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von Gersdorff, H.

Publications and source records attributed to von Gersdorff, H..

10 recordsLinked to original sources

Pre-Sensory Spontaneous Activity Accelerates Coordinated Maturation of Synaptic Partners and Drives Transition to the Mature Physiological Phenotype

Pre-sensory (ps), peripherally-generated spontaneous activity (SA) is important for establishing basic topography of central components of sensory pathways. However, roles for psSA in sculpting connections at the single neuron level and in driving functional maturation of postsynaptic targets are difficult to isolate and therefore little explored. We capitalized on the temporal onset of cochlea-generated psSA just prior to growth of the calyx of Held (CH), the largest nerve terminal in the mammalian brain, and its well-defined circuit topography to explore the causal roles for psSA in targeted synaptogenesis and postsynaptic functional maturation. To this end, we developed a viral vector to rapidly express tetanus neurotoxin (TeNT), which blocks neurotransmission, and selectively introduced it into CH-forming neurons at the onset of psSA. TeNT expression did not prevent but delayed and altered the developmental trajectory of neural circuit maturation, which in sum prevented the postsynaptic neuron from acquiring its mature phasic firing phenotype. Thus, psSA initiates and drives circuit maturation along central sensory pathways, but alternative mechanisms can partially compensate in its absence.

neuroscience↗

Astrocyte gap junctions and Kir channels contribute to K+ buffering and regulate neuronal excitability

ABSRACTAstrocytes are connected in a functional syncytium via gap junctions, which is thought to contribute to maintenance of extracellular K+ homeostasis. The prevailing hypothesis is that K+ released during neuronal firing is taken up by astrocytes via Kir channels and then distributed among neighboring astrocytes via gap junctions. Previous reports examining the role of Kir channels and gap junctions have shown both hyperexcitability and depression when each mechanism is blocked. Here, we tested the effect of blocking Kir channels and gap junctions, both independently and simultaneously, on field activity of cortical slices in response to a 3 s, 20 Hz stimulation train. Independently blocking either Kir channels or gap junctions increased the amplitude of the first fEPSC (field excitatory post-synaptic current) in response to a stimulation train, followed by suppression of fEPSCs during sustained stimulation. Surprisingly, blocking both gap junctions and Kir channels enhanced the suppression of neuronal activity, resulting in a [~]75% decrease in fiber volley (pre-synaptic action potentials) amplitude in the first response, followed by a fast and strong suppression of sustained fEPSCs. Our results demonstrate that blocking Kir channels and gap junctions can increase the excitability of neurons when firing is sparse, but suppression results when the firing frequency is increased to cortical physiological ranges. This suggest that K+ buffering via Kir and gap junctions, likely mediated by astrocytes, together play a critical role in maintaining neuronal excitability, particularly during sustained activity.

neuroscience↗

Synaptic facilitation enhances the reliability and precision of high frequency neurotransmission

