PubMed Health⌕ Search

Biomedical subjects

E García Austt

Publications and source records attributed to E García Austt.

At least 19 recordsLinked to original sources
PubMed1977

Analysis of unit pairs in the hippocampus.

Unit pairs were recorded from dorsal hippocampus in curarized rats injected with physostigmine, during spontaneous activity and stimulation of hippocampal afferents. Interactions between neurons and with the theta (theta) rhythm were investigated with statistical procedures which included: autocorrelations, crossocorrelations, peristimulus-time-histograms (PSTHs) and joint-peristimulus-scatter-diagrams (JPSs). Three types of pairs were found: (1) theta pairs, with rhythmical bursting units phaselocked with theta; (2) non-theta pairs, having non-rhythmical cells; and (3) mixed pairs. Theta pairs showed periodical crossrelation between units which fired in phase or out of phase. Non-theta pairs could interact or not. Many interacting non-theta pairs showed a degree of phaselocking with theta. Mixed pairs were rare, but when interacting they always revealed positive periodical crosscorrelations. Stimulus-elicited phase relationships (reset) and rhythmical interactions within the theta pairs suggest a common source for their rhythmicity and reset. In related non-theta pairs the stimulus usually modified their interactions suggesting loose functional connections.

Animals↗
PubMedDate not supplied

Nocturnal growth hormone surges in type 1 diabetes mellitus are both sleep- and glycemia-dependent: assessment under continuous sleep monitoring.

Our work has studied the relationship between nocturnal growth hormone (GH) surges, sleep and glycemia in seven conventionally treated type 1 diabetic patients under continuous sleep monitoring and the results were compared to those found in five age-matched healthy controls. On the experimental day, sleep was monitored from 24.00 to 07.00. Blood glucose levels and GH were assayed in both groups. As a group the diabetics had nocturnal GH responses higher than those in controls. However, the sleep-related GH release is not abnormally high in patients who maintain strict normoglycemia. Early-night hypoglycemia and/or rapidly decreasing blood glucose concentrations enhance sleep-related GH secretion in diabetics, whereas hypoglycemia not associated with slow-wave sleep (SWS) causes a moderate increase in GH. Late-onset nocturnal hypoglycemia is not potent enough to stimulate GH. It is proposed that in diabetics sleep-related GH production is probably not abnormally elevated within a wide range of stable glucose levels, but when these thresholds are crossed or when there is a rapid decrease in blood glucose, then GH secretion is inversely related to the changing blood glucose. Therefore, our study supports the conclusion that sleep-related GH secretion is finely modulated by the actual glycemic fluctuations in diabetic patients.

Adult↗