Nerve Spike Research Articles

A Model of Frequency Coding in the Central Auditory Nervous System

A phenomenological model for neural coding in the central auditory system is presented. This model is based on average rate-place codes and the hypothesis is that the rate-place code present in the population of low spontaneous rate nerve fibres is adequate to account for frequency discrimination thresholds across the entire audible frequency range. The activity of a population of nerve fibres in response to an input pure tone is calculated and a neural spike train pattern is generated. An optimal central observer estimates the input frequency from the spike train pattern. The model output is the frequency difference limen at the specific input frequency, determined from the estimated input frequency. It is shown that a rate-place code can account for psychoacoustically observed frequency difference limens. The model also supports the hypothesis that a human listener does not make full use of all the information relevant to frequency that is available in auditory nerve spike trains.

Ingestion of sugar diets correlates with spike activity in labellar chemosensilla of the flesh‐fly,Neobellieria(=Sarcophaga)bullata

Abstract.Female 2‐day‐old Neobellieria (= Sarcophaga) bullata (Parker) (Diptera: Sarcophagidae) were exposed to different concentrations of sucrose, glucose and fructose in a single‐choice potometer, and the volume ingested in the first hour was measured. Nerve spike activity in response to the same sugars was recorded from medium labellar taste hairs of similar flies by tip‐recording. Two classes of chemosensory cells responded to sucrose, glucose and fructose. Cell 1 showed an increasing spike activity with sugar concentration, whereas cell 2 did not; cell 1 was identified as the ‘sugar cell'.For both spike activity in cell 1 and feeding, sucrose was the most stimulatory sugar. The dose–response curves for glucose and fructose crossed over at about 200 mm. At higher concentrations, glucose was more stimulatory for both cell 1 and for feeding, and at lower concentrations, fructose. The pattern of spike activity supports a separate location on the sensory cells of receptors for pyranose and fructose forms of sugar. The strong correlation between volume ingested and spike activity indicates that sugar feeding is controlled by sensory input from the ‘sugar' cells of labellar chemosensilla. Moreover, the results suggest that the flies do not distinguish between these sugars except by apparent ‘sweetness'.

Mode of action of β-carboline convulsants on the insect nervous system and their potential as insecticides

Little information is available on the actions of β-carboline convulsants on insect GABA receptors or their potential as insecticides. Accordingly, two compounds (3-ethoxy-β-carboline, 3-EBC; dimethoxy-β-carboline-3-methyl ester, DMCM) were studied for their effects on Drosophila melanogaster larval neuron discharge and also in lethality bioassays on adult female D. melanogaster and adult male Blattella germanica. Recordings of nerve spiking in the isolated larval central nervous system showed that 3-EBC and DMCM inhibited nerve discharge, and this inhibitory effect was not additive with that of GABA, confirming that the inhibition was expressed through an action on the GABA receptor. Nerve blockage induced by β-carbolines could not be reversed by picrotoxinin, indicating that there may exist some overlap or negative allosteric coupling between the picrotoxinin and β-carboline binding sites. DMCM and 3-EBC effectively antagonized the effects of exogenously applied GABA in nerve preparations from insecticide-susceptible larvae. In contrast, preparations from the rdl strain of D. melanogaster, which possesses a GABA receptor that is highly resistant to cyclodienes and related convulsants, were less sensitive to the GABA antagonist effect of DMCM. Neither of the β-carbolines produced any appreciable mortality in insects, even when synergized with piperonyl butoxide or S,S,S-tributyl phosphorotrithioate, The toxicity of the β-carbolines is probably limited by their relatively weak effects on the GABA receptor and perhaps also by pharmacokinetic factors. These considerations, coupled with the cross-resistance observed in cyclodiene-resistant insects, suggest that the currently available β-carbolines are not viable as lead compounds for insecticide screening efforts. © 1997 SCI.

Is loudness simply proportional to the auditory nerve spike count?

