Biomedical subjects

M Bijak

Publications and source records attributed to M Bijak.

At least 37 records · Page 2Linked to original sources

PubMed1999

[Modular PC-based data acquisition and processing system for biological signals].

The data acquisition system described here is designed for biomedical research and permits the recording of up to eight biological signals simultaneously. A personal computer using the Windows 95 operating system is employed for data monitoring, data processing and analysis during experiments. The system has been designed for reliability, economy, flexibility and ease of handling, with the aim of achieving universal application. To avoid interface incompatibility, problems with transfer protocols and the data formats of commercially available products, analog signals are used for further processing. The individual input channels are electrically isolated from one another and the PC to avoid ground loops, and for reasons of safety. An isolated voltage supply is available for pre-amplifiers and bridges. A bandwidth of 0-5 kHz and the maximum sampling rate of 12.5 kHz suffice to pick up higher frequency signals such as EMG and ENG. The modular software and hardware concepts permit the use of almost any desktop or laptop PC as a central processing unit. The PC handless documentation, data acquisition, data analysis and the preparation of publications. If needed, further analytical functions can be added in modular form. Finally, the option of saving data in the ASCII format permits processing of results with such standard software packages as Excel, Access, Matlab and Origin.

Signal Processing, Computer-Assisted↗

PubMed1998

Antidepressant treatment influences group I of glutamate metabotropic receptors in slices from hippocampal CA1 region.

We investigated the effects of repeated electroconvulsive shock or imipramine treatment on inositol phosphate accumulation and on the reactivity of neurons to metabotropic glutamate (mGlu) receptor agonists in rat hippocampal slices. (1S,3R)-1-carboxycyclopentane-3-acetic acid (1S,3R-ACPD), a nonselective mGlu receptor agonist, caused a concentration-dependent increase in inositol phosphate in slices from the CA1 region of the hippocampus, an effect that was not modified by imipramine or electroconvulsive shock treatment. 1S,3R-ACPD or the selective agonist of the I group of mGlu receptor, (R,S)-3,5-dihydroxyphenylglycine ((R,S)-3,5-DHPG), produced a concentration-dependent increase of the population spike recorded in the CA1 cell layer. This effect of 1S,3R-ACPD was markedly attenuated by both repeated imipramine and electroconvulsive shock treatment, and the action of (R,S)-3,5-DHPG was markedly attenuated by prolonged imipramine treatment (electroconvulsive shock was not tested). Our results indicate that antidepressant treatment may induce a subsensitivity of group I mGlu receptors when assessed by electrophysiological but not biochemical measures.

Action Potentials↗

PubMed1997

Repeated treatment with antidepressant drugs induces subsensitivity to the excitatory effect of 5-HT4 receptor activation in the rat hippocampus.

The effect of repeated treatment with various antidepressant drugs on the reactivity of CA1 neurons to the 5-HT4 receptor agonist zacopride was examined. Zacopride decreased the calcium-activated afterhyperpolarization and adaptation, it also elicited a slow membrane depolarization associated with an increase in input resistance. All those effects may have contributed to the zacopride-induced increase in the amplitude of population spikes, evoked in the CA1 cell layer by stimulation of the Schaffer collateral/commissural pathway. The later effect of zacopride was concentration-dependent and was antagonized by the 5-HT4 receptor antagonist DAU 62805. Repeated (14 days, twice daily), but not single, administration of the antidepressant drugs imipramine, citalopram, fluvoxamine and paroxetine (10 mg/kg) attenuated the effect of zacopride on population spikes. Because inhibitory 5-HT1A and excitatory 5-HT4 receptors are colocalized on pyramidal neurons, and our previous data demonstrated an increase in the 5-HT1A receptor-mediated inhibition after repeated treatment with antidepressants, we conclude that treatment with antidepressant drugs may enhance the inhibitory effect of 5-HT directly, by increasing the 5-HT1A receptor responsiveness, and indirectly, by inducing subsensitivity to the 5-HT4 receptor activation.

Animals↗

PubMed1997

Effects of serotonin through serotonin1A and serotonin4 receptors on inhibition in the guinea-pig dentate gyrus in vitro.

