The temporal frequency response function of pattern ERG and VEP: changes in optic neuritis

Steady-state pattern electroretinograms (PERGs) and visual evoked potentials (VEPs) in response to sinusoidal gratings (2 c/deg), sinusoidally counterphased at closely spaced temporal frequencies (TFs) between 4 and 28 Hz, were recorded from 11 patients with unilateral optic neuritis (ON; 11 affected eyes and 10 healthy fellow eyes) and 7 age-matched normal subjects (7 eyes). Amplitude and phase of responses' second harmonics were measured. Responses' apparent latencies were estimated from the rate at which phase lagged with TF. When compared to control values, mean PERG and VEP amplitudes of ON eyes were reduced (by about 0.4 log units) at both low (5–10 Hz) and high (16–20 Hz) TFs. Mean PERG amplitudes of fellow eyes were selectively reduced at low TFs (by about 0.3 log units). Mean PERG apparent latencies of both ON and fellow eyes were delayed (by 15 and 9 ms, respectively). Mean VEP apparent latency of ON eyes was delayed at both low and high TFs (by 24 and 30 ms, respectively), while that of fellow eyes was selectively delayed at high TFs (by 28 ms). The results in ON eyes indicate non-selective abnormalities of PERG and VEP generators responding at both low and high TFs. VEP TF losses may be in part accounted for by corresponding PERG losses. In the fellow eyes of patients, more selective PERG and VEP TF abnormalities may suggest differential impairment of retinal and postretinal subsystems responding better to low and high TFs (i.e. parvo-and magnocellular streams).     

The effects of stimulus rates upon median,ulnar and radial nerve somatosensory evoked potentials

We examined the effect of stimulus rates on the somatosensory evoked potential (SEP) amplitude following stimulation of the median nerve (MN) and the ulnar nerve (UN) at the elbow or wrist, and the radial nerve (RN) at the wrist in 12 normal subjects. We measured the amplitude of frontal (P14-N18-P22-N30) and parietal peaks (P14-N20-P26-N34) at a stimulus rate of 1.1, 3.5 and 5.7 Hz. The amplitude attenuation was found at frontal P22 and N30 and to a lesser degree at parietal N20 and P26 peaks with an increasing stimulus rate from 1.1 to 5.7 Hz. The amplitude attenuation was greatest at the elbow when compared to the wrist stimulation for both MN and UN. The attenuation was least for wrist stimulation for the RN. The UN block by local anesthesia just distal to the stimulus electrode at the elbow abolished the amplitude attenuation caused by the fast stimulus rate. The observed amplitude attenuation with the faster stimulus rate is probably due, in part, to interference from the “secondary” afferent inputs. The secondary afferent inputs arise from peripheral receptor stimulation (muscle, joint and/or cutaneous) as a subsequent effect of efferent volleys initiated from the point of stimulation. The greater number of peripheral receptors being activated as more proximal sites of stimulation in a mixed nerve would result in greater attenuation of the SEP recorded from scalp electrodes. We postulate that the attenuation of frontal peaks by the fast stimulus rate is due to the frontal projection of interfering “secondary” afferent inputs.     

背景光对图形视网膜电图空间调谐特性的影响

本工作应用背景光压抑闪光视网膜电图(FERG),考察对图形视网膜电图(PERG)的空间调谐特性的影响,并与无背景光时的结果进行比较。背景光使全屏幕闪光诱发的FERG基本压抑。在这种条件下,同屏幕的图形刺激所诱发的PERG的振幅显示一定的低空间频率衰减(LSFA)。FFT分析表明,当时间频率为3.91Hz时,PERG的二次谐波呈现十分明显的LS-FA,与无背景光时的结果吻合得很好;当时间频率为7.81Hz时,也表现出LSFA,而无背景光时则缺如。这些结果表明,无背景光时记录的PERG振幅在低空间频率区偏高确实是由于混杂有亮度特异性成分—FERG。但是,PERG振幅所显示的LSFA仍不如二次谐波那么明显,这可能是因为FERG中存在的非线性成分未为背景光所完全压抑,仍然混杂在低频区的PERG反应中。     

The origin of the electroretinogram induced by structured stimuli in man

The Authors studied the checkerboard pattern electroretinogram (PERG) behaviour in normal subjects and in patients suffering from traumatic lesion of optic nerve, demyelinating optic neuritis, axonal optic neuritis, retinal vascular disorders and retinitis pigmentosa in order to verify the PERG origin. According to our data the PERG appears to originate from ganglion cells since the signal diminished or disappeared in axonal lesion of optic nerve, as a result of retrograde ganglion cell degeneration. Furthermore, the demyelinating lesions of optic nerve were not able to modify the PERG wave. In patients suffering from retinal receptor disturbances the flash electroretinogram (FERG), which is probably an expression of receptor activity, was greatly impaired, whereas PERGs were either normal or less impaired than FERGs. These data demonstrate the different origin of PERG and FERG.     

