Biomedical subjects

H Pawelzik

Publications and source records attributed to H Pawelzik.

11 recordsLinked to original sources

PubMed2005

Patients with ALS can use sensorimotor rhythms to operate a brain-computer interface.

People with severe motor disabilities can maintain an acceptable quality of life if they can communicate. Brain-computer interfaces (BCIs), which do not depend on muscle control, can provide communication. Four people severely disabled by ALS learned to operate a BCI with EEG rhythms recorded over sensorimotor cortex. These results suggest that a sensorimotor rhythm-based BCI could help maintain quality of life for people with ALS.

Aged↗

PubMed2003

Modulation of inhibitory autapses and synapses on rat CA1 interneurones by GABA(A) receptor ligands.

To determine whether autaptic inhibition plays a functional role in the adult hippocampus, the action potential afterhyperpolarisations (spike AHPs) of CA1 interneurones were investigated in 25 basket, three bistratified and eight axo-axonic cells. The spike AHPs showed two minima in all regular-spiking (5), burst-firing (3) and in many fast-spiking cells (17:28). The fast component had a time-to-peak (TTP) of 1.2 +/- 0.5 ms, the slower TTP was very variable (range of 3.3-103 ms). The AHP width at half-amplitude (HW) was 12.5 +/- 5.7 ms in fast-spiking, 29.3 +/- 18 ms in regular-spiking and 99.7 +/- 42 ms in burst-firing cells. Axo-axonic cells never establish autapses, and the fast-spiking variety showed narrow (HW: 3.9 +/- 0.7 ms) spike AHPs with only one AHP minimum (TTP: 0.9 +/- 0.1 ms). When challenged with GABA(A) receptor modulators, spike AHPs in basket and bistratified cells were enhanced by zolpidem (HW by 18.4 +/- 6.2 % in 10:15 cells tested), diazepam (45.2 +/- 0.5 %, 6:7), etomidate (43.9 +/- 36 %, 6:8) and pentobarbitone sodium (41 %, 1:1), and were depressed by bicuculline (-41 +/- 5.7 %, 5:8) and picrotoxin (-54 %, 1:1), and the enhancement produced by zolpidem was reduced by flumazenil (-31 +/- 13 %, relative to the AHP HW during exposure to zolpidem, 3:4). Neuronal excitability was modulated in parallel. The spike AHPs of three axo-axonic cells tested showed no sensitivity to etomidate, pentobarbitone or diazepam. Interneurone-to-interneurone inhibitory postsynaptic potentials (IPSPs), studied with dual intracellular recordings, had time courses resembling those of the spike AHPs. The IPSP HW was 13.4 +/- 2.8 ms in fast-spiking (n = 16) and 28.7 +/- 5.8 ms in regular-spiking/burst-firing cells (n = 6), and the benzodiazepine1-selective modulator zolpidem strongly enhanced these IPSPs (45 +/- 28 %, n = 5). Interneurones with spike AHPs affected by the GABA(A) receptor ligands exhibited 3.8 +/- 1.9 close autaptic appositions. In three basket cells studied at the ultrastructural level 6 of 6, 1 of 2 and 1 of 2 close appositions were confirmed as autapses. Therefore, in the hippocampus autaptic connections contribute to spike AHPs in many interneurones. These autapses influence neuronal firing and responses to GABA(A) receptor ligands.

Action Potentials↗

PubMed2000

Double immunofluorescence, peroxidase labelling and ultrastructural analysis of interneurones following prolonged electrophysiological recordings in vitro.

Inhibitory hippocampal and neocortical interneurones comprise a physiologically, morphologically and neurochemically heterogenous cell population. To identify the roles each class of interneurone plays within a given circuit it is necessary to correlate the electrophysiological properties of individual cells with their neurochemistry and morphology at both the light and electron microscopic level. However, the optimal conditions required for any one part of the protocol typically compromise the results from another. We have developed a protocol which allows the neurochemical content, gross morphology and ultrastructure details of biocytin-filled neurones to be recovered following long, dual intracellular recordings in thick mature slices maintained in an interface recording chamber, helping define sub-populations which could not otherwise be determined. Dual immunofluorescence is performed by incubating the tissue in monoclonal and polyclonal antibodies simultaneously, prior to visualization of biocytin-labelling with precipitation of a peroxidase reaction product. By using a biotinylated anti-avidin D antibody (Vector Laboratories), the intensity of this precipitation can be enhanced further where necessary. It is envisaged that this protocol can not only help determine the neurochemical content of cells recorded in similar in vivo studies, but that the ability to amplify peroxidase labelling in poorly filled cells is also of interest.

