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Biomedical subjects

L K Kaczmarek

Publications and source records attributed to L K Kaczmarek.

At least 127 records · Page 7Linked to original sources
PubMed1979

Flux of labeled compounds in biochemical oscillations.

If a labeled compound (e.g., a radioisotopically or chemically labeled metabolite) is introduced into any biochemical reaction system, the label will be removed by catabolic reactions and replaced by unlabeled compound through anagolic reactions. It is shown that the removal of labeled compounds is particularly efficient if the rates of the catabolic steps are able to oscillate. This is demonstrated by comparing reaction schemes that maintain the same mean fluxes and concentrations of metabolites and the same overall chemical affinity but which differe in that the rate of catabolism is either constant or oscillates as a function of time. Simple analyses are presented for both small and large oscillations of undefined wave form and for sinusoidal oscillations. The enhanced removal of labeled compounds from oscillating reaction systems is also documented by numerical computation on a nonlinear model system. It is suggested that this ability to remove labeled compounds may have provided a selective advantage for the evolution of some biological oscillations.

Kinetics↗
PubMed1978

Neurotransmitter modulation, phosphodiesterase inhibitor effects, and cyclic AMP correlates of afterdischarge in peptidergic neurites.

The neuroendocrine bag cells in the abdominal ganglion of Aplysia generate a long-lasting synchronous afterdischarge upon brief stimulation of an afferent pathway. After this afterdischarge the cells become refractory to further synaptic stimulation. We find that synchrony, afterdischarge, and prolonged refractoriness are properties that can be expressed in the isolated asomatic neurites of the bag cells. We have distinguished two independent types of refractoriness. The first (type I) is seen as a failure of action potentials generated in the tips of bag cell neurites to invade cell somata. The second form of refractoriness (type II) controls the duration of afterdischarge such that stimuli after the first afterdischarge produce only very short afterdischarges or fail to elicit an afterdischarge. Type II refractoriness is sensitive to serotonin and certain of its analogues, and to dopamine and the methylxanthine phosphodiesterase inhibitors. Extracellularly applied serotonin suppresses an ongoing afterdischarge while dopamine and the phosphodiesterase inhibitors, when applied at the end of the first afterdischarge, generate a subsequent afterdischarge of long duration without further electrical stimulation. None of these compounds influenced the degree of type I refractoriness. We have shown that both serotonin and dopamine stimulate the formation of cyclic AMP in the bag cell clusters and in the pleurovisceral connectives and that the occurrence of an afterdischarge is associated with a specific increase in total cyclic AMP in bag cell bodies. Moreover, afterdischarges can be generated in unstimulated preparations by extracellular application of the cyclic AMP analogues, 8-benzylthio-cyclic AMP or 8-methylthio-cyclic AMP. Our data suggest that serotonin and/or dopamine may control bag cell activity and that activation of adenylate cyclase is linked to bag cell afterdischarge.

Action Potentials↗
PubMed1975

Modification of the direct cortical response by taurine.

The effects of taurine on the direct cortical response have been studied in immobilized cats (with local analgesia). The primary negative component of the response was inverted in polarity by the topical application of 25 mM taurine while the later slow negative component was considerably augmented. These effects are identical to those observed with 25 mM GABA. Pentobarbital anesthesia produced little qualitative change in the effects of taurine. With stronger stimuli in the presence of taurine, rhythmic waves followed each stimulus both at the cortical surface and at a depth of 1000 mum. An increase in the EEG amplitude following topical taurine was generally localized to the cortical surface but in certain experiments, could be recorded at cortical depths up to 1000 mum.

Animals↗
PubMed1975

Extracellular release of cerebral macromolecules during potassium- and low-calcium-induced seizures.

Cerebral cortex of cat was incubated with 14C-lysine and 3H-glucosamine. Subsequent superfusion of the surface of the cortex resulted in the release into the superfusate of a variety of 14C- and 3H-labeled compounds including proteins, glycoproteins, and gangliosides. The release of 14C- and 3H-labeled macromolecules could be considerably enhanced by topical addition of 40 mM K+, WHICH INDUCED Epileptiform EEG activity. Peaks in efflux could also be correlated with the onset of seizures induced by superfusion with low (0.75 mM) Ca2+ media. Control experiments in which the cortex was prelabeled with 14C-carboxyl-inulin and 3H2O indicate that the release of macromolecules was not a direct consequence of the altered blood flow that may occur during convulsions.

Animals↗
PubMed1971

Subcellular distribution of taurine and cysteinesulphinate decarboxylase in developing rat brain.

The concentration of taurine and the activities of cysteinesulphinate decarboxylase and glutamate decarboxylase have been measured in rat brain. During development, taurine exhibited a decrease in concentration unrelated to the activity of cysteinesulphinate decarboxylase which increased during the same period. The distribution of taurine in subcellular fractions of adult and 7-day-old rat brain was typical of most amino acids, whereas half of the cysteinesulphinate decarboxylase activity was found in the nerve-ending cytoplasm. In anatomical distribution, taurine displayed great regional heterogeneity but both cysteinesulphinate decarboxylase and glutamate decarboxylase were more evenly distributed. Hypertaurinaemia was shown to have no effect on the entry of glycine into the brain or on its utilization in protein synthesis.

Amino Acids↗