It is often asserted that the physiological correlate of loudness is the simple sum of the spike activity produced by all neurons in the auditory nerve (the auditory nerve spike count). We will refer to this hypothesis as the spike count hypothesis. The spike count hypothesis has been tested in the past using models of the auditory periphery and in almost all cases, the hypothesis has been supported. Our new technique for recording a compound potential from the chinchilla auditory nerve, the perstimulus compound action potential (PCAP), makes possible the measurement of the growth of the auditory nerve spike count, thus providing data that can be used to test the spike count hypothesis empirically. It was observed that the growth of the auditory nerve spike count in response to a 1-kHz pure tone (in dB/dB) is 33% shallower than the growth of loudness for a 1-kHz tone, and this discrepancy increases to 66% for an 8-kHz tone. In addition, "equal-count" contours were constructed in a manner analogous to equal-loudness contours. It was found that as reference intensity increases, equal-count contours become sharply curved upward at high frequencies whereas equal-loudness contours become increasingly flat. These differences are unlikely to be the result of the cross-species comparison, since the discrepancies are mostly attributable to the skewed pattern of spread of excitation along the basilar membrane, a property shared by humans and chinchillas. Therefore, we conclude that the simple sum of the spike activity in the auditory nerve cannot be the physiological correlate of loudness.

Neural contributions to the perstimulus compound action potential: implications for measuring the growth of the auditory nerve spike count as a function of stimulus intensity.

The perstimulus compound action potential (PCAP), unlike the more familiar compound action potential (CAP), can be recorded in response to asynchronous as well as synchronous auditory nerve activity. When all neurons contribute equally to the PCAP, the area under the PCAP (the PCAP area) is proportional to the number of action potentials fired by auditory nerve neurons (the auditory nerve spike count). The auditory nerve spike count is one proposed code for stimulus intensity, and our goal is to use the PCAP to test this hypothesis. In this study, two independent tests were developed to measure the contributions of neurons to the PCAP as a function of their characteristic frequency (CF). The test results were verified using a model of the auditory periphery designed to calculate the auditory nerve spike count as a function of pure tone intensity and frequency. In nearly all experiments, neurons having CFs that span contiguous three or four octave bands contribute equally to the PCAP. For pure tones that stimulate only those neurons contributing equally to the PCAP, the PCAP area grows over intensity ranges frequently exceeding 80 dB, and in one case equaling 108 dB. These results demonstrate that the auditory nerve spike count, at least for pure tones, is capable of encoding changes in stimulus intensity over the entire dynamic range of the auditory system.

Energy detection and temporal integration in the noctuid A1 auditory receptor

The temporal integration of the A1 auditory receptor of two species of noctuid moths (Lepidoptera, Noctuidae) was investigated. Tympanal nerve spikes were recorded while stimulating the ear with broad band clicks. Thresholds were measured for single clicks, pairs of clicks with a separation of 1–20 ms, and trains of up to 8 clicks at separations of 1–2 ms. The average threshold for single clicks was 52.9 dB peSPL (SD 1.7 dB, n = 40) for Noctua pronuba and 50.1 dB peSPL (SD 4.0 dB, n = 27) for Spodoptera littoralis. The thresholds for double clicks with a 1 ms separation were lower than the thresholds for single clicks. The difference decreased as the separation between the clicks was increased. The results were fully consistent with an energy detector model (a leaky integrator with an exponential decay) with a time constant of about 4 ms. The results are compared to previously published results with pure tone intensity/duration trading. A common underlying mechanism is suggested, based on the passive electric properties of the receptor cell membrane. It is suggested, that the time constant revealed in the present study characterizes auditory receptors in general, and is related to the short time constants in vertebrate audition.

Depolarization is a critical event in hypoxia-induced glomus cell secretion.

Hypoxia chemotransduction within the carotid body is generally believed to be mediated by the glomus cells. Neurotransmitters (primarily dopamine) are stored within glomus cells in dense-cored vesicles, and catecholamine secretion is enhanced by hypoxia. Glomus cells are apposed to afferent terminals of the sinus nerve, and hypoxia-induced release of catecholamines leads to increased sinus nerve spiking activity. Two theories have evolved in an attempt to elucidate the cellular mechanisms involved in hypoxia-induced glomus cell secretion. In one model, hypoxia inhibits an oxygen-sensitive K+ channel, leading to depolarization, activation of voltage-dependent Ca2+ currents, and enhanced secretion of catecholamine due to increased intracellular calcium (Gonzalez et al, 1994). In support of this model, several investigators have observed an inhibition of glomus cell K+ current by hypoxia during patch-clamp recording of isolated glomus cells, and this inhibition appears to be correlated with an increase in [Ca2+]i and enhanced secretion (Montoro et al, 1996). In contrast, others have observed an increase in [Ca2+]i during hypoxia in the absence of extracellular calcium, implicating a second model, in which hypoxia causes release of calcium from intracellular stores, leading to enhanced secretion (Biscoe et al, 1989a; Biscoe & Duchen, 1990). In this second model, depolarization and calcium influx are not important events in the stimulus cascade. This is supported further by observations that membrane potential may actually hyperpolarize, rather than depolarize, during stimulation (Biscoe & Purves, 1989b).