Animals↗

PubMed2000

Differential sensitivity to Zolpidem of IPSPs activated by morphologically identified CA1 interneurons in slices of rat hippocampus.

Hippocampal pyramidal cells express several alpha-subunits, which determine the affinity of GABAA (gamma-aminobutyric acid) receptors for benzodiazepine site ligands. This study asked whether inhibitory postsynaptic potentials (IPSPs) elicited by specific interneuronal subclasses were differentially sensitive to the alpha1-preferring agonist Zolpidem, i.e. whether different receptors mediate different inhibitory connections. Paired intracellular recordings in which the presynaptic cell was an interneuron and the postsynaptic cell a CA1 pyramid were performed in slices of adult rat hippocampus. Resultant IPSPs were challenged with Zolpidem, cells filled with biocytin and identified morphologically. IPSPs elicited by fast spiking (FS) basket cells (n = 9) were enhanced more than IPSPs elicited by regular spiking (RS) basket cells (n = 10). At FS basket cell synapses the efficacy of Zolpidem was equivalent to that of Diazepam, while RS basket cell IPSPs are enhanced 50% less by Zolpidem than by Diazepam. Thus, while alpha1 subunits may dominate at synapses supplied by FS basket cells, RS basket cell synapses also involve alpha2/3 subunits. Two bistratified cell IPSPs tested with Zolpidem did not increase in amplitude, despite powerful enhancements of bistratified cell IPSPs by Diazepam, consistent with previous indications that these synapses utilize alpha5-containing receptors. Enhancements of basket cell IPSPs by Zolpidem and Diazepam were bi- or triphasic with steep amplitude increases separated by plateaux, occurring 10-15, 25-30 and 45-55 min after adding the drug to the bath. The entire enhancement was, however, blocked by the antagonist Flumazenil (n = 7). Flumazenil, either alone (n = 3), or after Zolpidem, reduced IPSP amplitude to approximately 90% of control, suggesting that alpha4-containing receptors were not involved.

Animals↗

PubMed1999

Modulation of bistratified cell IPSPs and basket cell IPSPs by pentobarbitone sodium, diazepam and Zn2+: dual recordings in slices of adult rat hippocampus.

Simultaneous intracellular recordings from presynaptic Stratum pyramidale interneurons and postsynaptic pyramidal cells in adult rat hippocampal slices were performed to investigate the strength of the modulation of single-axon inhibitory postsynaptic potentials (IPSPs) by the GABAA receptor modulators pentobarbitone, diazepam and zinc. The processing of biocytin-filled interneurons for light microscopy revealed that these single-axon IPSPs were generated by basket cells (n = 33), bistratified cells (n = 18) and axo-axonic cells (n = 2). The IPSPs generated by these three groups of interneurons had amplitudes and widths at half amplitude with similar ranges, but when bistratified cell IPSPs were compared with basket cell IPSPs with similar half widths their rise times were slower. Pentobarbitone sodium (250 microM) powerfully enhanced 13 tested IPSPs generated by all three cell types. Amplitudes were enhanced by 82 +/- 56%, 10-90% rise times by 150 +/- 101% and the widths at half amplitude by 71 +/- 29%. Diazepam (1-2 microM) also increased all IPSPs tested, although the changes were more moderate in basket cell IPSPs (amplitudes increased by 19 +/- 11%, n = 8) than in bistratified cell IPSPs (amplitudes increased by 66 +/- 48%, n = 5). Basket cell IPSP 10-90% rise times and widths at half amplitude were not significantly increased. Bistratified cell IPSP 10-90% rise times were increased by 44 +/- 24% and the widths at half amplitude by 32 +/- 35%. The one tested IPSP generated by an axo-axonic cell was also diazepam-sensitive. Zinc, 250 microM, decreased four out of 10 IPSPs generated by basket cells and four out of five IPSPs generated by bistratified cells. The one tested axo-axonic cell IPSP was zinc-insensitive. These data suggest that IPSPs generated in CA1 pyramidal cells by basket and bistratified cells display different pharmacologies and may be mediated by different receptors or receptor combinations.

