chronically implantable 3D printed chamber specifically designed to accommodate a rodent head-mounted system (RodentPACK) onto a NHP's head. We recorded EEG signal for more than a year, confirmed quality of the signal, and the ability to use the data to monitor sleep activity. We also used two of our epileptic animals to validate the embedded alarm system for real time seizure monitoring. While initially not designed for NHP, but with a minimum number of adaptions, this telemeter is in fact perfectly suitable for NHP experiments. Since early medical intervention during seizures is critical to avoid status epilepticus and to save the animal's life, real time seizures monitoring is becoming a safety requirement in many NHP studies. This method refines the current seizure monitoring methods for NHP and creates a flexible telemetry solution.

Effect on human platelets of catecholamines at levels achieved in the circulation.

Epinephrine at concentrations varying between 3.3 and 12.5 nM had no effect on blood platelets when added alone, but augmented the in vitro platelet response to collagen and thrombin. Both aggregation and secretion responses were enhanced. Norepinephrine produced similar effects but was 50-60% less active than epinephrine. The minimum concentration of epinephrine or norepinephrine to achieve potentiation of platelet responses was even lower in the presence of 5-hydroxy- tryptamine. In contrast to the effects observed with higher concentrations of catecholamines, the synergistic interaction of these low concentrations of catecholamines with other agonists was not transient. The augmented response to catecholamines was mediated by platelet alpha 2-adrenoceptors. The response was inhibited by aspirin indicating that metabolism of arachidonic acid contributes to the synergy between low concentrations of catecholamines and other agonists. These studies show that the levels of the hormones epinephrine and norepinephrine obtained in circulating blood in humans, can be sufficient to enhance platelet responses. The action of catecholamines on platelets may be important in hemostasis and could provide an explanation for the association between certain risk factors and cardiovascular disease.

Collagen increases cytoplasmic free calcium in human platelets.

The role of changes in cytoplasmic free calcium in response to collagen was studied in human platelets loaded with the fluorescent calcium indicator, quin2. In the presence of 1mM external calcium, collagen caused a biphasic increase in cytoplasmic free calcium. In the absence of external calcium, there was a much smaller increase in cytoplasmic free calcium. These findings suggest that collagen increases cytoplasmic free calcium, partly by discharge of internal calcium, but mainly by stimulating calcium influx. Inhibition of cyclooxygenase by aspirin markedly reduced the second phase of the calcium response. Removal of ADP with apyrase resulted in complete inhibition of the second phase of the calcium response. The combination of apyrase and aspirin completely inhibited aggregation and the shape change caused by collagen. The calcium-entry blocking agent, verapamil, also inhibited the second phase of the calcium response to collagen. The increase in cytoplasmic free calcium is fast enough to be involved in the platelet response to collagen and these findings suggest that ADP and metabolites of arachidonic acid mediate the second phase of the calcium response to collagen.