A system for aligning video‐recorded visual data and high‐quality multichannel recordings of simultaneously occurring signals

SUMMARYAn electronic circuit is described which provides a unique number for each video frame, and which is superimposed on the frame as a 4‐digit light‐emitting diode display using a second camera and videomixer. The number is also encoded as a simple voltage waveform which is recorded separately together with electrical signals giving information about events related to, and coincident with, the visual data, for example nerve spike trains. Sophisticated computer analysis of signals can thus be related accurately to microscopical visual information processed by video analysis.

Amplitude enhancement is seen in the cochlear nerve but not at, or before, the afferent synapse

The amplitude of the cochlear nerve compound action potential (CAP) produced by a moderate intensity tonal stimulus (S 2) can be enhanced when S 2 is preceded by a low intensity S 1 of the same frequency. The presence of S 1, had no observable influence on the threshold of the CAP to S 2. Enhancement was not observed in the cochlear microphonics or summating potentials. Deactivation of the contralateral olivocochlear bundle did not influence enhancement. Tetrodotoxin (TTX) was applied to the round window to block cochlear nerve spike activity, resulting in a residual EPSP-like potential, as described in the guinea pig by Dolan et al. (1989). Kainic acid, in turn, eliminated this EPSP-like response. Even though some differences were found in the responses of the gerbil and their guinea pig preparation to TTX and kainic acid, enhancement was not observed in this residual potential. When enhancement was observed at the level of the CAP, it was also observed at brainstem levels. It is suggested that enhancement originates within the cochlear nerve axons.

Fractal patterns in auditory nerve-spike trains

The authors discuss the following topics: traditional renewal point process models; long-term correlations; self-similarity of neuronal firing rates; power-law behavior of the Fano-factor time curve; change in the firing pattern induced by the presence of a stimulus; neural information processing with fractal nerve spikes; biophysical origin of the fractal behavior; fractal point-process model; short-term correlations.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>

Modulation of cochlear nerve spike rate by cardiac activity in the gerbil

Among primary auditory axons with characteristic frequencies (CFs) below 2500 Hz, a substantial subpopulation was found in which spike activity was driven by cardiac events. The presence of cardiac-driven activity was inferred from cycle histograms triggered on the peak of the electrocardiogram (ECG). This driven activity was either like a simple onset response (often followed by a reduction of spike activity to below background level), or as a longer lasting series of peaks and troughs. In two axons with high CFs (7 kHz and 12.5 kHz), cardiac-driven suppression was observed. Recordings made by a probe microphone revealed the presence of heart-related sound in the external ear canal. The onset of that sound coincided with the onset of cardiac-driven spike activity (and suppression).

The neuroethology of sound production in tiger moths (Lepidoptera, Arctiidae)

When stimulated either acoustically or tactually, certain species of arctiid moths rhythmically emit trains of clicks from metathoracic tymbals. The purpose of the experiments presented here was to determine the location within the central nervous system (CNS) of the proposed tymbal central pattern generator (CPG) in Cycnia tenera. Motor neuron impulses that underlie tymbal activation were recorded extracellularly from the tymbal nerve while moths were subjected to selective severing of the suboesophageal, prothoracic, pterothoracic and abdominal ganglia connectives. Motor output evoked by either acoustic or tactile stimulation originates from a common CPG because tymbal nerve spikes in both cases are similar in amplitude, waveform and rhythmicity. Our results showed: (1) removal of the CNS posterior of the second abdominal neuromere had no effect, (2) removal of the head decreased the responsiveness of the animal to acoustic stimulation and, (3) severing the connectives between the prothoracic and pterothoracic ganglia abolished responses to acoustic stimuli and diminished responses to tactile stimuli. We conclude that although the minimal circuitry sufficient for activating the tymbals resides in the pterothoracic ganglion, the prothoracic and cephalic ganglia are required for the normal, and in particular, auditory-evoked operation of the tymbal CPG.

Role of sympathetic nerve inhibition in the vasodepressor effect of bromocriptine in normotensive and hypertensive rats.

