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Biomedical subjects

A Ebel

Publications and source records attributed to A Ebel.

At least 37 records · Page 2Linked to original sources
PubMed1986

Expression of cholinergic markers in the developing chick embryo spinal cord.

The expression of cholinergic neurotransmission in the developing spinal cord was followed with pre- and postsynaptic cholinergic markers and histoautoradiographic determinations of cholinergic receptors and ultrastructural studies. Two distinct steps in the development of cholinergic markers were evident. The first step of cholinergic expression occurs early in development and its characterized by a sudden and large increase in choline acetyltransferase activity, whereas the high affinity choline uptake mechanism remains undetectable and few muscarinic receptors are detectable. This phenomenon possibly reflects the expression of high choline acetyltransferase gene activity in developing neurons which are still not synaptically connected. The second step is also characterized by a sharp rise of choline acetyltransferase activity. This rise parallels an active development of high affinity choline uptake and big increase in both number and density of muscarinic receptors. Also nicotine receptors increase, as revealed by histoautoradiography. Specific morphogenetic events, such as the increase of synaptic junctions with postsynaptic thickenings and numerous presynaptic clear vesicles, occur at the same time. Such interactions may contribute to the full maturity of cholinergic neurotransmission of the spinal cord.

Acetylcholinesterase↗
PubMed1985

Somatostatin levels in the central nervous system of the Snell dwarf mouse; is somatostatin excess the primary molecular defect in the dw/dw dwarfism?

The Snell dwarf mouse (dw/dw) shows significantly decreased somatostatin levels in the hypothalamus whereas more or less increased somatostatin concentrations are observed in any central extrahypothalamic sites studied. These opposite results in hypothalamus and extrahypothalamic areas may be linked to the apparently distinct neurohormonal and neuromodulatory functions of somatostatin in the brain. They also provide arguments for the assumption of a primary somatostatin excess which could be related to the dwarf mutation. In hypothalamus, the severe defect in growth hormone of the dwarf mutant may rapidly lead, by failure of a pituitary retro-control, to a reduction in the presumed initially elevated somatostatin levels. In central extrahypothalamic sites, known to escape to GH retro-action, higher somatostatin levels remain.

Animals↗
PubMed1985

Cholinergic neurotransmission in the central nervous system of the Snell dwarf mouse.

An unequal decrease in cholinergic activity has been evidenced in discrete brain areas in the growth hormone, thyroid-stimulating hormone and prolactin deficient Snell dwarf mouse. The effect of the mutation's pituitary deficit on central cholinergic mechanisms appears to be selective: Normally high cholinergic activity areas such as striatum, olfactory tubercles, and hippocampus show strong alterations in this neurotransmitter system. Structures which appear earlier in ontogenesis are less affected, if at all. The lack of pituitary hormones seems to have effects on choline acetyltransferase activity and/or synthesis as well as on the development of high affinity (H.A.) cholinergic uptake mechanisms, both strongly defective in hippocampus and striatum. Therefore, a lower density of cholinergic terminals can be inferred. Furthermore, our observations are consistent with a close functional coupling of the choline H.A. transport and of subsequent choline acetylation. Acetylcholinesterase activity does not seem to be affected. Moreover, a compensatory effect at the postsynaptic level may have occurred due to developmental or functional plasticity for cholinergic responsiveness. In conclusion, the dwarf mouse seems to be a useful model for a better understanding of the influences of growth hormone and thyroid hormones on the development of central cholinergic mechanisms. It also provides the possibility to attempt a functional restoration of the deficient cholinergic neurotransmission and the behavioral disturbances which may be linked to them, by hormone replacement.

Acetylcholinesterase↗
PubMed1985

Dopamine and serotonin metabolism in striatum and in the septohippocampal pathway of the Snell dwarf mouse.

Dopamine and serotonin neurotransmission has been investigated in striatum and in the septohippocampal pathway of the locomotor activity and memory deficient Snell dwarf mouse. In striatum a sharp decrease in 3-MT levels with a concomitant decrease in DA turnover is indicative of a strong decrement in the functional activity of striatal dopaminergic terminals in the mutant mouse. The observed enhancement in serotoninergic markers (5HT, 5HIAA, 5 HTP), at the opposite, provide evidence for an altered relationship between serotonin and dopamine striatal neurotransmission in the mutant mouse as compared to the normal mouse. Impairment in dopamine and serotonin neurotransmission has also been observed in the septohippocampal pathway where the removal of acidic metabolites of these neurotransmitters from brain appears to be disturbed. The data presented here are discussed with regard to previously noted alterations in cholinergic activity as well as to the behavioral disturbances of the dwarf mutant.

Animals↗
PubMed1980

Changes in hippocampal cholinergic activity following learning in mice.

A short bar-press operant conditioning acquisition session with food reward on continuous reinforcement was shown to induce a decrease (13.5%) of hippocampal choline acetyltransferase activity in mice. Such an effect seems to be specific to this kind of learning since no change was observed in several control groups, including a group of mice submitted to another type of conditioning in the same apparatus. It is suggested that these enzymatic modifications might be responsible for the delayed improvement of performance observed on retention of this task.

Acetylcholinesterase↗
PubMed1980

Study of some enzyme activities in cultured chick embryo brain nerve cells treated by chick embryo brain extracts.