The role of serotonin1A and serotonin4 receptors in the modulation of synaptic inhibition in the dentate gyrus of guinea-pig hippocampal slices was studied. The effects of serotonin (5-hydroxytryptamine) on hilar neurons and on inhibitory postsynaptic potentials in granule cells were compared using intracellular recording in the presence of glutamatergic receptor antagonists. On the basis of electrophysiological properties hilar neurons were classified as type I neurons (presumably inhibitory) and type II neurons (presumably excitatory). Serotonin hyperpolarized a proportion of type I hilar neurons (60%) and decreased their input resistance through activation of a K+-conductance. This effect was mediated by serotonin1A receptors since it was mimicked by the selective serotonin1A receptor agonist (+/-)-8-hydroxy-dipropylaminotetralin hydrobromide and blocked by the selective serotonin1A receptor antagonist (+) WAY 100135. In some type I hilar neurons (40%) neither serotonin nor (+/-)-8-hydroxydipropylaminotetralin hydrobromide induced a membrane hyperpolarization. Instead, serotonin induced an excitatory response, depolarizing the cells and blocking the slow afterhyperpolarization. Similar effects were seen in all hilar neurons after blockade of serotonin1A receptors. They were mimicked by the serotonin4 receptor agonist zacopride. Serotonin induced either decreases or increases in the frequency of spontaneous GABA(A) receptor-mediated inhibitory postsynaptic potentials in granule cells via activation of serotonin1A and of serotonin4 receptors, respectively. 4-aminopyridine-evoked GABA(B) receptor-mediated inhibitory postsynaptic potentials were inhibited by serotonin via activation of serotonin1A receptors. However, after blockade of serotonin1A receptors, serotonin increased the frequency of GABA(B)-inhibitory postsynaptic potentials through the activation of serotonin4 receptors. We conclude that a proportion of inhibitory neurons in the dentate area does not express serotonin1A receptors and is excited by serotonin. Other inhibitory neurons express serotonin1A receptors and are inhibited by serotonin.

Animals↗

PubMed1997

[The foramen sternale: a minor anomaly--great relevance].

PURPOSE: Evaluation of the incidence of a midline sternal foramen, as a developmental anomaly, in order to avoid fatal complications following sternal puncture of sternal acupuncture treatment. MATERIAL AND METHODS: 100 chest computed tomograms were evaluated in reference to the incidence of this anomaly and its various features. RESULTS: The variety of CT aspects ranged from very incomplete types with only sandglass-like retraction of sternal cortex, to a complete foraminal defect. The incidence of midline sternal foramen in a feature bearing a risk of complication, is approximately 6%. CONCLUSION: We conclude that--if sternal acupuncture is planned in the region of corpus--previous radiographs should be done to rule out this anomaly. Furthermore, we strongly recommend the acupuncture technique of the "Wiener Schule", which prescribes a safe superficial-oblique approach to the sternum.

Acupuncture Therapy↗

PubMed1997

Useful applications and limits of battery powered implants in functional electrical stimulations.

Battery powered stimulation implants have been well-known for a long time as heart pacemakers. In the last few years, fully implantable stimulators have been used in the field of functional electrical stimulation (FES) for applications like dynamic cardiomyoplasty and electro-stimulated graciloplasty for fecal incontinence. The error rate of battery powered implants is significantly smaller than that for conventional stimulator systems, and the quality of life for the patients is increased because the need for an external power and control unit is eliminated. The use of battery powered implants is limited by the complexity of the stimulation control strategies and the battery capacity. Therefore, applications like the stimulation of lower extremities for walking, cochlea stimulation, or direct muscle stimulation cannot be supported. The improvement of implantable batteries, microcontrollers, and ultralow power products is ongoing. In the future, battery powered implants will also meet the requirements of complex applications. Systems for restoration of hand and breathing functions after spinal cord injury can be the next field of use for battery powered implants. For these purposes, we developed a battery powered multichannel implant with a sufficient life span for phrenic pacing. The problems during development and the limits of this system are described in this paper.