This study aimed to elucidate the mechanism of the hypotensive effect of bromocriptine (BRC), and to investigate whether or not the effects of BRC on the sympathetic nervous system are altered in hypertension. BRC was administered intravenously to normotensive and spontaneously hypertensive rats (SHR). It elicited hypotensive effects dose-dependently in urethane-anaesthetized normotensive rats, an effect which was antagonized with metoclopramide. Pretreatment with intravenous hexamethonium attenuated the hypotensive effect of BRC. BRC decreased plasma norepinephrine (NE) without inhibiting the sympathetic nerve spikes recorded from the postganglionic sympathetic nerve bundle. The hypotensive effect of BRC was significantly greater in SHR than in Wistar Kyoto Rats (WKY). Decrease in NE by BRC was also significantly greater in SHR than in WKY. These results suggest that the hypotensive effect of BRC is induced by suppression of NE release, not by inhibition of sympathetic nerve spikes, and that the dopaminergic presynaptic inhibition is attenuated in SHR.

A slope-based approach to spike discrimination in digitized data

A spike discrimination algorithm based on the analysis of spike up- and down-slopes can advantageously replace those based only on amplitude with a minimal increase of programming complexity and processing time. Such an algorithm was developed to sort muscle depolarizations from nerve spikes in electromyograms in insects. It could also be used to sort spikes according to their direction of travel in bipolar recordings from mixed nerves.

Non equilibrium oscillatory relaxation processes across biological membranes

Linear phenomenological equations relating fluxes and driving forces have been largely employed in the study of several phenomena in synthetic membrane systems. 1 These equations contain drag coefficients fulfilling Onsager reciprocity relations. 2,3 Biological membranes are endowed with the ability to allow the transport of ions and molecules against their own concentration gradients. These processes are made thermodynamically possible by a coupled passive transport of another component driven by its own concentration gradient. This kind of coupling cannot be treated as an Onsager coupling. 1 A theory developed by A.M. Liquori to deal with these phenomena is further developed in order to study relaxations around the steady state of the non Onsager coupled diffusion of two components across a membrane microphase containing an allosteric protein in local thermodynamic equilibrium binding at the interphases between the membrane and the two bathing solutions. 1 Starting from two first order linear differential equations describing the two non Onsager coupled fluxes, two second order linear differential equations have been derived which are valid near the steady state. Their solutions correspond to damped oscillations around the steady state. 4 These solutions may be used to deal with the fluxes of Na + and K + across a nerve membrane following stimulation producing the typical temporal changes of electrical potential associated to a nerve spike. 5,6,7,8. It is shown that the “resting state” of a nerve membrane behaves as a “strange attractor” 4,9,10.

Effects of ionic and non-ionic solutions on intradental nerve activity in the cat

Intradental nerve activity (INA) was recorded from cat canine teeth to determine whether solutions altering intradental nerve sensitivity were strongly correlated to the osmotic concentration of the solution or via a more direct action on intradental nerve excitability. The effects of various ionic and non-ionic solutions were tested in both deep and shallow dentinal cavities. With saline in the deep dentinal cavity a very low firing rate or resting nerve spike (action potentials) activity was recorded. When 3 M NaCl was placed in the same or similar cavity a high discharge rate of nerve spike activity was obtained. This 3 M NaCl elicited activity was utilized to determine the inhibitory or excitatory effects of various test agents on the intradental nerves. The following agents: MgCl 2, MgSO 4, and CaCl 2 were inhibitory to the INA response elicited by 3 M NaCl. Non-ionic solutions of urea or sucrose failed to evoke INA and they were also minimally effective in altering 3 M NaCl elicited activity. Shallow cavities were utilized to maintain the tubular structure of dentin relatively intact. In the shallow cavity preparations hypertonic sucrose or urea failed to evoke INA, even when dentin was etched with 50% citric acid for 2 min. The results suggest that the osmolarity of these solutions is a poor indicator of the INA.

Repetitive axonal discharges elicited by serotonin and intracellular adenosine 3′,5′-cyclic monophosphate in the crayfish neuromuscular junction

Experiments were carried out in the opener muscle of the claw of small crayfish. After pretreatment of the preparation with serotonin (5-HT), application of the membrane permeant analogue of adenosine 3′,5′-cyclic monophosphate (cAMP), 8-bromoadenosine 3′,5′-monophosphate was capable of evoking reversibly repetitive discharges in the inhibitory and excitatory axon. Reducing phosphodiesterase activity with application of either 3-isobutyl-1-methylxanthine or theophylline also elicited repetitive axonal discharges after 5-HT treatment. Moreover, application of forskolin dissolved in ethanol caused repetitive axonal discharges. The chemically induced presynaptic action potentials were detected mainly by their postsynaptic effects, i.e. by recording inhibitory and excitatory postsynaptic currents in voltage-clamped muscle fibres. In addition, nerve spikes were recorded extracellularly. It is concluded that 5-HT and intraaxonal cAMP alter membrane properties of the efferent axons innervating crayfish muscle.

