Biomedical subjects

Udo Kraushaar

Publications and source records attributed to Udo Kraushaar.

3 recordsLinked to original sources

PubMed2005

Inhibitory postsynaptic potentials carry synchronized frequency information in active cortical networks.

Temporal precision in spike timing is important in cortical function, interactions, and plasticity. We found that, during periods of recurrent network activity (UP states), cortical pyramidal cells in vivo and in vitro receive strong barrages of both excitatory and inhibitory postsynaptic potentials, with the inhibitory potentials showing much higher power at all frequencies above approximately 10 Hz and more synchrony between nearby neurons. Fast-spiking inhibitory interneurons discharged strongly in relation to higher-frequency oscillations in the field potential in vivo and possess membrane, synaptic, and action potential properties that are advantageous for transmission of higher-frequency activity. Intracellular injection of synaptic conductances having the characteristics of the recorded EPSPs and IPSPs reveal that IPSPs are important in controlling the timing and probability of action potential generation in pyramidal cells. Our results support the hypothesis that inhibitory networks are largely responsible for the dissemination of higher-frequency activity in cortex.

Action Potentials↗

PubMed2002

Characterization of GABA(A) and glycine receptors in neurons of the developing rat inferior colliculus.

GABA(A) receptors (GABA(A)Rs) and glycine receptors (GlyRs) expressed in developing neurons (P3-8) of the rat inferior colliculus (IC) were investigated using fast application of transmitters on nucleated patches and whole-cell patch-clamp recordings. At a holding potential of -60 mV and an E(Cl) close to 0 mV GABA and glycine activated inward currents with a half-maximal activation concentration of 127 microM and 353 microM, respectively. GABA(A)Rs activated and deactivated significantly faster than GlyRs (20-80% rise-time: 0.71 ms for GABA(A)Rs and 1.31 ms for GlyRs; amplitude-weighted decay time constant, tau(w), 22.4+/-1.3 ms for GABA(A)Rs and 108.7+/-32.9 ms for GlyRs). The tau(w) values for receptor desensitization were 26.8+/-1.9 ms for GABA(A)Rs and 177.9+/-47.2 ms for GlyRs. Recovery from desensitization was significantly faster for GlyRs (tau=334 ms) than for GABA(A)Rs (tau1=82 ms; tau2=3783 ms). The tau(w) values of GABA(A)R-mediated spontaneous and miniature inhibitory postsynaptic currents were not significantly different from those of GABA(A)Rs activated by fast application, but significantly different to the tau(w) of GlyRs activated by fast application. The different properties of GABA(A)Rs and GlyRs expressed in the same IC neuron suggest a distinct functional contribution to the development of inhibitory synapses in the IC.

Aging↗

PubMed2002

Presynaptic short-term depression is maintained during regulation of transmitter release at a GABAergic synapse in rat hippocampus.

To examine possible interactions between fast depression and modulation of inhibitory synaptic transmission in the hippocampus, we recorded from pairs of synaptically connected basket cells (BCs) and granule cells (GCs) in the dentate gyrus of rat brain slices at 34 degrees C. Multiple-pulse depression (MPD) was examined in trains of 5 or 10 inhibitory postsynaptic currents (IPSCs) evoked at frequencies of 10-100 Hz under several conditions that inhibit transmitter release: block of voltage-dependent Ca2+ channels by Cd2+ (10 microM), activation of gamma-amino-butyric acid type B receptors (GABA(B)Rs) by baclofen (10 microM) and activation of muscarinic acetylcholine receptors (mAchRs) by carbachol (2 microM). All manipulations led to a substantial inhibition of synaptic transmission, reducing the amplitude of the first IPSC in the train (IPSC1) by 72%, 61% and 29%, respectively. However, MPD was largely preserved under these conditions (0.34 in control versus 0.31, 0.50 and 0.47 in the respective conditions at 50 Hz). Similarly, a theta burst stimulation (TBS) protocol reduced IPSC1 by 54%, but left MPD unchanged (0.40 in control and 0.39 during TBS). Analysis of both fractions of transmission failures and coefficients of variation (CV) of IPSC peak amplitudes suggested that MPD had a presynaptic expression site, independent of release probability. In conclusion, different types of presynaptic modulation of inhibitory synaptic transmission converge on a reduction of synaptic strength, while short-term dynamics are largely unchanged.

Animals↗