Cardiomyoplasty↗

PubMed1997

Computer aided adjustment of the phrenic pacemaker: automatic functions, documentation, and quality control.

Electrical stimulation of the phrenic nerves of patients with complete ventilatory insufficiency with the Vienna respiratory pacemaker has been in clinical use since 1983. During the adjustment of stimulation parameters with this device, the following problems have occurred: for some measurements like the recruitment curve, series of complete inspiration cycles have to be stimulated, which causes the danger of muscle fatigue for unconditioned patients. The documentation is completed predominantly by hand, taking time and increasing the possibility of error. As a first step to solve these problems, we developed a new stimulation and measurement system. It consists of a PC with data acquisition hardware, the necessary sensors, and amplifier circuitry. The implanted stimulator is controlled via the parallel interface. The new system offers some advantages: computer control shortens the time for measurement and documentation, and the stress on the patient and the risk of error is reduced; synchronized measurement makes it possible to use single stimulation pulses instead of bursts and ramps to reduce diaphragm fatigue; digital signal processing improves measurement results and reproducibility; and help functions and self tests are provided, together with a graphical user interface. We used sensors for air flow, diaphragm EMG, and acceleration, on up to 8 channels simultaneously. Combined sample rates of up to 100 kS/s were possible. The system could be adapted for other uses involving functional electrical stimulation with our implantable nerve stimulators. Using this equipment saves a lot of effort, and the adjustment process can be focused on improved stimulation results and better performance for the patient. Current research is studying implementation of automatic functions like acquisition of stimulation thresholds. This could result in a predominantly automated adjustment of the phrenic pacemaker and even in a closed-loop controlled system in the future.

Computer Simulation↗

PubMed1996

Imipramine increases the 5-HT1A receptor-mediated inhibition of hippocampal neurons without changing the 5-HT1A receptor binding.

The effect of repeated treatment with imipramine on the 5-HT1A receptor-mediated inhibition of a population spike was studied in the rat CA1 hippocampal region ex vivo. Serotonin (5-hydroxytryptamine, 5-HT) and the selective 5-HT1A receptor agonist 8-hydroxy-2-(dipropylamino)tetralin (8-OH-DPAT) decreased dose-dependently the amplitude of population spikes; this effect was blocked by the selective 5-HT1A receptor antagonist (S)-N-tert-butyl-3-[4-(2-methoxyphenyl)piperazin-1-yl]-2-phenylpro panamide dihydrochloride [(S)-WAY 100135]. Repeated (14 days, twice daily), but not single, administration of imipramine (10 mg/kg) shifted the dose-response curves for serotonin and 8-OH-DPAT to the left. Repeated treatment with imipramine did not change the density of 5-HT1A receptors in the hippocampus as measured by autoradiography using [3H]8-OH-DPAT as a ligand. The latter findings indicate that the imipramine-induced increase in the responsiveness of hippocampal neurons to stimulation of 5-HT1A receptors may not involve an increase in the density of this receptor subtype. To find out whether the efficacy of the postreceptor transduction mechanism is changed by repeated treatment with imipramine, we examined the effect of baclofen. The baclofen-induced inhibition of the population spike was not changed by imipramine. Our results suggest that repeated treatment with imipramine induces sensitization to the inhibitory effects of 5-HT1A receptor agonists in the hippocampus.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1996

Suppression by GABAB receptors of 4-aminopyridine-induced hyperactivity in guinea-pig dentate neurons.

Double intracellular recording from granule cells and hilar neurons was performed in hippocampal slices to study the effect of gamma-aminobutyric acid (GABA) receptor antagonists on the activity induced by the convulsant 4-aminopyridine (4-AP) in the dentate gyrus. 4-AP evoked GABA-mediated responses in granule cells and burst discharges in hilar neurons. In the presence of GABAB but not GABAA receptor antagonists, 4-AP evoked discharge activity in dentate granule cells. When both GABAA and GABAB receptors were blocked 4-AP induced synchronous 'paroxysmal depolarizing shift'-like activity in granule cells and hilar neurons. Our data indicate that GABAB receptor-mediated mechanisms protect dentate cells against the convulsant effects of 4-AP.