The small and tortuous volume of synaptic clefts limits the diffusion of Ca2+ ions during high frequency spiking. Extracellular Ca2+ levels ([Ca2+]o) of 0.8 mM or lower have been measured or calculated for different synapses. Here, we recorded evoked postsynaptic potentials (EPSP) and action potentials (AP) from young adult male and female mouse auditory brainstem principal neurons to investigate the relationship between neurotransmission reliability, stimulation frequency and [Ca2+]o. In 0.8 mM [Ca2+]o, we observed AP failures during afferent fiber stimulation at 100 Hz. Surprisingly, AP failures, EPSP-AP latency and jitter were all greatly reduced when stimulation frequency was increased to 500 Hz. Analysis of the EPSP/AP waveform revealed marked facilitation at 500 Hz that was not present at 100 Hz. Raising [Ca2+]o to 1.2 mM or 2.0 mM reduced or eliminated facilitation and, in these conditions, stimulation at 500 Hz increased the number of AP failures. In 0.8 mM [Ca2+]o, afferent fiber stimulation over a broad range of frequencies from 10-1000 Hz produced three different types of spiking responses: Type I cells exhibited band-pass filtering, with best response at approximately 500 Hz, Type II cells exhibited low-pass filtering above 600 Hz, and Type III cells exhibited shallow band-pass filtering centered at approximately 300 Hz. To predict AP success or failure, we built a model based on three factors: size of the EPSP, membrane potential immediately prior to the synaptic event and the number of preceding failures. We conclude that synaptic facilitation can contribute positively to the maintenance of reliable and precise high frequency neurotransmission in the auditory brainstem. Significance StatementFacilitation of evoked postsynaptic currents is a common feature of synapses. The strength of facilitation and its role in reaching spike threshold depends on intrinsic properties of the synapse, stimulation frequency, and extracellular Ca2+ concentration ([Ca2+]o). Physiological levels of [Ca2+]o can vary from 0.8 to 1.2 mM depending on synaptic activity. In the mouse Medial Nucleus of the Trapezoid Body, synaptic facilitation is readily observable in slice experiments using relatively low (0.8 mM) [Ca2+]o, but is partially or completely obscured by short-term synaptic depression when [Ca2+]o is high (1.2 or 2.0 mM). Here we show that facilitation can rescue the reliability of high-frequency (500 Hz) action potential firing in low [Ca2+]o, resulting in band-pass filter transmission.

neuroscience↗

Dopamine regulates the membrane potential and glycine release of AII amacrine cells via D1-like receptor modulation of gap junction coupling.

Dopamine plays a pivotal role in adjusting the flow of information across the retina as luminance changes from night to day. Here we show, under dim photopic conditions, that both dopamine and a D1-like receptor (D1R) agonist hyperpolarized the resting membrane potential (Vm) of AII amacrine cells (AII-ACs). Surprisingly, in the presence of glutamatergic and GABAergic synaptic blockers that isolate glycinergic synapses, D1R agonists are without effect. However, a D1R antagonist depolarized Vm and reduced the input resistance of AII-ACs in wild type mice, but not in Cx36-/- mice. Accordingly, D1R antagonists enhanced tonic glycinergic transmission to type-2 OFF-cone bipolar cells (OFF-CBCs). D1Rs thus adjust the Vm and excitability of AII-ACs and, thereby, the level of glycine release to OFF-CBCs by regulating gap junction coupling with ON cone bipolar cells. Our findings provide insights into how the retina may use dopamine to adapt crossover inhibitory microcircuits during changes in luminance.

neuroscience↗

Cortical Betz cells analogue in songbirds utilizes Kv3.1 to generate ultranarrow spikes

Complex motor skills in vertebrates require specialized upper motor neurons with precise action potential (AP) firing. To examine how diverse populations of upper motor neurons subserve distinct functions and the specific repertoire of ion channels involved, we conducted a thorough study of the excitability of upper motor neurons controlling somatic motor function in the zebra finch. We found that robustus arcopallialis projection neurons (RAPNs), key command neurons for song production, exhibit ultranarrow spikes and higher firing rates compared to neurons controlling non-vocal somatic motor functions (AId neurons). This striking difference was primarily due to the expression of a high threshold, fast-activating voltage-gated K+ channel, Kv3.1 (KCNC1). RAPN properties thus mirror those of the sparse, specialized Betz cells in the motor cortex of humans and other primates, which also fire ultranarrow spikes enabled by Kv3.1 expression. These large layer 5 pyramidal neurons are involved in fine digit control and are notably absent in rodents. Our study thus provides evidence that songbird RAPNs and primate Betz cells have convergently evolved the use of Kv3.1 to ensure precise, rapid AP firing required for fast and complex motor skills.

neuroscience↗

Trophoblast glycoprotein is required for efficient synaptic vesicle exocytosis from retinal rod bipolar cells.

