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C Stricker

Publications and source records attributed to C Stricker.

11 recordsLinked to original sources
PubMed1996

Statistical analysis of amplitude fluctuations in EPSCs evoked in rat CA1 pyramidal neurones in vitro.

1. EPSCs were evoked in CA1 pyramidal neurones of young rats in vitro by extracellular stimulation of axons in a restricted stratum radiatum field, and were recorded using the whole-cell technique. 2. Quantal fluctuations in EPSC amplitude could be demonstrated for nineteen of fifty EPSCs analysed. Quantal currents (at the soma) ranged from 2.6 to 9.5 pA (after correction for the access resistance) with a mean of 4.0 +/- 2.0 pA. 3. Quantal variance was negligible for the majority (13/19) of the EPSCs. However, a large quantal variance (with a coefficient of variation > 0.4) is one possible reason why a large number of the EPSCs (29/50) could not be shown to have quantal fluctuations. 4. The statistical pattern of fluctuations in the amplitude of the majority of the quantal EPSCs (18/19) could not be described by conventional models of transmitter release. 5. The time course of the EPSC and a compartmental model of CA1 pyramidal neurones were used to calculate synaptic location. The quantal current (at the soma) was independent of the electrotonic location of the synapse at which it was evoked. The peak quantal conductance generating each quantal current ranged from 0.5 to 6.8 nS (mean 1.3 +/- 1.4 nS), its magnitude increasing with distance from the soma. The mean peak conductance is likely to be generated by the opening of at least 60-160 AMPA channels.

Animals↗
PubMed1996

Changes in quantal parameters of EPSCs in rat CA1 neurones in vitro after the induction of long-term potentiation.

1. Long-term potentiation (LTP) was induced in EPSCs evoked in CA1 pyramidal neurones of young rats in vitro by extracellular stimulation of stratum radiatum. Low frequency stimulation was paired with postsynaptic depolarization to induce LTP, using whole-cell recording techniques. 2. Sufficient control and potentiated records were obtained under stable recording conditions to allow a quantal analysis of eleven EPSCs. The fluctuations in amplitude of all eleven EPSCs were quantized before conditioning stimulation, and they remained quantized after LTP induction, usually with an increased quantal variance. 3. Quantal current was increased by conditioning for nine out of eleven EPSCs. The increase in quantal current was correlated with the percentage increase in the EPSC. For only two EPSCs could the entire potentiation be attributed to an increase in quantal current. 4. The amplitude fluctuations of five control EPSCs could be described by binomial statistics, but after conditioning the binomial description held for only one of these EPSCs. For this EPSC, conditioning caused the release probability to increase from 0.39 +/- 0.05 to 0.47 +/- 0.02. 5. Quantal content was increased by conditioning stimulation for ten out of eleven EPSCs. The increase in quantal content was correlated with the percentage increase in the EPSC. However, for only four EPSCs could the entire potentiation be attributed to an increase in quantal content. 6. Most EPSCs were evoked with a high proportion of response failures. The probability of response failures decreased in eight out of eleven EPSCs following the induction of LTP. There was a negative correlation between the change in the probability of response failures and the amount of LTP. 7. The minimal number of sites at which transmission occurred increased for ten out of eleven EPSCs following LTP induction. Increases in the minimal number of active sites following conditioning were associated with decreases in the probability of response failures for seven out of eleven EPSCs. 8. The induction of LTP usually resulted in changes in the time course of the EPSCs. Cable analysis using a passive compartmental model of a CA1 pyramidal cell suggested that these time course changes were associated with shifts in the average electrotonic location of the active sites following LTP induction, rather than being caused by an increased duration of synaptic current. 9. LTP expression involves postsynaptic modifications to enhance the synaptic current at active sites. New sites are recruited, and our data cannot be used to determine if this is a result of a pre- or a postsynaptic change. Evidence for an increase in release probability was found for one EPSC.

Animals↗
PubMed1996

Genes specifying receptors for F18 fimbriated Escherichia coli, causing oedema disease and postweaning diarrhoea in pigs, map to chromosome 6.

The study comprised 236 pigs selected for resistance or susceptibility to oedema disease. The susceptibility to colonization of the small intestine by an Escherichia coli strain causing oedema disease was determined: (1) by monitoring faecal excretion of weaned pigs orally inoculated with E. coli strain O139:K12(B):H1:F18ab serotype; and (2) by an in vitro adhesion assay using an F18ab positive E. coli strain and small intestinal enterocyte preparations. Susceptibility to adhesion by these bacteria was shown to be controlled by a dominant (B) allele of the ECF18R locus and resistance by the alternative recessive allele (b). Pigs were typed for 14 blood group systems, 11 biochemical polymorphisms and the polymorphism at nucleotide 1843 of the RYR1 locus. Linkage was demonstrated between the locus for F18 E. coli receptors and the loci S, RYR1, GPI, EAH, A1BG and PGD (Z > 20). The most likely gene orders are: S-ECF18R-RYR1-GPI-PGD or GPI-RYR1-ECF18R-S-PGD. The recombination frequencies between ECF18R-S and ECF18R-RYR1 were estimated to be theta = 0.5% and 3.1%, respectively.

Adhesins, Bacterial↗
PubMed1995

Linkage analysis with an alternative formulation for the mixed model of inheritance: the finite polygenic mixed model.

This paper presents an extension of the finite polygenic mixed model of Fernando et al. (1994) to linkage analysis. The finite polygenic mixed model, extended for linkage analysis, leads to a likelihood that can be calculated using efficient algorithms developed for oligogenic models. For comparison, linkage analysis of 5 simulated 4021-member pedigrees was performed using the usual mixed model of inheritance, approximated by Hasstedt (1982), and the finite polygenic mixed model extended for linkage analysis presented here. Maximum likelihood estimates of the finite polygenic mixed model could be inferred to be closer to the simulated values in these pedigrees.