Age Factors↗

PubMed1998

CA1 pyramidal to basket and bistratified cell EPSPs: dual intracellular recordings in rat hippocampal slices.

1. Dual intracellular recordings in the CA1 region of adult rat hippocampal slices and biocytin filling of synaptically connected cells were used to study the excitatory postsynaptic potentials (EPSPs) elicited in basket (n = 7) and bistratified interneurones (n = 7) by action potentials activated in simultaneously recorded pyramidal cells. 2. Interneurones could be subdivided according to their electrophysiological properties into classical fast spiking, burst firing, regular spiking and fast spiking cells with a rounded spike after-hyperpolarization. These physiological classes did not, however, correlate with morphological type. EPSPs were not recorded in regular spiking cells. 3. Average EPSP amplitudes were larger in bistratified cells (range, 0.5-9 mV) than in basket cells (range, 0. 15-3.6 mV) and the probability of obtaining a pyramidal cell-interneurone EPSP was also higher for the bistratified cells (1:7) than for the basket cells (1:22). EPSP 10-90 % rise times in bistratified cells (0.7-2 ms) and their widths at half-amplitude (3. 9-11.2 ms) were slightly longer than in basket cells (rise times, 0.4-1.6 ms; half-widths, 2.2-9.7 ms). 4. The majority of these EPSPs (6 of 8 tested) increased in amplitude and duration with postsynaptic depolarization, although in two (of 4) basket cells the voltage relation was conventional. 5. All EPSPs tested in both basket (n = 7) and bistratified cells (n = 5) decreased in amplitude with repetitive presynaptic firing. The average amplitudes of second EPSPs elicited within 15 ms of the first were between 34 and 94 % of the average amplitude of the first EPSP. Third and fourth EPSPs in brief trains were further depressed. This depression was associated with an increase in the incidence of apparent failures of transmission indicating a presynaptic locus.

Animals↗

PubMed1998

A peptide derived from a neurite outgrowth-promoting domain on the gamma 1 chain of laminin modulates the electrical properties of neocortical neurons.

Laminins form a family of large multidomain glycoproteins of the extracellular matrix. The cellular distribution of laminin immunoreactivity in the adult mammalian central nervous system suggests an important role for laminins in mature brain function in addition to their role during brain development. To characterize the effects of this group of extracellular matrix molecules on mature brain function, intracellular recording techniques were applied to in vitro slice preparations of the rat neocortex. The experiments show that a peptide homologous to the C-terminal part of the gamma 1 chain of laminin modulates the electrical activity of pyramidal neurons in the adult neocortex of the rat. The peptide is part of the neurite outgrowth-promoting domain of the gamma 1 chain on the E8 fragment of laminin and it displays the neurite outgrowth-promoting activity of the native laminin molecule. Perfusion of in vitro brain slices with the peptide increased the input resistance of the neuronal membrane. In addition, a rise in inward rectification could be observed. These events were accompanied by a strong increase in direct excitability of the treated neurons. Immunohistochemistry techniques were applied to sections of the adult rat neocortex and hippocampus to demonstrate the presence of both the neurite outgrowth-promoting domain and the native laminin in the adult brain. An antiserum raised against the neurite outgrowth-promoting domain on the gamma 1 chain of laminin, which also recognized the free synthetic peptide, showed immunoreactivity on neurons. In addition, a population of glial fibrillary acidic protein-positive astrocytes in the hippocampus displayed immunoreactivity for this antibody. These results were confirmed by using several antibodies directed against the whole laminin-1 molecule. Neurons in the neocortex and hippocampus, as well as astrocytes in the hippocampus, demonstrated immunoreactivity for antibodies directed against the whole laminin-1 molecule. The results suggest that laminins containing the gamma 1 chain have the potential to modulate neuronal activity. This effect may be mediated either by direct cell-cell contact from surrounding cells, or through the neuronal expression of laminin or laminin-like molecules which are inserted into the neuronal cell membrane.

Animals↗

PubMed1994

Thyrotropin-releasing hormone enhances excitatory postsynaptic potentials in neocortical neurons of the rat in vitro.

