The Effect of Propofol Anesthesia on Rebound Spiking

Data show a relationship of cellular resonance and network oscillations in the entorhinal cortex to the spatial periodicity of grid cells. This paper presents a model that simulates the resonance and rebound spiking properties of entorhinal neurons to generate spatial periodicity dependent upon phasic input from medial septum. The model shows that a difference in spatial periodicity can result from a difference in neuronal resonance frequency that replicates data from several experiments. The model also demonstrates a functional role for the phenomenon of theta cycle skipping in the medial entorhinal cortex.

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Rebound Spiking as a Neural Mechanism for Surface Filling-in

Journal of Cognitive Neuroscience ◽

10.1162/jocn.2010.21512 ◽

2011 ◽

Vol 23 (2) ◽

pp. 491-501 ◽

Cited By ~ 6

Author(s):

Hans Supèr ◽

August Romeo

Keyword(s):

Computational Modeling ◽

Visual Information ◽

Sensory Information ◽

Neural Mechanism ◽

Photoreceptor Cells ◽

Blind Spot ◽

Visual Signals ◽

Surround Inhibition ◽

Surface Filling ◽

Rebound Spiking

Perceptual filling-in is the phenomenon where visual information is perceived although information is not physically present. For instance, the blind spot, which corresponds to the retinal location where there are no photoreceptor cells to capture the visual signals, is filled-in by the surrounding visual signals. The neural mechanism for such immediate filling-in of surfaces is unclear. By means of computational modeling, we show that surround inhibition produces rebound or after-discharge spiking in neurons that otherwise do not receive sensory information. The behavior of rebound spiking mimics the immediate surface filling-in illusion observed at the blind spot and also reproduces the filling-in of an empty object after a background flash, like in the color dove illusion. In conclusion, we propose rebound spiking as a possible neural mechanism for surface filling-in.

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Normal and rebound impulse firing in retinal ganglion cells

Visual Neuroscience ◽

10.1017/s0952523807070101 ◽

2007 ◽

Vol 24 (1) ◽

pp. 79-90 ◽

Cited By ~ 14

Author(s):

PRATIP MITRA ◽

ROBERT F. MILLER

Keyword(s):

Action Potential ◽

Retinal Ganglion Cells ◽

Visual Information ◽

Ganglion Cells ◽

Resting Membrane Potential ◽

Voltage Response ◽

Retinal Ganglion ◽

Action Potential Firing ◽

Impulse Frequency ◽

Rebound Spiking

Given that the action potential output of retinal ganglion cells (RGCs) determines the nature of the visual information that is transmitted from the retina, an understanding of their intrinsic impulse firing characteristics is critical for an appreciation of the overall processing of visual information. Recordings from RGCs within an isolated whole-mount retina preparation showed that their normal impulse firing from the resting membrane potential (RMP) was linearly correlated in its frequency with the stimulus intensity. In addition to describing the relationship between the magnitude of the current injection and the resulting impulse frequency (F/I relationship), we have characterized the properties of individual action potentials when they are elicited from the RMP. In contrast, hyperpolarizing below the RMP revealed that RGCs displayed a time dependent anomalous rectification, manifested by the appearance of a depolarizing sag in their voltage response. When an adequate period of hyperpolarization was terminated, a fast phasic period of “rebound excitation” was observed, characterized by a brief phasic burst of impulse activity. When compared to equivalent action potential firing evoked by depolarizing from the RMP, rebound spiking was associated with a lower threshold and shorter latency for impulse activation as well as a prominent, phasic, burst-like doublet, or triplet of impulses. The rebound action potential had a more positive voltage overshoot and displayed a higher peak rate of rise in its upstroke than those correspondingly generated by depolarizing current pulses from the RMP. Blocking sodium spikes with TTX confirmed that the preceding hyperpolarization led to the recruitment and subsequent generation of a transient depolarizing voltage overshoot, which we have termed the net depolarizing overshoot (NDO). We propose that the NDO boosts the generation of sodium spikes by triggering rebound spikes on its upstroke and crest, thus accounting for the observed voltage dependent change in the firing pattern of RGCs.