Somatosensory evoked potentials at rest and during movement in Parkinson's disease: evidence for a specific apomorphine effect on the frontal N30 wave

Studies attempting to relate the abnormalities of the frontal N30 components of the somatosensory evoked potentials (SEPs) to motor symptoms in Parkinson's disease (PD) have shown contradictory results. We recorded the frontal and parietal SEPs to median nerve stimulation in 2 groups of PD patients: a group of 17 patients presenting the wearing-off phenomenon, and a group of 10 untreated PD patients. The results were compared with a group of 13 healthy volunteers of the same age and with a group of 10 non-parkinsonian patients. All parkinsonian and non-parkinsonian patients were studied before (“off” condition) and after a subcutaneous injection of apomorphine (“on” condition). The gating effects of a voluntary movement (clenching of the hand) on the SEPs were also studied for the wearing-off group of PD patients (in states off and on) in comparison with the healthy subjects. At rest and in the off condition the amplitude of the frontal N30 was significantly reduced in the 2 groups of PD patients. We demonstrate that the movement gating ability of the PD patient is preserved in spite of the reduced amplitude of the frontal N30. This result suggests that the specific change in the frontal N30 in PD is not the consequence of a continuous gating of the sensory inflow by a motor corollary discharge. Clinical motor improvement induced by apomorphine was associated with a significant enhancement of the frontal N30 wave. In contrast, the subcortical P14 and N18 waves and the cortical N20, P22, P27 and N45 were not statistically modified by the drug. Apomorphine infusion did not change the absolute reduced voltage of the N30 reached during the movement gating. While the frontal N30 component of the non-parkinsonian patients was significantly lower in comparison to healthy subjects, this wave did not change after the apomorphine administration. In the wearing-off PD patient group the frontal N30 increment was positively correlated with the number of off hours per day. This specific apomorphine sensitivity of the frontal N30 was interpreted as a physiological index of the dopaminergic modulatory control exerted on the neuronal structures implicated in the generation of the frontal N30.     

Dissociable Neural Response Signatures for Slow Amplitude and Frequency Modulation in Human Auditory Cortex

Natural auditory stimuli are characterized by slow fluctuations in amplitude and frequency. However, the degree to which the neural responses to slow amplitude modulation (AM) and frequency modulation (FM) are capable of conveying independent time-varying information, particularly with respect to speech communication, is unclear. In the current electroencephalography (EEG) study, participants listened to amplitude- and frequency-modulated narrow-band noises with a 3-Hz modulation rate, and the resulting neural responses were compared. Spectral analyses revealed similar spectral amplitude peaks for AM and FM at the stimulation frequency (3 Hz), but amplitude at the second harmonic frequency (6 Hz) was much higher for FM than for AM. Moreover, the phase delay of neural responses with respect to the full-band stimulus envelope was shorter for FM than for AM. Finally, the critical analysis involved classification of single trials as being in response to either AM or FM based on either phase or amplitude information. Time-varying phase, but not amplitude, was sufficient to accurately classify AM and FM stimuli based on single-trial neural responses. Taken together, the current results support the dissociable nature of cortical signatures of slow AM and FM. These cortical signatures potentially provide an efficient means to dissect simultaneously communicated slow temporal and spectral information in acoustic communication signals.     

The pattern electroretinogram: N95 amplitudes in normal subjects and optic neuritis patients

Recent work has suggested that the N95 peak of the transient pattern electroretinogram (PERG) may be a more sensitve indicator of the late stages of retinal function prior to optic nerve activation than the P50 peak. In the report, we show that a new measure of N95 amplitude, based on digital filtering methods to identify a non-linear baseline measurement, greatly reduced the amplitude variation in a population of 50 normal subjects when compared with two other plausible measures. We then used that new measure to follow the time course of N95 amplitudes in 12 optic neuritis patients. It was found that mintenance of a normal N95 amplitude at 6 months after onset of optic neuritis was always associated with excellent clinical recovery as measured by visual fields, acuity, presence or absence of an afferent pupil and optic atrophy, and contrast sensitivity (CS). Loss of N95 amplitude to below laboratory limits of normal was associated with abnormalities in these indicators of visual function. This study supports the idea that the N95 peak represents retinal ganglion cell function.     