Several lines of evidence suggest a modulatory effect of thyrotropin-releasing hormone (TRH) on synaptic transmission in the mammalian neocortex. In the present study, the effects of this tripeptide on intracellularly recorded neocortical pyramidal neurons were investigated using rat in vitro brain slice preparations. TRH (5 microM and 50 microM) added to the perfusion medium concentration-dependently increased the excitability of pyramidal neurons, reflected by the number of spikes evoked by a depolarizing current pulse and by the augmentation of the time integral of glutamatergic excitatory postsynaptic potentials (EPSPs). TRH increased preferentially the time integrals of the late components of EPSPs (1-EPSPs) and increased their voltage-dependence. The early components of the EPSPs (e-EPSPs) were changed to much lesser extent. Iontophoretically applied D-2-amino-5-phosphonovalerate (D-APV) antagonized the TRH-induced increase of the 1-EPSPs. TRH also markedly enhanced the depolarizing responses evoked by iontophoretically applied N-methyl-D-aspartate (NMDA), while the depolarizing responses evoked by (R,S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and L-glutamate were not significantly affected. The depolarizing inward rectification present in all neurons studied was augmented by the higher concentration of TRH. The effects of TRH were incited after about 5 min and were long-lasting. In most neurons the effects of TRH on neuronal excitability did not completely recover during the 45 min washout period. The present data suggest that some of the non-hormonal actions of TRH in the neocortex may be due to an enhancement of glutamatergic synaptic transmission.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗

PubMed1992

Actions of vasoactive intestinal polypeptide (VIP) on neocortical neurons of the rat in vitro.

The action of vasoactive intestinal polypeptide (VIP) was studied using intracellular recording techniques in neocortical neurons of the rat in vitro. When added to the perfusion medium, VIP enhanced direct excitability and increased the amplitude of the excitatory postsynaptic potential (EPSP). Effects of VIP were long-lasting and in most cases not fully reversible within the observation period. The present results suggest a role for VIP in long-lasting peptidergic modulation of excitatory synaptic components as well as direct excitability of neocortical pyramidal neurons of the adult rat.

Animals↗

PubMed1991

Actions of noradrenaline on neocortical neurons in vitro.

The effects of noradrenaline (NA) and alpha- and beta-adrenergic agonists on neocortical neurons in rat brain slices were studied by intracellular recording. NA added to the perfusion medium decreased the orthodromically evoked excitatory postsynaptic potential (EPSP) and increased the neuronal excitability on current injection. The decrease of the EPSP by NA was mimicked by alpha-adrenoceptor activation. The beta-adrenergic agonist, isoprenaline, increased the neuronal excitability to current injections similarly to NA. In addition, isoprenaline markedly increased the amplitude of a late component of the EPSP (I-EPSP). The increase of the I-EPSP was long-lasting (up to 90 min). Since this late component of the EPSP is blocked by the NMDA (N-methyl-D-aspartate)-antagonist APV (D-2-amino-5-phosphonovalerate), an enhancement of this excitatory synaptic transient via beta-adrenoceptors may be relevant for the facilitatory effect of NA on neuronal plasticity.

2-Amino-5-phosphonovalerate↗

PubMed1987

[Doppler echocardiography normal values in various types of mitral valve prostheses].

To determine the value of Doppler echocardiography for the normal clinical use in functional diagnostics of prosthetic mitral valves, and to determine normal values for different types of prosthetic valves, 136 patients with different types of prosthetic mitral valves with the same external diameter (29 mm) were examined. For pressure half-time (t1/2) there were higher values for Starr-Edwards (SE) (n = 18) and Lillehei-Kaster (LK) prostheses (n = 10) (113 +/- 29 and 125 +/- 29 ms) than for Saint Jude-Medical (SJM) (n = 56), Björk-Shiley (BS) (n = 40) and Ionescu-Shiley valves (IS) (n = 12) (78 +/- 16, 82 +/- 17 and 93 +/- 28 ms, p less than 0.001), as well as for the orifice and for the mean diastolic gradient (delta p). The upper permissible limits of t1/2 and delta p were 104 ms and 4.1 mm Hg for SJM, and 111 and 4.8 for BS valves respectively. Day-to-day variability (n = 30) was 5.0% (0.0-14.4%, if t1/2 greater than 100 ms: 0.0-6.0%), the correlation was r = 0.97. The duration of implantation did not have any influence on prosthetic mitral valve function. These normal values and limits form a basis for the evaluation of prosthetic mitral valves in the future.

Adult↗