Brain extracts from 8-day-old chick embryos have been shown to influence morphological development of dissociated brain cells from 7-day-old chick embryos in culture. Stimulatory effects on size of the neuronal somas and on growth of long processes were observed by adding the cytosol of the brain extract or the dialysate of the cytosol. These morphological changes parallel modifications of various enzyme activities according to the age of the cultures. Adenyl cyclase, (Na+,K+)- and Mg2+-ATPase, 5'-nucleotidase, choline acetyltransferase, and acetylcholinesterase activities were studied between 5 and 14 days of culture. Adenyl cyclase activity was strongly stimulated at 8 days by both extracts. (Na+,K+)- and Mg2+-ATPase activities were stimulated in 8-day-old cultures only by the dialysate. 5'-Nucleotidase activity was stimulated in 8-day-old cultures by the dialysate and in 11-day-old cultures by both extracts. Choline acetyltransferase activity was stimulated by the cytosol in 8-day-old cultures and by the dialysate in 11-day-old cultures. The total acetylcholinesterase activity was higher in 8-, 11-, and 14-day-old cultures treated with the cytosol. When the cells were treated with the dialysate, the activity was only higher in 14-day-old cultures. We also found that following the addition of brain extracts, the specific activity of the enzymes we studied was enhanced and became close to the values found in vivo during embryogenesis. Thus in parallel to the morphological modifications observed in nerve cell cultures treated by embryo brain extracts, biochemical variations especially involved in synaptogenesis and membrane development could be measured.

Acetylcholinesterase↗
PubMed1979

Cholinergic involvement in ethanol intoxication and withdrawal-induced seizure susceptibility.

The enzymes of the cholinergic system have been investigated in discrete brain areas in alcohol-dependent rats, which were still intoxicated or were undergoing withdrawal. The ethanol intoxication resulted in a slight, but significant increase in choline acetyltransferase (CAT) activity in the caudate nucleus both 1 and 7 h after the last dose of ethanol. We also found a significant decrease in CAT activity in the temporal limbic cortex while rats were highly intoxicated. All other brain regions investigated, e.g., cerebellum, pons-medulla, frontoparietal cortex, hypothalamus and septum showed unchanged CAT activity. Rats were also analysed immediately following the onset of a withdrawal-induced audiogenic convulsive seizure where, in addition to the striatum, depressed CAT activity was observed in the hippocampus. In all the analysed situations acetylcholinesterase activity remained unchanged. These results show that ethanol intoxication leads to a perturbation in the synthetic capacity of acetylcholine in certain defined brain structures and that this may have some correlation to the observed behavioural impairments.

Acetylcholinesterase↗
PubMed1978

Conduction studies of the saphenous nerve in healthy subjects.

An easily performed and reproducible method is described for the antidromic determination of conduction velocity in the saphenous nerve. Eighty nerves were studied in 40 healthy subjects and the mean values obtained were as follows: latency 3.6 +/- 0.4 msec, conduction velocity 41.7 +/- 3.4 m/sec, amplitude 9.0 muV. This new technique should be useful in the electrodiagnostic evaluation of peripheral neuropathy, femoral neuropathy and saphenous nerve entrapment syndrome.

Adult↗
PubMed1977

Regional acetylcholine turnover rates in the brains of three inbred strains of mice: correlation with some interstrain behavioural differences.

The hypothesis that the genetically determined behavioural differences which exist between the inbred mouse strains Balb/c, DBA/2 and C57Bl/6 may be related to differences in acetylcholine metabolism in certain regions of the brain has been tested. In vivo ACh turnover rates have been measured in three regions (hippocampus, caudate nucleus and frontal-parietal cortex) of the brains of each strain by following the rate of formation of labelled ACh, in these regions, after a pulse intravenous injection of a tracer dose of 3H labelled choline. Focused microwave procedures were used for the rapid fixation of brain tissue and Ch and ACh radioactivities were determined following their electrophoretic separation. Steady-state concentrations of Ch and ACh were measured by a sensitive radio-enzymatic method. Significant interstrain differences in ACh turnover rates are reported for each of the brain regions studied with the order of metabolic activity being Balb/c greater than DBA/2 greater than C57 Bl/6 in each case. These results are interpreted as being in agreement with previous reports on correlations between learning ability or locomotor activity and regional activities of choline acetyltransferase in the brains of these inbred strains. The correlations between the in vivo ACh turnover rates and (1) interstrain differences in behavioural measures and (2) regional choline acetyltransferase activities are discussed.

Acetylcholine↗
PubMed1977

Effects of hippocampal electrical stimulation on longterm memory and on cholinergic mechanisms in three inbred strains of mice.

Two sets of experiments have been carried out in an attempt to determine the role of hippocampal cholinergic mechanisms in a long-term memory storage. Three inbred strains of mice were presented with two different learning tasks in order to estimate their long-term retention abilities as well as changes in this ability after a post-trial hippocampal stimulation. In parallel experiments the enzymes involved in acetylcholine metabolism were studied under different experimental conditions. Our results indicate: (a) The capacity for long-term memory of the BALB/c line is much greater than that of either the C57BL/6 or C57BR strain. (b) Hippocampal post-trial electrical stimulation leads to an improvement of this capacity in the BALB/c strain. This phenomenon is less pronounced in C57BL/6 and non-existent in C57BR mice. (c) Choline acetyltransferase activity in the hippocampus is significantly higher in BALB/c than in the other two strains. In BALB/c this enzyme activity is greatly changed by the post-trial stimulation whereas in the C57BL/L strain only a slight variation of enzyme activity is observed. No modification occurs in C57BR. The results suggest that the more active acetylcholine synthesizing enzyme in the hippocampus of BALB/c may be related to a greater acetylcholine availability, thus favoring the establishment of a long-term memory, perhaps by releasing greater amounts of acetylcholine in the hippocampus immmediately after the learning session. The electrical stimulation of the hippocampus acts to magnify or accelerate this phenomenon. It is suggested that the efficiency of the stimulation would be related to the genetically determined higher cholinergic activity of the hippocampus.

Acetylcholine↗