Genetic Linkage↗
PubMed1994

Statistical analysis of synaptic transmission: model discrimination and confidence limits.

Procedures for discriminating between competing statistical models of synaptic transmission, and for providing confidence limits on the parameters of these models, have been developed. These procedures were tested against simulated data and were used to analyze the fluctuations in synaptic currents evoked in hippocampal neurones. All models were fitted to data using the Expectation-Maximization algorithm and a maximum likelihood criterion. Competing models were evaluated using the log-likelihood ratio (Wilks statistic). When the competing models were not nested, Monte Carlo sampling of the model used as the null hypothesis (H0) provided density functions against which H0 and the alternate model (H1) were tested. The statistic for the log-likelihood ratio was determined from the fit of H0 and H1 to these probability densities. This statistic was used to determine the significance level at which H0 could be rejected for the original data. When the competing models were nested, log-likelihood ratios and the chi 2 statistic were used to determine the confidence level for rejection. Once the model that provided the best statistical fit to the data was identified, many estimates for the model parameters were calculated by resampling the original data. Bootstrap techniques were then used to obtain the confidence limits of these parameters.

Algorithms↗
PubMed1994

Statistical models of synaptic transmission evaluated using the expectation-maximization algorithm.

Amplitude fluctuations of evoked synaptic responses can be used to extract information on the probabilities of release at the active sites, and on the amplitudes of the synaptic responses generated by transmission at each active site. The parameters that describe this process must be obtained from an incomplete data set represented by the probability density of the evoked synaptic response. In this paper, the equations required to calculate these parameters using the Expectation-Maximization algorithm and the maximum likelihood criterion have been derived for a variety of statistical models of synaptic transmission. These models are ones where the probabilities associated with the different discrete amplitudes in the evoked responses are a) unconstrained, b) binomial, and c) compound binomial. The discrete amplitudes may be separated by equal (quantal) or unequal amounts, with or without quantal variance. Alternative models have been considered where the variance associated with the discrete amplitudes is sufficiently large such that no quantal amplitudes can be detected. These models involve the sum of a normal distribution (to represent failures) and a unimodal distribution (to represent the evoked responses). The implementation of the algorithm is described in each case, and its accuracy and convergence have been demonstrated.

Algorithms↗
PubMed1989

The contribution of the N- and C-terminal regions of steroid receptors to activation of transcription is both receptor and cell-specific.

Normalized dose response-curves for transcriptional activation of reporter genes were obtained by co-transfecting them with increasing amounts of wild-type (wt) progesterone (PR), glucocorticoid (GR) and oestrogen (ER) expression vectors. Marked differences in both shape and magnitude of the stimulation were observed depending on whether HeLa or CV1 cells were transfected. In HeLa cells the transcriptional stimulation from a reporter gene containing the hormone responsive element (RE) present in the mouse mammary tumour virus (MMTV) long terminal repeat (LTR) increased as increasing amounts (from 0.05 to 7.5 micrograms) of PR expression vector were transfected, whereas no such increase was observed in CV1 cells above 1 microgram of the same vector. In contrast, a PR mutant lacking the hormone binding domain (HBD, region E), exhibited increasing constitutive activity with increasing amounts of PR expression vector, such that in CV1 cells, but not in HeLa cells, similar activities were measured for the mutant and wt PR when 5 micrograms expression vectors were transfected. Western blot analyses indicated that the differences between the two cell lines were not due to differences in the amount of receptor proteins. Using the same MMTV LTR-based reporter gene, cell-specific differences were also detected between the dose-response curves obtained for the human GR and a mutant which lacks the HBD. A PR mutant in which the N-terminal A/B region was deleted exhibited no (CV1 cells) or less than 5% (HeLa cells) of the wt-activity, whereas the corresponding GR mutant stimulated efficiently transcription in both cell lines. Identical studies with the wt human ER or a mutant truncated for the N-terminal A/B region resulted in bell-shaped dose-response curves in both HeLa and CV1 cells, whereas an ER mutant lacking the HBD was weakly active in either cell line. These data demonstrate cell- and receptor-specificity for the transcriptional activation functions present in the A/B region and the HBD of various steroid receptors and suggest that limiting factors mediate their action. The present study also emphasizes the need of establishing dose-response curves to correctly assess the relative contribution of the different regions of steroid hormone receptors in activation of transcription.

Amino Acid Sequence↗
PubMed1989

Influences of morphology and topography of motoneurons and muscle spindle afferents on amplitude of single fiber excitatory postsynaptic potentials in cat.

Excitatory postsynaptic potentials (e.p.s. p.s.) elicited by impulses in single muscle spindle afferent fibers from the medial gastrocnemius (m.g.) muscle were recorded intracellularly from homonymous and heteronymous motoneurons in order to study factors that influence the amplitudes of such responses. Impulses in large afferent fibers elicited larger single-fiber e.p.s.p.s. than those in smaller afferents. Mean e.p.s.p. amplitudes were related exponentially to afferent conduction velocities of both Ia and spindle group II fibers. The closer a motoneuron was to the spinal entry point of an afferent fiber, the larger was the mean e.p.s.p. amplitude evoked in it. Impulses in the same afferent fiber elicited larger e.p.s.p.s in small than large motoneurons when the two cells were located at the same craniocaudal levels. Other factors being equal, the single-fiber e.p.s.p.s evoked in homonymous and heteronymous motoneurons were approximately equal in amplitude. Relatively simple morphological and topographical explanations for the findings were advanced and their functional significance for orderly recruitment in partitioned and unpartitioned reflexes was described.

Action Potentials↗