4-Aminopyridine↗

PubMed1996

The effects of paroxetine given repeatedly on the 5-HT receptor subpopulations in the rat brain.

Effects of paroxetine (10 mg/kg PO, twice daily, 14 days) on 5-HT receptor subpopulations in the brain were evaluated pharmacologically, electrophysiologically and biochemically in male Wistar rats. Imipramine was used for comparison. Repeated paroxetine antagonized the 8-OH-DPAT-induced behavioural syndrome (a 5-HT1A effect); imipramine showed similar, yet weaker, activity. The 5-HT-or 8-OH-DPAT-induced inhibition of population spikes in hippocampal slices was increased by both those repeated antidepressants. Repeated (or acute) paroxetine decreased the density of and increased the affinity for 5-HT1A receptors ([3H]-8-OH-DPAT used as ligand) in the hippocampus, while imipramine induced opposite effects. m-Chlorophenyl piperazine (m-CPP)-evoked exploratory hypoactivity, a 5-HT2C effect, was reduced by repeated paroxetine, but not by imipramine. Either of the antidepressants given repeatedly antagonized TFMPP-induced hyperthermia (another putative 5-HT2C effect). 5-HTP-induced head twitches (a 5-HT2A effect) were inhibited by repeated paroxetine or imipramine. Either antidepressant given repeatedly decreased the density of 5-HT2A receptors ([3H]-ketanserin as a ligand) in the brain cortex, but did not change their affinity. The present results indicate that paroxetine given repeatedly induces secondary changes in 5-HT2 receptors, which lead to reduction of the 5-HT2 neurotransmission (reduced responsiveness of 5-HT2 postsynaptic receptors). The consequences of the secondary changes in 5-HT1A receptors, found here still await clarification.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1996

Inhibitory effect of NPY on the picrotoxin-induced activity in the hippocampus: a behavioural and electrophysiological study.

The effect of neuropeptide Y (NPY) on the picrotoxin-induced activity was studied in rat brain hippocampal slices in vitro and after intrahippocampal injection in vivo. In the hippocampal slices, NPY (0.1-0.5 microM) inhibited the picrotoxin-induced epileptiform activity recorded extracellularly in CA1 and CA3 hippocampal pyramidal cells. Similar inhibition was induced by the Y2 receptor agonist NPY13-36, which indicates that the effect of NPY was due to activation of Y2 receptors. In behavioural studies, rats with chronically implanted cannulae were injected unilaterally into the CA1 hippocampal region with a 1 ml volume of the studied substances. Picrotoxin in a dose of 1 mg (1.6 nmol) induced behavioural excitation, shakes and weak signs of epileptic behaviour. NPY in a dose of 2 mg (470 pmol), but not 1 mg, inhibited some excitatory effects of picrotoxin, but did not change the epileptic symptoms. The obtained results suggest that NPY has an inhibitory action in the hippocampus, which can be observed in vitro and also in a behavioural study.

Animals↗

PubMed1996

Vienna phrenic pacemaker--experience with diaphragm pacing in children.

Eight children, five boys and three girls, aging from 2 to 13 years (M = 9 +/- 3) were treated with the "Vienna phrenic pacemaker". Indication for implantation was central alveolar hypoventilation syndrome (CAH) in one case and total ventilatory insufficiency due to high cervical cord or brain stem lesion (SCI) in seven cases. Four electrodes were applied to each phrenic nerve via sternotomy. Both hemidiaphragms were paced synchronously with increasing duty cycles to condition the diaphragms for continuous electrophrenic respiration (EPR). EPR could be performed successfully in all children but one. Four children could achieve chronical EPR, one is in conditioning period. Two patients could not be discharged from hospital due to parental neglect and died after two and three years of intermittent stimulation. Six children could be discharged from hospital, two of them died after one and four years of chronic pacing. In one case tracheotomy could be closed definitively. Ventilatory insufficiency due to CAH and SCI can be treated even in children with diaphragm pacing, provided the indication for implantation, containing medical and social aspects, was made correctly. Diaphragm pacing probably will not lengthen life of severely injured children but it can increase the quality of their life and therefore should be preferred to positive pressure mechanical ventilation.

