A method for recording evoked local field potentials in the primate dentate gyrus in vivo.

Recording evoked local field potentials (LFPs) in the hippocampus in vivo has yielded us useful information about the neural mechanisms of learning and memory. Although this technique has been used in studies of the hippocampus of rodents, lagomorphs, and felines, it has not yet been applied to the primate hippocampus. Here, we report a method for recording evoked LFPs in the hippocampus of monkeys. A stimulation electrode and a recording electrode were implanted in the perforant pathway and dentate gyrus, respectively, under the guidance of electrophysiological recording. With a low stimulus intensity just above the threshold, the potential appeared as a slow positive-wave component, which was regarded as field excitatory postsynaptic potential (putative fEPSP); as stimulation intensity increased, the fEPSP amplitude increased, followed by a sharp negative component which was regarded as putative population spike. When the coordinates of the recording or stimulation electrode were moved stepwise, we observed a systematic change in the waveforms of evoked LFPs; this change corresponded to the structural arrangement through which the electrode passed. In a test for short-term synaptic plasticity by paired-pulse stimulation, potentials evoked by the second pulse were influenced by the first one in a manner dependent on interpulse intervals. In a test for long-term synaptic plasticity by high-frequency stimulation, the slopes of the fEPSPs and the area of population spikes were increased for more than 1 h. These results indicate that the method developed in the present study is useful for testing theories of hippocampal functions in primates.

Sleep-stage correlates of hippocampal electroencephalogram in primates.

It has been demonstrated in the rodent hippocampus that rhythmic slow activity (theta) predominantly occurs during rapid eye movement (REM) sleep, while sharp waves and associated ripples occur mainly during non-REM sleep. However, evidence is lacking for correlates of sleep stages with electroencephalogram (EEG) in the hippocampus of monkeys. In the present study, we recorded hippocampal EEG from the dentate gyrus in monkeys overnight under conditions of polysomnographical monitoring. As result, the hippocampal EEG changed in a manner similar to that of the surface EEG: during wakefulness, the hippocampal EEG showed fast, desynchronized waves, which were partly replaced with slower waves of intermediate amplitudes during the shallow stages of non-REM sleep. During the deep stages of non-REM sleep, continuous, slower oscillations (0.5-8 Hz) with high amplitudes were predominant. During REM sleep, the hippocampal EEG again showed fast, desynchronized waves similar to those found during wakefulness. These results indicate that in the monkey, hippocampal rhythmic slow activity rarely occurs during REM sleep, which is in clear contrast to that of rodents. In addition, the increase in the slower oscillations of hippocampal EEG during non-REM sleep, which resembled that of the surface EEG, may at least partly reflect cortical inputs to the dentate gyrus during this behavioral state.

Hyponatremia due to an excess of arginine vasopressin is common in children with febrile disease.

Hypotonic fluids are commonly used for treating hospitalized children. However, an excess of arginine vasopressin (AVP) with impaired free water excretion is thought to contribute to the development of hyponatremia in febrile children. The aim of this two-part study was to define the clinical relationship between hyponatremia and excess AVP. In a retrospective study carried out between 2001 and 2005, we found that approximately 17% of the hospitalized patients had hyponatremia [serum sodium (Na) < 135 mEq/l] upon admission and that the ratio of patients with hyponatremia was significantly higher among febrile patients than among afebrile patients. In a subsequent prospective study, we examined 73 hospitalized patients who presented with acute febrile diseases accompanied by hyponatremia (serum Na <134 mEq/l). Almost all of these patients demonstrated excess AVP, defined as high plasma AVP levels (>1 pg/ml). There were no significant relationships between the levels of AVP and other laboratory variables, including serum sodium, serum osmolality, atrial natriuretic peptide, and brain natriuretic peptide. About 30% (22/73) of the patients fulfilled the criteria of the syndrome of inappropriate secretion of antidiuretic hormone. These findings suggest that fever and other nonosmotic stimuli lead directly to excess AVP and hyponatremia. We therefore recommend that isotonic fluids should be used for patients with prolonged fever and hyponatremia.