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Intrinsic and synaptic homeostatic plasticity in motoneurons from mice with glycine receptor mutations

Journal of Neurophysiology ◽

10.1152/jn.00728.2013 ◽

2014 ◽

Vol 111 (7) ◽

pp. 1487-1498 ◽

Cited By ~ 12

Author(s):

M. A. Tadros ◽

K. E. Farrell ◽

P. R. Schofield ◽

A. M. Brichta ◽

B. A. Graham ◽

...

Keyword(s):

Glycine Receptor ◽

Firing Frequency ◽

Homeostatic Plasticity ◽

Current Decay ◽

Decay Times ◽

Brainstem Slices ◽

The Difference ◽

Rebound Spiking ◽

Whole Cell Recordings

Inhibitory synaptic inputs to hypoglossal motoneurons (HMs) are important for modulating excitability in brainstem circuits. Here we ask whether reduced inhibition, as occurs in three murine mutants with distinct naturally occurring mutations in the glycine receptor (GlyR), leads to intrinsic and/or synaptic homeostatic plasticity. Whole cell recordings were obtained from HMs in transverse brainstem slices from wild-type ( wt), spasmodic ( spd), spastic ( spa), and oscillator ( ot) mice (C57Bl/6, approximately postnatal day 21). Passive and action potential (AP) properties in spd and ot HMs were similar to wt. In contrast, spa HMs had lower input resistances, more depolarized resting membrane potentials, higher rheobase currents, smaller AP amplitudes, and slower afterhyperpolarization current decay times. The excitability of HMs, assessed by “gain” in injected current/firing-frequency plots, was similar in all strains whereas the incidence of rebound spiking was increased in spd. The difference between recruitment and derecruitment current (i.e., Δ I) for AP discharge during ramp current injection was more negative in spa and ot. GABAA miniature inhibitory postsynaptic current (mIPSC) amplitude was increased in spa and ot but not spd, suggesting diminished glycinergic drive leads to compensatory adjustments in the other major fast inhibitory synaptic transmitter system in these mutants. Overall, our data suggest long-term reduction in glycinergic drive to HMs results in changes in intrinsic and synaptic properties that are consistent with homeostatic plasticity in spa and ot but not in spd. We propose such plasticity is an attempt to stabilize HM output, which succeeds in spa but fails in ot.

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The mechanism of ethanol action on midbrain dopaminergic neuron firing: a dynamic-clamp study of the role of Ih and GABAergic synaptic integration

Journal of Neurophysiology ◽

10.1152/jn.00162.2011 ◽

2011 ◽

Vol 106 (4) ◽

pp. 1901-1922 ◽

Cited By ~ 30

Author(s):

Takashi Tateno ◽

Hugh P. C. Robinson

Keyword(s):