Adolescent↗

PubMed1996

[Pruritometer 1: Portable measuring system for quantifying scratching as an objective measure of cholestatic pruritus].

Objective assessment of subjective symptoms such as pruritus always presents problems, which can often be resolved only indirectly. The objectification of pruritus was necessitated by a study on the efficacy of a serotonin antagonist used as treatment of cholestatic pruritus. In the present paper, a portable measuring system for the indirect objective assessment of pruritus via the quantification of scratching is described. A piezoelectric scratch-vibration sensor for attachment to the middle finger of the patient's dominant hand was developed. A sensor interface detects the scratching signals and generates pulses that are then summed in an adapted sports watch. The entire system-Pruritometer 1- is worn by the patient like a wrist watch, and is characterized by ease of handling. Acceptance by the patient is reported to be good. A statistically good correlation between measured (Pruritometer) and visually counted scratches was demonstrated. Pruritometer 2, which will enable scratch frequency and intensity distribution over time to be determined, is presently being developed.

Cholestasis, Intrahepatic↗

PubMed1996

Monoamine modulation of the synaptic inhibition in the hippocampus.

Changes in the strength of synaptic inhibition have profound effects on the functions of cortical neurones. Accumulating evidence suggests that inhibitory synaptic transmission may be the target of actions of monoamines. In the hippocampal dentate gyrus, norepinephrine and serotonin (5-HT) have multiple direct and indirect actions on the presumed inhibitory hilar neurones. These effects are mediated through distinct mechanisms and signalled by different receptor subtypes. The predominant effects of norepinephrine are excitatory and are mediated by beta-adrenergic receptors. Accordingly, both the GABAA- and GABAB-receptor-mediated inhibition in granule cells is enhanced by activation of the beta-adrenergic receptor. 5-HT has more complex effects inhibiting a subpopulation of the hilar neurones and exciting other hilar cells. Study of the effects of 5-HT on inhibition in granule cells revealed that 5-HT enhanced Cl-IPSPs and blocked K-IPSPs. These results are in line with the suggestion that Cl- and K-IPSPs in granule cells are generated by two distinct populations of inhibitory neurones.

Animals↗

PubMed1996

Electrical stimulation to restore respiration.

Electrical stimulation has been used for over 25 years to restore breathing to patients with high quadriplegia causing respiratory paralysis and patients with central alveolar hypoventilation. Three groups have developed electrical pacing systems for long-term support of respiration in humans. These systems consist of electrodes implanted on the phrenic nerves, connected by leads to a stimulator implanted under the skin, and powered and controlled from a battery-powered transmitter outside the body. The systems differ principally in the electrode design and stimulation waveform. Approximately 1,000 people worldwide have received one of the three phrenic pacing devices, most with strongly positive results: reduced risk of tracheal problems and chronic infection, the ability to speak and smell more normally, reduced risk of accidental interruption of respiration, greater independence, and reduced costs and time for ventilatory care. For patients with partial lesions of the phrenic nerves, intercostal muscle stimulation may supplement respiration.

Electric Stimulation Therapy↗

PubMed1996

Prolonged treatment with antidepressants increases the 5-HT1A-mediated inhibition of hippocampal neurons without changing the 5-HT1A receptor binding.

The effect of repeated treatment with antidepressant drugs imipramine, (+)oxaprotiline and paroxetine on neuronal responsiveness to 5-HT and the 5-HT1A receptor agonist 8-OH-DPAT was examined in the hippocampal slice preparation from the rat. 5-HT and 8-OH-DPAT decreased the amplitude of population spikes evoked in the CA1 cell layer by electrical stimulation of the stratum radiatum. The antidepressant drugs, administered for 2 weeks, produced a significant increase in the inhibitory effect of 5-HT and 8-OH-DPAT. Repeated treatment with imipramine did not change the density of 5-HT1A receptors in the hippocampus suggesting that the increase in 5-HT1A responsivity may not involve an increase in the receptor density.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1995

A physiological role for GABAB receptors and the effects of baclofen in the mammalian central nervous system.

