Biomedical subjects

S K Kodali

Publications and source records attributed to S K Kodali.

3 recordsLinked to original sources

PubMed1996

Intercellular calcium waves in neurons.

Spontaneous intercellular Ca2+ waves were observed in groups of neurons in two different culture preparations: primary mouse cortical neurons and GT1-1 immortalized neurons. Waves of increased intracellular Ca2+ concentration propagated at rates of 100-200 microns/s over as many as 200 cells and were abolished by the removal of extracellular calcium, by nimodipine, by tetrodotoxin, and by the gap junction inhibitor octanol. A sister clone of the GT1 line, GT1-7 neurons, showed no intercellular Ca2+ waves and were found to have a significantly lower level of connexin26 mRNA than the GT1-1 line. Although we cannot definitively rule out a role for synaptic communication, we propose that intercellular Ca2+ waves in cultured neurons are generated by Ca2+ influx caused primarily by the propagation of depolarization via gap junctions. Intercellular Ca2+ signaling via gap junctions may represent an important mechanism for nonsynaptic neuronal signaling.

Animals↗

PubMed1995

Stimulation of A1 adenosine receptors mimics the electroencephalographic effects of sleep deprivation.

N6-Cyclopentyladenosine (CPA), an A1 adenosine receptor agonist, increased EEG slow-wave activity in nonREM sleep when administered either systemically (0.1-3 mg/kg) or intracerebroventricularly (3.5-10 micrograms) in the rat. The power spectrum of EEG changes (as calculated by Fourier analysis) matched that produced by total sleep deprivation in the rat. The effects of CPA on the nonREM-sleep EEG were dose-dependent. These findings suggest that adenosine is an endogenous mediator of sleep-deprivation induced increases in EEG slow-wave activity, and therefore that increased adenosine release is a concomitant of accumulation of sleep need and may be involved in homeostatic feedback control of sleep expression.

Adenosine↗

PubMed1994

Scoring transitions to REM sleep in rats based on the EEG phenomena of pre-REM sleep: an improved analysis of sleep structure.

Algorithms for scoring sleep/waking states and transitions to REM sleep (NRTs) in rats are presented and validated. Both algorithms are based on electroencephalographic (EEG) power in delta (0.5-4.0 Hz), theta (6-9 Hz) and sigma (10-14 Hz) frequency bands, and electromyogram (EMG) intensity. Waking is scored when EMG intensity is high or (sigma power).(theta power) is low. Nonrapid eye movement (NREM) sleep is scored in nonwaking epochs having high (delta power)/(theta power). Rapid eye movement (REM) sleep is scored in nonwaking epochs having low (delta power)/(theta power). NRTs are identified by the EEG phenomena of the pre-REM sleep phase of NREM sleep. Algorithms are validated by comparison with records scored independently by two investigators based on visual examination of EEGs and EMGs. The sleep/waking-state scoring algorithm produces greater than 90% agreement with visual scoring. The NRT-scoring algorithm produces 88-92% agreement with visual scoring. Scoring NRTs based on the phenomena of the pre-REM sleep phase of NREM sleep, instead of relying solely on REM sleep expression for identification of REM sleep onset, reveals a significant population of brief REM sleep episodes that are ignored by most sleep cycle analyses and allows independent quantification of REM sleep timing and maintenance.

Algorithms↗