Rod bipolar cells (RBCs) faithfully transmit light-driven signals from rod photoreceptors in the outer retina to third order neurons in the inner retina. Recently, significant work has focused on the role of leucine-rich repeat (LRR) proteins in synaptic development and signal transduction at RBC synapses. We previously identified trophoblast glycoprotein (TPBG) as a novel transmembrane LRR protein localized to the dendrites and axon terminals of RBCs. We now examine the effects on RBC physiology and retinal processing of TPBG genetic knockout in mice using immunofluorescence and electrophysiological techniques. The scotopic electroretinogram showed a modest increase in the b-wave and a marked attenuation in oscillatory potentials in the TPBG knockout. No effect of TPBG knockout was observed on the RBC dendritic morphology, TRPM1 currents, or RBC excitability. Because scotopic oscillatory potentials primarily reflect RBC-driven rhythmic activity of the inner retina, we investigated the contribution of TPBG to downstream transmission from RBCs to third-order neurons. Using electron microscopy, we found shorter synaptic ribbons in TPBG knockout axon terminals in RBCs. Time-resolved capacitance measurements indicated that TPBG knockout reduces synaptic vesicle exocytosis and subsequent GABAergic reciprocal feedback without altering voltage-gated Ca2+ currents. Thus, TPBG is required for normal synaptic ribbon development and efficient neurotransmitter release from RBCs to downstream cells. Our results highlight a novel synaptic role for TPBG at RBC ribbon synapses and support further examination into the mechanisms by which TPBG regulates RBC physiology. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/501380v2_ufig1.gif" ALT="Figure 1"> View larger version (18K): org.highwire.dtl.DTLVardef@13d5916org.highwire.dtl.DTLVardef@a3c259org.highwire.dtl.DTLVardef@12c74e0org.highwire.dtl.DTLVardef@1ad43a8_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

A subtype of melanopsin ganglion cells encodes ground luminance

Visual input to the hypothalamus from intrinsically photosensitive retinal ganglion cells (ipRGCs) influences several functions including circadian entrainment, body temperature, and sleep. ipRGCs also project to nuclei such as the supraoptic nucleus (SON), which is involved in systemic fluid homeostasis, maternal behavior, and appetite. However, little is known about the SON-projecting ipRGCs or their relationship to well-characterized ipRGC subtypes. Using a GlyT2Cre mouse line, we identify a subtype of ipRGCs restricted to the dorsal retina that selectively project to the SON. These ipRGCs form a non-overlapping tiled mosaic that is limited to a dorsal region of the retina, forming a substrate for encoding ground luminance. Optogenetic activation of their axons demonstrates they release the neurotransmitter glutamate and that the SON is retinorecipient, receiving synaptic input from dorsal ipRGCs. Our results challenge the idea that ipRGC dendrites overlap to optimize photon capture and suggests non-image forming vision operates to sample local regions of the visual field.

neuroscience↗

Resurgent Na+ currents promote ultrafast spiking in projection neurons that drive fine motor control

The underlying mechanisms that promote precise spiking in upper motor neurons controlling fine motor skills are not well understood. Here we report that projection neurons in the adult zebra finch song nucleus RA display: 1) robust high-frequency firing, 2) ultra-short half-width spike waveforms, 3) superfast Na+ current inactivation kinetics and 4) large resurgent Na+ currents (INaR). These spiking properties closely resemble those of specialized pyramidal neurons in mammalian motor cortex and are well suited for precise temporal coding. They emerge during the critical period for vocal learning in males but not females, coinciding with a complete switch of modulatory Na+ channel subunit expression from Nav{beta}3 to Nav{beta}4. Dynamic clamping and dialysis of Nav{beta}4s C-terminal peptide into juvenile RA neurons provide evidence that this subunit, and its associated INaR, promote neuronal excitability. We propose that Nav{beta}4 underpins INaR that facilitates precise, prolonged, and reliable high-frequency firing in upper motor neurons.

neuroscience↗

Dendritic speeding of synaptic potentials in an auditory brainstem principal neuron