The inhibitory neurotransmitter GABA acts in the mammalian brain through two different receptor classes: GABAA and GABAB receptors. GABAB receptors differ fundamentally from GABAA receptors in that they require a G-protein. GABAB receptors are located pre- and/or post-synaptically, and are coupled to various K+ and Ca2+ channels presumably through both a membrane delimited pathway and a pathway involving second messengers. Baclofen, a selective GABAB receptor agonist, as well as GABA itself have pre- and post-synaptic effects. Pre-synaptic effects comprise the reduction of the release of excitatory and inhibitory transmitters. GABAergic receptors on GABAergic terminals may regulate GABA release, however, in most instances spontaneous inhibitory synaptic activity is not modulated by endogenous GABA. Post-synaptic GABAB receptor-mediated inhibition is likely to occur through a membrane delimited pathway activating K+ channels, while baclofen, in some neurons, may activate K+ channels through a second messenger pathway involving arachidonic acid. Some, but not all GABAB receptor-gated K+ channels have the typical properties of those G-protein-activated K+ channels which are also gated by other endogenous ligands of the brain. New, high affinity GABAB antagonists are now available, and some pharmacological evidence points to a receptor heterogeneity. The pharmacological distinction of receptor subtypes, however, has to await final support from a characterization of the molecular structure. The function importance of post-synaptic GABAB receptors is highlighted by a segregation of GABAA and GABAB synapses in the mammalian brain.

Animals↗

PubMed1995

Adrenergic modulation of hilar neuron activity and granule cell inhibition in the guinea-pig hippocampal slice.

To study the effects of norepinephrine on synaptic inhibition in the dentate gyrus, intracellular recordings were made from hilar neurons in the guinea-pig hippocampal slice. The effects of norepinephrine on hilar neurons were compared with changes in the frequency of spontaneous inhibitory postsynaptic potentials recorded from granule cells. Hilar neurons comprised two electrophysiologically distinct groups: type I hilar neurons displayed a pronounced single spike afterhyperpolarization and little spike frequency accommodation, type II hilar neurons had small afterhyperpolarizations and pronounced spike frequency accommodation. The majority of recordings were from type I hilar neurons which are presumably inhibitory to granule cells. In most instances, effects of norepinephrine (2-10 microM) on hilar neurons could be mimicked by the beta-adrenergic agonist isoproterenol (0.1-1 microM). Isoproterenol induced a slight depolarization, blocked a slow afterhyperpolarization and, in type II neurons, reduced spike frequency accommodation. These effects were associated with an increase in the spontaneous discharge rate and an enhancement of spontaneous excitatory and inhibitory postsynaptic potentials. In accordance, isoproterenol and norepinephrine increased the frequency of inhibitory postsynaptic potentials in granule cells. In the presence of the non-N-methyl-D-aspartate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and the N-methyl-D-aspartate receptor antagonist CGP 37849, isoproterenol and norepinephrine also increased the frequency of Cl- -dependent inhibitory postsynaptic potentials in granule cells. Under this experimental condition, however, norepinephrine reduced the discharge rate of type I hilar neurons through an effect on alpha-receptors. In the presence of GABAA receptor blockers, norepinephrine increased the frequency of spontaneously occurring K(+)-dependent inhibitory postsynaptic potentials in granule cells. Accordingly, the frequency of burst discharges in type I hilar neurons was increased. We suggest that the discrepancy in the effect of norepinephrine on the discharge rate of presumed inhibitory hilar neurons and the frequency of Cl- -dependent inhibitory postsynaptic potentials in granule cells results from a direct effect of norepinephrine on GABAergic terminals because norepinephrine also enhanced the frequency of tetrodotoxin-resistant inhibitory postsynaptic potentials in granule cells. Thus, the net effect of synaptically released norepinephrine on synaptic inhibition in the dentate gyrus will be determined by opposing actions of alpha- versus beta-receptor stimulation at the synapse on hilar neurons.

Animals↗