Hcn Channels ◽

Dynamic Clamp ◽

Gabaergic Interneurons ◽

Channel Current ◽

Midbrain Dopaminergic Neuron ◽

Rebound Spiking ◽

Perforated Patch Clamp ◽

Clamp Study

Hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels are expressed in dopaminergic (DA) neurons of the ventral tegmental area (VTA) as well as in DA and GABAergic neurons of the substantia nigra (SN). The excitation of DA neurons induced by ethanol has been proposed to result from its enhancing HCN channel current, Ih. Using perforated patch-clamp recordings in rat midbrain slices, we isolated Ih in these neurons by voltage clamp. We showed that ethanol reversibly increased the amplitude and accelerated the activation kinetics of Ih and caused a depolarizing shift in its voltage dependence. Using dynamic-clamp conductance injection, we injected artificial Ih and fluctuating GABAergic synaptic conductance inputs into neurons following block of intrinsic Ih. This demonstrated directly a major role of Ih in promoting rebound spiking following phasic inhibition, which was enhanced as the kinetics and amplitude of Ih were changed in the manner induced by ethanol. Similar effects of ethanol were observed on Ih and firing rate in non-DA, putatively GABAergic interneurons, indicating that in addition to its direct effects on firing, ethanol will produce large changes in the inhibition and disinhibition (via GABAergic interneurons) converging on DA neurons. Thus the overall effects of ethanol on firing of DA cells of the VTA and SN in vivo, and hence on phasic dopamine release in the striatum, appear to be determined substantially by its action on Ih in both DA cells and GABAergic interneurons.

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Fast A-type currents shape a rapidly adapting form of delayed short latency firing of excitatory superficial dorsal horn neurons that express the NPY Y1 receptor

10.1101/2021.02.18.431823 ◽

2021 ◽

Author(s):

Ghanshyam P. Sinha ◽

Pranav Prasoon ◽

Bret N. Smith ◽

Bradley K. Taylor

Keyword(s):

Spinal Cord ◽

Dorsal Horn ◽

Short Latency ◽

Superficial Dorsal Horn ◽

Firing Patterns ◽

Future Studies ◽

Dorsal Horn Neurons ◽

Y1 Receptor ◽

Reporter Mice ◽

Rebound Spiking

ABSTRACTNeuroanatomical and behavioral evidence indicates that neuropeptide Y Y1 receptor-expressing interneurons (Y1-INs) in the superficial dorsal horn (SDH) are predominantly excitatory and contribute to chronic pain. Using an adult ex vivo spinal cord slice preparation from Y1eGFP reporter mice, we characterized firing patterns in response to steady state depolarizing current injection of GFP-positive cells in lamina II, the great majority of which expressed Y1 mRNA (88%). Randomly sampled and Y1eGFP neurons exhibited five firing patterns: tonic (TF), initial burst (IBF), phasic (PF), delayed short-latency <180 ms (DSLF), and delayed long-latency >180 ms (DLLF). When studied at resting membrane potential, most RS neurons exhibited delayed firing, while most Y1eGFP neurons exhibited phasic firing and not delayed firing. A preconditioning membrane hyperpolarization produced only subtle changes in the firing patterns of randomly sampled neurons, but dramatically shifted Y1eGFP neurons to DSLF (46%) and DLLF (24%). In contrast to randomly sampled DSLF neurons which rarely exhibited spike frequency adaptation, Y1eGFP DSLF neurons were almost always rapidly adapting, a characteristic of nociceptive-responsive SDH neurons. Rebound spiking was more prevalent in Y1eGFP neurons (6% RS vs 32% Y1eGFP), indicating enrichment of T-type calcium currents. Y1eGFP DSLF neurons exhibited fast A-type potassium currents that are known to delay or limit action potential firing, and these were of smaller current density as compared to randomly sampled DSLF neurons. Our results inspire future studies to determine whether tissue or nerve injury downregulates channels that contribute to A-currents, thus potentially unmasking T-type calcium channel activity and membrane hyperexcitability in Y1-INs, leading to persistent pain.KEYPOINTSNeuropeptide Y Y1 receptor-expressing neurons in the dorsal horn of the spinal cord contribute to chronic pain.For the first time, we characterized the firing patterns of Y1-expressing neurons in Y1eGFP reporter mice.Under hyperpolarized conditions, most Y1eGFP neurons exhibited fast A-type potassium currents and delayed, short-latency firing (DSLF).Y1eGFP DSLF neurons were almost always rapidly adapting and often exhibited rebound spiking, characteristics of spinal pain neurons under the control of T-type calcium channels.These results inspire future studies to determine whether tissue or nerve injury downregulates the channels that underlie A-currents, thus unmasking membrane hyperexcitability in Y1- expressing dorsal horn neurons, leading to persistent pain

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