Principal cells of the medial nucleus of the trapezoid body (MNTB) in the mammalian auditory brainstem receive most of their strong synaptic inputs directly on the cell soma. However, these neurons also grow extensive dendrites during the first four postnatal weeks. What are the functional roles of these dendrites? We studied the morphology and growth of the dendrites in the mouse MNTB using both electron microscopy and confocal fluorescence imaging from postnatal day 9 (P9; pre-hearing) to P30. The soma of principal cells sprouted 1 to 3 thin dendrites (diameter ~ 1.5 microns) by P21 to P30. Each dendrite bifurcated into 2-3 branches and spanned an overall distance of about 80 to 200 microns. By contrast, at P9-11 the soma had 1 to 2 dendrites that extended for only 25 microns on average. Patch clamp experiments revealed that the growth of dendrites during development correlates with a progressive decrease in the input resistance, whereas acute removal of dendrites during brain slicing leads to higher input resistances. Accordingly, recordings of excitatory postsynaptic potentials (EPSPs) evoked by afferent fiber stimulation show that EPSP decay is faster in P21-24 neurons with intact dendrites than in neurons without dendrites. This dendritic speeding of the EPSP reduces the decay time constant 5-fold, which will impact significantly synaptic current summation and the ability to fire high-frequency spike trains. These data suggest a novel role for dendrites in auditory brainstem neurons: the speeding of EPSPs for faster and more precise output signal transfer.\n\nSignificance StatementAuditory circuits that compute sound localization express different types of specialized synapses. Some are capable of fast, precise and sustained synaptic transmission. As the paradigm example, principal cells of the MNTB receive a single calyx-type nerve terminal on their soma and this large excitatory synapse produces fast and brief supra-threshold EPSPs that can trigger trains of high frequency spikes. However, these neurons also extend thin and long dendrites with unknown function. We examined the relationship between dendritic morphology, passive electrical properties and EPSP waveform. We found that more mature neurons with intact dendrites have lower input resistances and short EPSP waveforms, ideally suited for conveying precise timing information, whereas immature neurons with shorter dendrites and higher input resistance have longer lasting EPSPs.

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How to build a fast and highly sensitive sound detector that remains robust to temperature shifts

Frogs must have sharp hearing abilities during the warm summer months to successfully find mating partners. This study aims to understand how frog hair cell ribbon-type synapses preserve both sensitivity and temporal precision during temperature changes. We performed in vitro patch-clamp recordings of hair cells and their afferent fibers in bullfrog amphibian papillae under room (23-25{degrees}C) and high (30-33{degrees}C) temperature. Afferent fibers exhibited a wide heterogeneity in membrane input resistance (Rin) from 100 M{Omega} to 1000 M{Omega}, which may contribute to variations in spike threshold and firing frequency. At higher temperatures, most fibers increased their frequency of action potential firing due to an increase in spontaneous EPSC frequencies. Hair cell resting membrane potential (Vrest) remained surprisingly stable during temperature increases, although both inward Ca2+ current and outward K+ current increased in amplitude. This increase in Ca2+ current may explain the higher spontaneous EPSC frequencies. The larger \"leak currents\" at Vrest lowered Rin and produced higher electrical resonant frequencies. However, lower Rin should decrease sensitivity to sound detection via smaller receptor potentials. Using membrane capacitance measurements, we suggest that hair cells can partially compensate for this reduced sensitivity by increasing exocytosis efficiency and the size of the readily releasable pool of synaptic vesicles. Furthermore, paired recordings of hair cells and their afferent fibers showed that synaptic delays become shorter and multivesicular release becomes more synchronous at higher temperatures, which should improve temporal precision. Altogether, our results explain many previous in vivo observations on the temperature dependence of spikes in auditory nerves.\n\nSignificance StatementThe vertebrate inner ear detects and transmits auditory information over a broad dynamic range of sound frequency and intensity. It achieves remarkable sensitivity to soft sounds and precise frequency selectivity. How does the ear of cold-blooded vertebrates maintain its performance level as temperature changes? More specifically, how does the hair cell to afferent fiber synapse in bullfrog amphibian papilla adjust to a wide range of physiological temperatures without losing its sensitivity and temporal fidelity to sound signals? This study uses in vitro experiments to reveal the biophysical mechanisms that explain many observations made from in vivo auditory nerve fiber recordings. We find that higher temperature facilitates vesicle exocytosis and electrical tuning to higher sound frequencies, which benefits sensitivity and selectivity.

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