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Biomedical subjects

A Ebel

Publications and source records attributed to A Ebel.

At least 19 recordsLinked to original sources
PubMed1992

Distribution of cholinergic neurons in the chick spinal cord during embryonic development. Comparison of ChAT immunocytochemistry with AChE histochemistry.

The location of cholinergic neurons was studied during the development of the chick embryo spinal cord. A comparison between choline acetyltransferase (ChAT) immunocytochemistry and acetylcholinesterase (AChE) histochemistry was performed. ChAT-positive neurons could be detected only from embryonic day 9 (E9) onwards by the FITC technique and from E12 onwards by the PAP technique. These neurons were located mainly in the medial and lateral motor columns in the ventral horn of the gray matter and some of them were observed in the intermediate region of the spinal cord. AChE-containing cell bodies were much more numerous than the ChAT immunoreactive ones and were distributed in the ventral horn of the gray matter, the intermediate gray region and mostly off the apical part of the dorsal horn. ChAT should provide a reliable and specific marker for cholinergic neurons.

Acetylcholinesterase↗
PubMed1991

Are chronic alcohol-induced central vasopressin changes determinant in strain dependency of tolerance in mice?

As vasopressin (VP) has been related to tolerance, we were interested in following central VP levels after chronic alcohol exposure of two selected mouse lines (C57Bl and Balb/c). Strongly elevated VP and VP mRNA levels have been noted, in particular in the hypothalamus. The phenomenon is much more marked in Balb/c mice than in C57Bl; in extrahypothalamic areas in the changes in VP noted in septum and amygdala are only apparent in Balb/c mice. Hypothalamic norepinephrine and serotonin, known to partly control VP release, also reacts in a strain dependent manner to alcohol. This study provides neurochemical evidence that long term ethanol intoxication selectively activates central vasopressinergic and aminergic neurons in mice. Such activation appears to be strain dependent; therefore it may be related to the unequal capacities of these strains to adapt to chronic alcohol intoxication. Such phenomena may partly account for differences between individuals in tolerance to chronic alcohol in men.

Animals↗
PubMed1990

Alcohol withdrawal-induced changes in brain biogenic amines in mice: influence of the genotype.

Alterations in striatal and hippocampal dopamine (DA) and serotonin (5HT) activities were investigated in two inbred strains of mice (C57B1 and Balb/c) after 3 withdrawal periods following 5 months chronic ethanol administration. Two groups of animals with different levels of ethanol administration (15% and 30%, v/v) were examined. A striking strain dependency has been noted. Striatal dopaminergic mechanisms of the Balb/c strain are profoundly disturbed in both groups. In contrast no changes were noted for either transmitter activities in C57B1 mice at any withdrawal time studied. Strain dependency has also been noted for hippocampal serotonin neurotransmission, since only Balb/c mice showed a progressive decrease in 5HT levels. These impairments observed in striatum and hippocampus could be involved in motor incoordinations and convulsions often associated with the withdrawal syndrome. The differences in withdrawal effects we noted between the two strains may be linked to the specific chemical neuroanatomy of the strains. Such specificities could be implied in the well known variability of withdrawal induced behavior in man.

Animals↗
PubMed1989

Effects of basic fibroblast growth factor (bFGF) on choline acetyltransferase activity and astroglial reaction in adult rats after partial fimbria transection.

Adult rats received a partial and unilateral transection of the fimbria. They received then intracerebroventricular (i.c.v.) injections of 5 microliters of Tris, half of them containing 2.5 ng of basic fibroblast growth factor (bFGF). They were injected twice a week for 4 weeks. At the end of this period, choline acetyltransferase (ChAT) activity was measured in the hippocampus. ChAT activity, which was decreased by the fimbria transection, was higher (by about 20%) in medial hippocampus of the bFGF group compared with the Tris group. In addition, bFGF enhanced the lesion-induced astroglial reaction by changing the morphology of the astrocytes and increasing the apparent number of these reactive astrocytes.

Animals↗
PubMed1988

Responses of cholinergic markers to a pre- or a postsynaptic pharmacological blockage in the developing chick embryo spinal cord.

The response of cholinergic markers to pre- or postsynaptic blockage was followed during development of the chick embryo spinal cord, to understand better the maturation sequence of the developing cholinergic synapse. It has been shown that the developing neurotransmitter system is able to react to pre- or postsynaptic disturbances by compensatory mechanisms, as early as 7.5 days of incubation. From 12.5 days of incubation the synaptic reactivity to such blockage changes in complexity as well as in nature. At this developmental stage muscarinic receptors show capacity for intrinsic regulation, similar to that of the adult nervous system. These results together with our previous studies clearly demonstrate that 12.5-15.5 days of embryonic life appears to be a crucial period in ontogenesis of the cholinergic neurotransmission in the chick embryo spinal cord.

Animals↗
PubMed1987

Influence of mouse genotype on responses on central neurotransmitters to long-term alcohol exposure in striatum and hippocampus.

A striking strain dependency in response of central neuromediators (dopamine, serotonin, acetylcholine activities and somatostatin) to various periods of alcohol treatment has been noted in striatum and hippocampus in mice. For biogenic amines the C57Bl strain loses tolerance to prolonged alcohol injury earlier than the Balb/c strain. At the opposite the Balb/c strain exhibits a remarkable long lasting tolerance for cholinergic activity. The unequal capacity to adapt, also appears to depend on the nervous structure and the neurotransmitter considered. Such discrepancies may underly differences in behavioral changes observed in alcoholics.

Animals↗
PubMed1986

Effects of hormone therapy on the central cholinergic neurotransmission of the Snell dwarf mouse.

Effects of growth and thyroid hormone therapy on central cholinergic neurotransmission has been followed in the cholinergic-deficient Snell dwarf mouse. Growth hormone and thyroxine can reverse the neurotransmission impairment even in adulthood. Furthermore, it appears that in the dw/dw mouse, hormone deficiency becomes determinant only after the critical period of neurogenesis, in a late postnatal developmental stage. At first sight, these observations show that the disturbed cholinergic neurotransmission of the mutant might be linked to the pituitary and thyroxine deficiency that is characteristic of this mouse. Hormone therapy selectively stimulates cholinergic activity in cholinergic-deficient structures, where it reactivates presynaptic markers. The differential responsiveness of the neuroanatomical and neurochemical targets could be linked to different regulatory hormone effects or to timing in respect to sensitivity to hormones during development.

Acetylcholinesterase↗
PubMed1986

Genotypic differences in age and chronic alcohol exposure effects on somatostatin levels in hippocampus and striatum in mice.

Somatostatin contents of striatum, hippocampus, and pons medulla have been followed in two inbred strains of mice (C57B1/6J and Balb/cJ) with aging and long term alcohol exposure (over a 25 month period of intoxication). Marked strain dependent differences in basic levels of somatostatin and genotypic variations in reactivity of this neuropeptide to aging processes and chronic alcohol exposure were demonstrated. The Balb/c strain exhibits a significant age dependent decrease in striatal and hippocampal somatostatin levels whereas the C57B1 mice remain unchanged until the 27 month. Moreover, only the Balb/c strain reacts to chronic alcohol exposure, showing a significant increase in somatostatin levels in those structures affected by the aging process. Such genotypic differences may be involved in man in specific pathologies in aged individuals and in alcohol induced behavioral alterations in alcoholics.

Aging↗
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↗
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↗