Pattern ERG: effects of reference electrode site,stimulus mode and check size

We studied monocular pattern ERG (PERG) in 10 normal subjects and a patient with optic neuritis. No clinically significant PERG could be recorded from the occluded eye with any reference (ipsilateral ear or temple, or midfrontal), indicating that cross-contamination is not present with binocular testing. Ipsilateral temple reference minimized VEP (P100/N100) contribution to the PERG N95 which occurred with ipsilateral ear or midfrontal reference. The conclusions were confirmed by results from the patient, who had marked monocular delay of a normal amplitude P100. Twenty-four subjects were tested with monocular and binocular stimulation using an ipsilateral temple reference. There were differences in PERG latencies and amplitudes although the interside amplitude ratio showed smaller differences with binocular stimulation. Increasing check size (17, 35 and 70 min) decreased P50 and N95 latencies and increased P50 amplitude.     

Cytokine profile in the synovial fluid of patients with temporomandibular joint disorders: A systematic review

The aim of this study was to review the cytokine profiles in the synovial fluid (SF) of patients with temporomandibular joint disorders (TMJD). Databases were searched from 1965 till September 2015 using different combinations of the following key words: “Temporomandibular joint”; “Cytokine”; “disorder”; and “synovial fluid” and “inflammation”. Titles and abstracts of studies identified using the above-described protocol were screened and checked for agreement. Full-texts of articles judged by title and abstract to be relevant were read and independently evaluated. Hand-searching of the reference lists of potentially relevant original and review articles was also performed. The pattern of the present systematic review was customized to mainly summarize the relevant data. Fifteen studies were included. In 12 studies, cytokine profile of patients with TMJD was assessed using enzyme linked immunosorbent assay; and in 2 studies, histological analysis was performed to assess the cytokine profile of patients with TMJD. Patients with TMJD presented raised levels of interleukin (IL)-6 in 8 studies, IL-1beta (1β) in 5 studies and tumor necrosis factor-alpha (TNF-α) in 5 studies. Two studies showed no significant difference in TNF-α levels in patients with and without TMJD; and IL-1β levels were comparable in patients with and without TMJD in 2 studies. Raised levels of IL-6, TNF-α, IL-1β, IL-8, and IFN-γ in the SF have been associated with inflammation in patients with TMJD. Cytokines IL-10, osteoclastogenesis inhibitory factor/osteoprotegerin (OCIF/OPG), and VEGF found in the SF of TMJs could have an anti-inflammatory effect.     

Differentiation of the bimodal stimuli in a frog's retina

In work electric activity of frog's retina was investigated by silent substitution technique. Electroretinogram was recorded as a response to abrupt exchange of the referent stimulus-line with fixed values of luminance and orientation to test lines with varied luminance and orientations. As a result of the analysis it has been allocated two types of responses of a retina. The response to onset-offset of a stimulus-line was similar to the response at homogeneous illumination of a retina (ERG), and was characterized by both the high amplitude of b-wave (hundreds mkV) and significant asymmetry of b- and d-waves. Whereas the same waves in response to substitution of the same stimuli were more symmetric and had on ten times smaller amplitudes. Such activity of frog's retina was referred as pattern electroretinogram (PERG) recorded in a high vertebrate's retina as response to stimuli whose contrast was temporally modulated. The analysis of interaction of luminance and line orientation channels in retina was carried out on the base of construction V-shaped functions of stimuli differentiation. It has shown, that activities of both channels are linearly summarized in PERG. It means independent and parallel functioning of these mechanisms. However, it takes the short subdivision of luminance, namely, when luminance of test line not far from luminance of referent line. At the same time, from the moment of the double prevalence of test line in relation to referent line, growth of PERG amplitude has nonlinearly form. Such two-stage changing of PERG amplitude speaks presence in a retina of a frog of two mechanisms of coding of luminance. One mechanism coding light intensity by power of the discharge, it forms the information on an absolute level of light in the environment. Its activity is caused basically, by receptors and cells of external plexiform layer and is submitted by b-wave of electroretinogram. Other mechanism submitted in PERG, is based on the vector code of stimulus, it forms the information on spatial and time differentiation of a light in the visual field and is connected, basically, with cells of internal plexiform layer of frog's retina.     

