PubMed Health⌕ Search

Biomedical subjects

R R Drucker-Colín

Publications and source records attributed to R R Drucker-Colín.

18 recordsLinked to original sources
PubMed1979

Neurophysiological and neurochemical studies on the action of the anticonvulsant gamma-hydroxy, gamma-ethyl, gamma-phenyl-butyramide.

The effect of gamma-hydroxy, gamma-ethyl, gamma-phenyl-butyramide (HEPB) on afterdischarges produced by hippocampal stimulation in cats was studied. HEPB notably diminished the duration of afterdischarges and in some cats blocked their propagation into the substantia nigra and the amygdala. HEPB treatment also antagonized the enhancement of afterdischarge duration produced by subconvulsive doses of bicuculline, whereas treatment with diphenylhydantoin strongly potentiated this effect of bicuculline. The intracisternal injection of HEPB or gamma-aminobutyric acid (GABA) in mice resulted in a potentiation of strychnine-induced convulsions. On the other hand, neurochemical experiments in mouse brain cortex slices and in synaptosomes demonstrated that HEPB did not affect the high affinity uptake of [3H] GABA, its spontaneous or Ca2+ dependent release stimulated by depolarizing K+ concentrations, and its Na+ independent binding to synaptic plasma membranes.

Amygdala↗
PubMed1977

The effects of various protein synthesis inhibitors on the sleep-wake cycle of rats.

The present investigation sought to determine the effects of Anisomycin (A), Chloramphenicol (ChA), Vincristine (V), and Penicilline G on the sleep-wake cycle of rats. It was found that both high and low doses of anisomycin decreased rapid eye movement (REM) sleep, while only high doses of ChA and V produced such a decrease. Slow wave sleep (SWS) was unaffected by these drugs. Penicilline G, on the other hand, had no effect on the sleep-wake cycle. It was further shown that the reduction of REM sleep was the result of a decrease in the number of REM periods rather than in the duration of each individual period. These results suggest that protein synthesis may participate in the mechanisms that trigger REM sleep.

Animals↗
PubMed1976

Convulsions or flaccid paralysis induced by ruthenium red depending on route of administration.

Ruthenium red was administered to mice and cats intracranially or intraperitoneally. In mice, intracisternal administration produced status epilepticus and tonic convulsions. In contrast, intraperitoneal administration induced total flaccid paralysis lasting several hours. These effects of Ruthenium red were partially blocked by the simultaneous administration of CaCl2. EDTA, at doses much greater than those of Ruthenium red, produced effects similar to those of the dye, which were also blocked by CaCl2 administration. In cats, intraventricular or intrahippocampal administration of Ruthenium red through a permanently implanted cannula produced after a few minutes subclinical paroxysmal activity in all brain regions recorded. After several hours the animals developed typical grand mal seizures. Intraperitoneal injection of Ruthenium red to cats did not affect the EEG but markedly depressed muscular activity. Administration of carbachol to the latter animals produced myoclonic responses. These results are discussed in relation to the inhibitory effect of Ruthenium red on Ca2+ transport and binding to membranes, and to the role of this cation on neurotransmitter release.

Animals↗
PubMed1976

Neurohumoral correlates of sleep: further biochemical and physiological characterization of sleep perfusates.

Twenty cats were prepared surgically with electrodes for recording the EEG, Eye Movements and EMG and a push-pull cannula system in the midbrain reticular formation (MRF) allowing the extraction of perfusates during wakefulness or REM sleep. Proteins in the perfusates were analyzed by Isoelectric Focusing (IEF) polyacrylamide gels and Sodium Dodesyl Sulphate (SDS) slab gels. In addition analysis of glycoproteins was done by gas chromatography. In some cats the contribution of cerebrospinal fluid (CSF) proteins to perfusate proteins from brain tissue was studied by intraventricular injections of labelled leucine. The effect of sleep alterations on the protein cycle during sleep and wakefulness was also studied. The results of these experiments showed that most of the proteins in the perfusates are acidic, and that REM sleep perfusates contain 2 proteins M.W. 73.000 and 45.000 not present in awake perfusates, CSF or serum. It was also shown that CSF proteins do not appear to contribute to the proteins in perfusates, and that altering the sleep wake cycle, induces changes in the rhythm of protein release in perfusates. It is suggested that some relatively large polypeptides may participate in the regulation of REM sleep.

Animals↗
PubMed1975

Changes in protein levels in perfusates of freely moving cats: relation to behavioral state.

Perfusates from the brains of freely moving cats, obtained by means of a push-pull cannula, contain high concentrations of proteins. The levels vary in a cyclic fashion and are higher during rapid eye movement sleep than during the waking state. The proteins represent a distinctive class of tissue protein and their changing levels appear to reflect an alteration in the protein content of the extracellular space of brain related to behavioral state.

Animals↗
PubMed1975

Growth hormone effects on sleep and wakefulness in the rat.

The sleep-wakefulness pattern and brain protein levels were determined in rats for 3 h following these conditions: administration of an inhibitor of protein synthesis (anisomycin), administration of several doses of rat growth hormone (GH) or thyrotropin, and administration of a combination of anisomycin + GH or thyrotropin. Anisomycin inhibited sleep and increased wakefulness, GH increased REM sleep, and thyrotropin produced no change. The combined administration of GH and anisomycin returned sleep to control levels. Anisomycin produced a time-dependent decrease in brain protein levels, GH produced changes in brain protein levels as compared to controls in the second hour only, and thyrotropin had no effect upon brain protein levels. The results are discussed in terms of the possible relationship between sleep and proteins.

Animals↗
PubMed1971

Anemia in sleep-deprived rats receiving anticoagulants.

Independent groups of rats were deprived of sleep and treated with the anticoagulant drugs phenylindanedione or dicoumarol for 1 to 8 days. These animals developed an extremely severe anemia which was accelerated by p-chlorophenylalanine. The red cell count and amount of hemoglobin decreased to half of normal values. No decrease occurred in animals subjected to any one single treatment. Histological examination indicated hemolysis, hypoplasia of hemopoietic organs, slight hemorrhage, but no evidence of stress. The severity of the anemia was inversely related to the amount of sleep permitted during sleep deprivation. This new syndrome demonstrates marked effects of sleep deprivation on both maturation and destruction of red blood cells. Depletion of serotonin by injection of parachlorophenylalanine blocked the increase in amount of brain waves of the type commonly seen in slow wave sleep but did not eliminate the production of these waves. This result is at variance with the theory that serotonin is the neurochemical responsible for the "priming" of slow wave sleep.

Anemia↗