PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 9279021

Analysis of single and multiple neuronal discharges as point processes: a computer program set.

A Eblen-Zajjur
View original source ↗Export metadata ↓

Abstract

The analysis of single or multiple neuron discharges as point processes has gained considerable importance for understanding the principles of information coding and processing in the central nervous system (CNS). Here, a set of programs written in BASIC language for microcomputers is described for the point process analysis of discharges of individual or multiple simultaneously recorded neurons as well as the mathematical basis of the methods implemented in these programs. The input data consist of one or more ASCII files with the spike or stimulus occurrence times generated by the spike sorting system used. Interspike interval histogram, autocorrelogram, autospectrum, cross-correlogram, joint impulse configuration scatter diagram, poststimulus time histogram and joint peristimulus time scatter diagram, together with other more conventional methods, are included in this package which provides graphical or alpha numeric results which can be printed or stored on disk for additional graphical or statistical analysis.

Explore related subjects

Action PotentialsAnimalsElectric StimulationElectronic Data ProcessingNeuronsRatsSoftwareJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Eblen-Zajjur. 1995. Analysis of single and multiple neuronal discharges as point processes: a computer program set.. https://pubmed.ncbi.nlm.nih.gov/9279021/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1999

Differential control of three after-hyperpolarizations in rat hippocampal neurones by intracellular calcium buffering.

1. The whole-cell recording technique, combined with internal perfusion, was used to study the effects of intracellular Ca2+ buffering on fast, medium and slow after-hyperpolarizations (fAHP, mAHP and sAHP) in hippocampal CA1 pyramidal neurones in rat brain slices at room temperature. 2. The action potentials and the fAHP were unaffected by 100 microM to 3 mM concentrations of the internally applied fast Ca2+ chelator BAPTA. At higher (10-15 mM) concentrations, BAPTA inhibited the fAHP and prolonged the decay of the action potential, suggesting that the corresponding large-conductance Ca2+-activated K+ channels are located close to the sites of Ca2+ entry during an action potential. Addition of Ca2+ to the BAPTA-containing solution (at a ratio of 4.5 [Ca2+] : 10 [BAPTA]) to maintain the control level of [Ca2+]i did not prevent the effects of high concentrations of BAPTA. 3. The mAHP, activated by a train of action potentials, was inhibited by internally applied BAPTA within the range of concentrations used (100 microM to 15 mM), and this effect could not be reversed or prevented by addition of Ca2+ to the BAPTA-containing solution. The inhibition of the mAHP by BAPTA could also be observed after blockade of the hyperpolarization-activated IQ type mixed Na+-K+ current (also known as Ih) component of the mAHP by bath-applied 3-5 mM Cs+, suggesting that the inhibition of the mAHP by BAPTA is due to inhibition of the depolarization-activated IM (muscarinic) type K+ current. 4. The sAHP, activated by a train of action potentials, was potentiated by 100-300 microM internally applied BAPTA, both with and without added Ca2+. At 1-2 mM or higher concentrations, the potentiation of the sAHP by BAPTA without added Ca2+ was transient and was followed by a fast decrease. With added Ca2+, however, BAPTA caused a persistent potentiation of the sAHP with more than a 10-fold increase in duration for periods exceeding 1 h even at concentrations of the buffer as high as 10-15 mM. Earlier reports showing a blockade of the sAHP by BAPTA, based on experiments without added Ca2+, were apparently due to a sharp reduction in intracellular free [Ca2+] and to a high intracellular concentration of the free buffer. 5. Internally applied BAPTA caused a prolongation of the spike discharge during an 800 ms-long depolarizing current step. At 100-300 microM BAPTA, but not at 1-2 mM or higher concentrations, this effect could be reversed by addition of Ca2+. The effects of BAPTA on the spike discharge occurred in parallel with the changes in the sAHP time course, which was more prolonged at higher concentrations of the buffer. 6. The concentration-dependent differential control of the three types of AHP in hippocampal neurones by BAPTA is related to modulation of intracellular Ca2+ diffusion by a fast acting mobile Ca2+ buffer.

Action Potentials↗
PubMed1999

Relationship between K+ channel down-regulation and [Ca2+]i in rat ventricular myocytes following myocardial infarction.

1. Cardiac hypertrophy and prolongation of the cardiac action potential are hallmark features of heart disease. We examined the molecular mechanisms and the functional consequences of this action potential prolongation on calcium handling in right ventricular myocytes obtained from rats 8 weeks following ligation of the left anterior descending coronary artery (post-myocardial infarction (MI) myocytes). 2. Compared with myocytes from sham-operated rats (sham myocytes), post-MI myocytes showed significant reductions in transient outward K+ current (Ito) density (sham 19.7 +/- 1.1 pA pF-1 versus post-MI 11.0 +/- 1.3 pA pF-1; means +/- s.e.m.), inward rectifier K+ current density (sham -13.7 +/- 0.6 pA pF-1 versus post-MI -10.3 +/- 0.9 pA pF-1) and resting membrane potential (sham -84.4 +/- 1.3 mV versus post-MI -74.1 +/- 2.6 mV). Depressed Ito amplitude correlated with significant reductions in Kv4.2 and Kv4.3 mRNA and Kv4.2 protein levels. Kv1.4 mRNA and protein levels were increased and coincided with the appearance of a slow component of recovery from inactivation for Ito. 3. In current-clamp recordings, post-MI myocytes showed a significant increase in [Ca2+]i transient amplitude compared with sham myocytes. Using voltage-clamp depolarizations, no intrinsic differences in Ca2+ handling by the sarcoplasmic reticulum or in L-type Ca2+ channel density (ICa,L) were detected between the groups. 4. Stimulation of post-MI myocytes with an action potential derived from a sham myocyte reduced the [Ca2+] transient amplitude to the sham level and vice versa. 5. The net Ca2+ influx per beat via ICa,L was increased about 2-fold in myocytes stimulated with post-MI action potentials compared with sham action potentials. 6. Our findings demonstrate that reductions in K+ channel expression in post-MI myocytes prolong action potential duration resulting in elevated Ca2+ influx and [Ca2+]i transients.

Action Potentials↗
PubMed1999

Analysis of integrate-and-fire neurons: synchronization of synaptic input and spike output.

A new technique for analyzing the probability distribution of output spikes for the integrate-and-fire model is presented. This technique enables us to investigate models with arbitrary synaptic response functions that incorporate both leakage across the membrane and a rise time of the postsynaptic potential. The results, which are compared with numerical simulations, are exact in the limit of a large number of small-amplitude inputs. This method is applied to the synchronization problem, in which we examine the relationship between the spread in arrival times of the inputs (the temporal jitter of the synaptic input) and the resultant spread in the times at which the output spikes are generated (output jitter). The results of previous studies, which indicated that the ration of the output jitter to the input jitter is consistently less than one and that it decreases for increasing numbers of inputs, are confirmed for three classes of the integrate-and-fire model. In addition to the previously identified factors of axonal propagation times and synaptic jitter, we identify the variation in the spike-generating thresholds of the neurons and the variation in the number of active inputs as being important factors that determine the timing jitter in layered networks. Previously observed phase differences between optimally and suboptimally stimulated neurons may be understood in terms of the relative time taken to reach threshold.

Action Potentials↗