Use of pattern electroretinography to differentiate acute optic neuritis from acute anterior ischemic optic neuropathy

The transient pattern electroretinogram (PERG) was recorded from 16 patients with acute neuritis and from 13 patients with acute non-arteritic ischemic optic neuropathy (AION). All patients were tested within 35 days from the the onset of visual symptoms and all had significant central visual field abnormalities in their affected eyes as quantified by automated perimetry. Analysis of the PERGs showed that the amplitude of the N95 peak was abnormally reduced for each eye affected with AION while it remained normal in optic neuritis. No significant alteration in P50 amplitude was observed in either condition. The loss of N95 amplitude in AION was highly correlated with the average depth of visual field loss (in decibels) within a radius of 10° of fixation. These results suggest that PERG could be used early in the course of optic neuropathy to distinguish optic neuritis from AION in those cases for which the diagnosis is still uncertain after the clinical examination.     

Roles of Glutathione (GSH) in Dopamine (DA) Oxidation Studied by Improved Tandem HPLC Plus ESI-MS

In this study, new procedure with improved tandem HPLC plus ESI-MS was utilized to decipher the protective role of glutathione (GSH) against dopamine (DA) oxidation. We demonstrated that auto-oxidation of DA could produce aminochrome (AM, a cyclized DA quinone), which could be effectively abrogated by reductants, especially by GSH. Furthermore GSH was demonstrated to be able to conjugate with AM to form various conjugates via condensation reactions without enzymatic catalysis. The GSH-AM conjugates tend to aggregate, possibly mediated by conjugated AM structures, but could be inhibited by GSH. We hypothesized that proteins conjugated by AM might facilitate Lewy body formation of Parkinson’s disease (PD) in dopaminergic neurons via similar polymerization. We proposed that GSH could protect dopaminergic neurons against DA-induced toxicity via various mechanisms. The imbalance between DA oxidation and GSH protective capacity could be a key factor contributing to PD. Strategies to use GSH analogues, GSH inducers or to control DA oxidation might work to control PD onset and development.     

Stimulus variability affects the amplitude of the auditory steady-state response

In this study we investigate whether stimulus variability affects the auditory steady-state response (ASSR). We present cosinusoidal AM pulses as stimuli where we are able to manipulate waveform shape independently of the fixed repetition rate of 4 Hz. We either present sounds in which the waveform shape, the pulse-width, is fixed throughout the presentation or where it varies pseudo-randomly. Importantly, the average spectra of all the fixed-width AM stimuli are equal to the spectra of the mixed-width AM. Our null hypothesis is that the average ASSR to the fixed-width AM will not be significantly different from the ASSR to the mixed-width AM. In a region of interest beamformer analysis of MEG data, we compare the 4 Hz component of the ASSR to the mixed-width AM with the 4 Hz component of the ASSR to the pooled fixed-width AM. We find that at the group level, there is a significantly greater response to the variable mixed-width AM at the medial boundary of the Middle and Superior Temporal Gyri. Hence, we find that adding variability into AM stimuli increases the amplitude of the ASSR. This observation is important, as it provides evidence that analysis of the modulation waveform shape is an integral part of AM processing. Therefore, standard steady-state studies in audition, using sinusoidal AM, may not be sensitive to a key feature of acoustic processing.     

Experience Drives Synchronization: The phase and Amplitude Dynamics of Neural Oscillations to Musical Chords Are Differentially Modulated by Musical Expertise

Musical expertise is associated with structural and functional changes in the brain that underlie facilitated auditory perception. We investigated whether the phase locking (PL) and amplitude modulations (AM) of neuronal oscillations in response to musical chords are correlated with musical expertise and whether they reflect the prototypicality of chords in Western tonal music. To this aim, we recorded magnetoencephalography (MEG) while musicians and non-musicians were presented with common prototypical major and minor chords, and with uncommon, non-prototypical dissonant and mistuned chords, while watching a silenced movie. We then analyzed the PL and AM of ongoing oscillations in the theta (4–8 Hz) alpha (8–14 Hz), beta- (14–30 Hz) and gamma- (30–80 Hz) bands to these chords. We found that musical expertise was associated with strengthened PL of ongoing oscillations to chords over a wide frequency range during the first 300 ms from stimulus onset, as opposed to increased alpha-band AM to chords over temporal MEG channels. In musicians, the gamma-band PL was strongest to non-prototypical compared to other chords, while in non-musicians PL was strongest to minor chords. In both musicians and non-musicians the long-latency (> 200 ms) gamma-band PL was also sensitive to chord identity, and particularly to the amplitude modulations (beats) of the dissonant chord. These findings suggest that musical expertise modulates oscillation PL to musical chords and that the strength of these modulations is dependent on chord prototypicality.     