Time domain processing of electric organ discharge waveforms by pulse-type electric fish.

We explored coastal streams, rivers, and swamps in the Guianas of South America and found eleven species of gymnotiform fishes with pulse discharges. Each species has a characteristic electric organ discharge (EOD) waveform of 0.5-5 ms duration; at least two species appear to have a natural sex difference in their EODs which is apparent when comparing large adult males and females. Three sensory coding mechanisms are proposed to explain how electric fish might be able to determine species and sex identity from such short electrical pulses. Spectral Coding: electroreceptors tuned to different frequencies encode the spectrum of the EOD as a cross-fiber stimulation pattern. Temporal Coding: EODs are encoded as a volley of nerve spikes patterned in the time domain. Scan Sampling: a receiver detects a signaler's EOD as an amplitude modulation or 'beat' set up by the combination of its own discharge with the signaler's. The receiver uses the modulation envelope to assess the signaler's EOD waveform. To distinguish between these three coding mechanisms, we tested the ability of one pulse gymnotiform, Hypopomus beebei, to discriminate one electric waveform from another by comparing the acceleration of the discharge rate to different stimuli. Stimuli are presented under two conditions: when the stimulus pulse train is free-running compared to the fish's pulse train, and when the stimulus train is phase-locked to the fish's discharge pulse train. Under the former condition scan sampling may be used; under the latter it will be impossible. Hypopomus discriminates the polarity of a single period sinusoidal stimulus under scanning conditions but does not discriminate under clamped conditions. Hypopomus gives the strongest response to single period sine waves of 670 Hz and weaker responses to sinusoids of lower and higher frequencies. Free-running and phase-locked stimuli evoke similar responses. Under free-running conditions, Hypopomus discriminates a series of EOD-like stimuli that have been phase-shifted by varying amounts, but under phase-locked conditions does not. Scan sampling is presented as a possible waveform recognition mechanism for pulse-discharging gymnotiform fishes.

Interspike interval dependency from arterial chemoreceptors.

The carotid body impulse generator has been previously characterized as a Poisson-type random process. We examined the validity of this characterization by analyzing sinus nerve spike trains for interspike interval dependency. Fifteen single chemoreceptive afferents were recorded in vivo under hypoxic-hypercapnic conditions, and approximately 1,000 consecutive interspike intervals for each fiber were timed and analyzed for serial dependence. The same set of intervals placed in shuffled order served as a control series without serial dependence. The original spike interval trains showed significantly negative first-order serial correlation coefficients and less variability in joint interval distributions than did the shuffled interval trains. These results suggest that the chemoreceptor afferent train is not random and may reflect a negative feedback system operating within the carotid body that limits variation about a mean frequency.

Pulse-number distribution for the neural spike train in the cat's auditory nerve.

Pulse-number distributions (PNDs) were recorded from primary afferent fibers in the auditory nerve of the cat, using standard extracellular microelectrode recording techniques. Pure-tone and broadband-noise stimuli were used. The number of neural spikes (pulses) n was measured in a set of contiguous intervals, each of duration T seconds. The quantity n varies from one interval to another. These data were then used to determine the PND, which is the probability p(n,T) of occurrence of n spikes in the time T, versus the number n. The estimated mean and variance of p(n,T) were obtained. Two different values of T were used. An unexpected observation was that the count mean-to-variance ratio R is relatively constant and independent of the stimulus intensity. Use of the PND as a statistical measure of the underlying neural point process has a number of virtues. For example, the PND readily exhibits the existence of spike clusters (e.g., pairs) for some units. The PND is essentially unaffected by time jitter and time quantization and provides a statistically significant measure for units firing at low rates. A study of the scaled and unscaled pulse-interval distributions (PIDs), under conditions of spontaneous firing, demonstrates that the occurrences of neural events are generally not describable by a renewal process. Our investigation shows that none of the point processes customarily used to model the auditory neural spike train is consistent with all of the data. It appears that the encoding of acoustic information into nerve spikes in the peripheral auditory system takes the form of a cluster point process similar to the Neyman-Scott type. For pure-tone excitation, the PND will be well represented as a multinomial distribution in this case.