RAGE upregulation and nuclear factor-kappaB activation associated with ageing rat cardiomyocyte dysfunction

Evidence suggests that ageing is a major risk factor for cardiac dysfunction. Interactions between advanced glycation endproducts (AGEs) and the receptor for AGEs (RAGE) are known to cause chronic cellular activation, including activation of nuclear factor-kappaB (NF-kappaB), which has been implicated as a causal factor in the ageing process. To assess whether cardiomyocyte contractile function and the interaction of AGEs with RAGE in the heart are altered in ageing, 25- and 2-month-old male rats were compared. Mechanical properties were assessed in ventricular myocytes using an edge-detection system, including peak twitch amplitude (PTA), time-to-PTA (TPS), time-to-75% relengthening (TR75) and maximal velocity of shortening/relengthening (+/-dL/dt) in ventricular myocytes. AGEs were detected by using a fluorescence assay. The expression of RAGE and NF-kappaB was assessed through a Western blot analysis. Compared with young myocytes, aged myocytes displayed a prolonged TR75 at 1 Hz. With increasing stimulus frequency (from 2 to 4 Hz), aged myocytes' PTA was significantly reduced relative to young myocytes. Aged rat hearts displayed high level of AGEs, RAGE upregulation and NF-kappaB activation. These findings demonstrate impaired cardiomyocyte relaxation and reduced tolerance to increased stimulus frequency in aged rats, which might be associated with enhanced AGEs, RAGE expression, and NF-kappaB activation.     

A novel strategy for intrastriatal dopaminergic cell transplantation: Sequential “nest” grafting influences survival and behavioral recovery in a rat model of Parkinson's disease

Neural transplantation in experimental parkinsonism (PD) is limited by poor survival of grafted embryonic dopaminergic (DA) cells. In this proof-of-principle study we hypothesized that a first regular initial graft may create a “dopaminergic” environment similar to the perinatal substantia nigra and consequently stimulate a subsequent graft. Therefore, we grafted ventral mesencephalic neurons sequentially at different time intervals into the same target localization. Rats with a unilateral lesion of the dopamine neurons produced by injections of 6-hydroxydopamine (6-OHDA) received E14 ventral mesencephalon derived grafts into the DA-depleted striatum. In the control group we grafted all 6 deposits on the first day (d0). The other 4 groups received four graft deposits distributed over 2 implantation tracts followed by a second engraftment injected into the same site 3, 6, 14 and 21 days later. Quantitative assessment of the survival of tyrosine hydroxylase-immunoreactive neurons and graft volume revealed best results for those DA grafts implanted 6 days after the first one. In the present study, a model of short-interval sequential transplantation into the same target-site, so called “nest” grafts were established in the 6-OHDA rat model of PD which might become a useful tool to further elucidate the close neurotrophic and neurotopic interactions between the immediate graft vicinity and the cell suspension graft. In addition, we could show that the optimal milieu was established around the sixth day after the initial transplantation. This may also help to further optimize current transplantation strategies to restore the DA system in patients with PD.     

Activation of CB2R with AM1241 ameliorates neurodegeneration via the Xist/miR-133b-3p/Pitx3 axis

Activation of cannabinoid receptor type II (CB2R) by AM1241 has been demonstrated to protect dopaminergic neurons in Parkinson's disease (PD) animals. However, the specific mechanisms of the action of the CB2R agonist AM1241 for PD treatment have not been characterized. Wild-type (WT), CB1R knockout (CB1-KO), and CB2R knockout (CB2-KO) mice were exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 1 week to obtain a PD mouse model. The therapeutic effects of AM1241 were evaluated in each group. Behavioral tests, analysis of neurotransmitters, and immunofluorescence results demonstrated that AM1241 ameliorated PD in WT animals and CB1-KO animals. However, AM1241 did not ameliorate PD symptoms in CB2-KO mice. RNA-seq analysis identified the lncRNA Xist as an important regulator of the protective actions of AM1241. Specifically, AM1241 allowed WT and CB1-KO animals treated with MPTP to maintain normal expression of Xist, which affected the expression of miR-133b-3p and Pitx3. In vitro, overexpression of Xist or AM1241 protected neuronal cells from death induced by 6-hydroxydopamine and increased Pitx3 expression. The CB2 receptor agonist AM1241 alleviated PD via regulation of the Xist/miR-133b-3p/Pitx3 axis, and revealed a new approach for PD treatment.     

Protection of Pattern Electroretinogram and Retinal Ganglion Cells by Oncostatin M after Optic Nerve Injury

Injury to retinal ganglion cell (RGC) axons leads to selective loss of RGCs and vision. Previous studies have shown that exogenous neurotrophic factors promote RGC survival. We investigated the neuroprotective effects of oncostatin M (OSM), a member of the IL-6 family of cytokines, on pattern electroretinogram (PERG) and RGC survival after optic nerve crush (ON-crush) in the mouse. BALB/C mice received ON-crush in the left eyes for either 4-second or 1-second duration (4-s or 1-s). Fluoro-gold retrograde labeling was used to identify RGCs. RGC function was assessed by PERG measurement. OSM or CNTF protein was injected intravitreally immediately after ON-crush. OSM responsive cells were identified by localization of increased STAT3 phosphorylation. Significant higher RGC survival (46% of untreated control) was seen in OSM-treated eyes when assessed 2 weeks after 4-s ON-crush as compared to that (14% of untreated control) of the PBS-treated eyes (P<0.001). In addition, PERG amplitude was significantly higher in eyes treated with OSM or CNTF 1 week after 1-s ON-crush (36% of baseline) as compared with the amplitude of PBS-treated eyes (19% of the baseline, P = 0.003). An increase in STAT3 phosphorylation was localized in Müller layer after OSM treatment, suggesting that Müller cells mediate the effect of OSM. Our results demonstrate that one single injection of either OSM or CNTF after ON-crush improves RGC survival together with their electrophysiological activity. These data provide proof-of-concept for using neurotrophic factors OSM and CNTF for RGC degenerative diseases, including glaucoma and acute optic nerve trauma.     

Mutant alpha-synuclein-induced degeneration is reduced by parkin in a fly model of Parkinson's disease.

Parkinson's disease (PD) patients show a characteristic loss of motor control caused by the degeneration of dopaminergic neurons. Mutations in the genes that encode alpha-synuclein and parkin have been linked to inherited forms of this disease. The parkin protein functions as a ubiquitin ligase that targets proteins for degradation. Expression of isoforms of human alpha-synuclein in the Drosophila melanogaster nervous system forms the basis of an excellent genetic model that recapitulates phenotypic and behavioural features of PD. Using this model, we analysed the effect of parkin co-expression on the climbing ability of aging flies, their life span, and their retinal degeneration. We have determined that co-expression of parkin can suppress phenotypes caused by expression of mutant alpha-synuclein. In the developing eye, parkin reduces retinal degeneration. When co-expressed in the dopaminergic neurons, the ability to climb is extended over time. If conserved in humans, we suggest that upregulation of parkin may prove a method of suppression for PD induced by mutant forms of alpha-synuclein.     

Frequency filter properties of lobster chemoreceptor cells determined with high-resolution stimulus measurement

1. We developed a high resolution, on-line stimulus measurement system for accurate control of chemical stimulus applications for Homarus americanus lateral antennule chemoreceptors. Focal stimulus presentations in an electrophysiological preparation with the receptor sensilla intact were measured at small spatial (30 μm) and time (5 ms) scales.
2. We tested 15 receptor cells with ten 100 ms pulses of 10⁴ M hydroxyproline at 0.5, 1, 2 and 4 Hz and with a single 8 s square pulse. Individual cells showed differences in their capabilities to resolve pulses (“flicker fusion”). At 2 Hz stimulation, some cells could follow stimulus pulses while others could not. At 4 Hz, 3 cells could still encode individual stimulus pulses accurately. The population resolved pulses up to 2 Hz; at 4 Hz, the population response to a pulse series approximated the response to a square pulse.
3. Repetitive stimulation caused a gradual decrease in the number of spikes and a gradual increase in first spike latency (“cumulative adaptation”). Increased stimulation frequency resulted in greater cumulative adaptation.
4. Since individual differences in adaptation and disadaptation rates of the receptor cells could not be attributed to measured stimulus variability in situ, lobster chemoreceptor cell populations have intrinsic temporal diversity which, we hypothesize, could be used to analyze pulsatile stimuli that occur in natural turbulent odor plumes.