Changes In Stimulus Intensity Research Articles

Sensitivity to interaural intensity differences of neurons in primary auditory cortex of the cat. I. types of sensitivity and effects of variations in sound pressure level.

1. Interaural intensity differences (IIDs) provide the major cue to the azimuthal location of high-frequency narrowband sounds. In recent studies of the azimuthal sensitivity of high-frequency neurons in the primary auditory cortex (field AI) of the cat, a number of different types of azimuthal sensitivity have been described and the azimuthal sensitivity of many neurons was found to vary as a function of changes in stimulus intensity. The extent to which the shape and the intensity dependence of the azimuthal sensitivity of AI neurons reflects features of their IID sensitivity was investigated by obtaining data on IID sensitivity from a large sample of neurons with a characteristic frequency (CF) > 5.5 kHz in AI of anesthetized cats. IID sensitivity functions were classified in a manner that facilitated comparison with previously obtained data on azimuthal sensitivity, and the effects of changes in the base intensity at which IIDs were introduced were examined. 2. IID sensitivity functions for CF tonal stimuli were obtained at one or more intensities for a total of 294 neurons, in most cases by a method of generating IIDs that kept the average binaural intensity (ABI) of the stimuli at the two ears constant. In the standard ABI range at which a function was obtained for each unit, five types of IID sensitivity were distinguished. Contra-max neurons (50% of the sample) had maximum response (a peak or a plateau) at IIDs corresponding to contralateral azimuths, whereas ipsi-max neurons (17%) had the mirror-image form of sensitivity. Near-zero-max neurons (18%) had a clearly defined maximum response (peak) in the range of +/- 10 dB IID, whereas a small group of tough neurons (2%) had a restricted range of minimal responsiveness with near-maximal responses at IIDs on either side. A final 18% of AI neurons were classified as insensitive to IIDs. The proportions of neurons exhibiting the various types of sensitivity corresponded closely to the proportions found to exhibit corresponding types of azimuthal sensitivity in a previous study. 3. There was a strong correlation between a neuron's binaural interaction characteristics and the form of its IID sensitivity function. Thus, neurons excited by monaural stimulation of only one ear but with either inhibitory, facilitatory, or mixed facilitatory-inhibitory effects of stimulation of the other ear had predominantly contra-max IID sensitivity (if contralateral monaural stimulation was excitatory) or ipsi-max sensitivity (if ipsilateral monaural stimulation was excitatory). Neurons driven weakly or not at all by monaural stimulation but facilitated binaurally almost all exhibited near-zero-max IID sensitivity. The exception to this tight association between binaural input and IID sensitivity was provided by neurons excited by monaural stimulation of either ear (EE neurons). Although EE neurons have frequently been considered to be insensitive to IIDs, our data were in agreement with two recent reports indicating that they can exhibit various forms of IID sensitivity: only 23 of 75 EE neurons were classified as insensitive and the remainder exhibited diverse types of sensitivity. 4. IID sensitivity was examined at two or more intensities (3-5 in most cases) for 84 neurons. The form of the IID sensitivity function (defined in terms of both shape and position along the IID axis) was invariant with changes in ABI for only a small proportion of IID-sensitive neurons (approximately 15% if a strict criterion of invariance was employed), and for many of these neurons the spike counts associated with a given IID varied with ABI, particularly at near-threshold levels. When the patterns of variation in the form of IID sensitivity produced by changes in ABI were classified in a manner equivalent to that used previously to classify the effects of intensity on azimuthal sensitivity, there was a close correspondence between the effects of intensity on corresponding types of azimuthal and IID sensitivity

Functional significance of the early component of the human blink reflex.

The relationship between the size of the first electromyographic (EMG) component of the cutaneous blink reflex (R1) and onset of eyelid closure in human adults was determined in 4 experiments in which R1 size was varied by different means: change in stimulus intensity, paired stimulation, and warning. Two-phase lid movements were frequently seen, with an early small movement followed by a large rapid movement. All experiments showed that larger R1s were associated with shorter latencies of both movements. This covariation was general across participants and was independent of shifts in the excitability of the blink reflex pathways indexed by R1 latency, R2 latency, and R2 area (R2 is the more prolonged, later EMG component). The results indicate that R1 acts first to evoke an early lid movement and second to facilitate eyelid closure by the later R2 burst. Identification of this second behavioral function for R1 aids the interpretation of other findings and encourages its use as a model system.

The effects of aging on information-processing channels in the sense of touch: III. Differential sensitivity to changes in stimulus intensity.

Detection thresholds and difference limens were measured for 16 subjects ranging from 19 to 91 years of age. The stimuli were 250-Hz bursts of vibration applied through a 3.0-cm2 contactor to the thenar eminence of the right hand. Detection thresholds were higher in older than in younger subjects, as were the absolute values of difference limens. When the difference limen was expressed in relative terms as the proportion by which two stimuli had to differ in amplitude to be discriminated (delta alpha/alpha), discriminative capacities were unaffected by aging except for stimuli slightly above the detection threshold, in which case the limens of older subjects were significantly higher than those of younger subjects. The results are consistent with the hypothesis that elevations in the detection thresholds of older subjects are the results of reduced afferent input to central brain centers that, with regard to their capacity to detect the presence of threshold-level stimuli and to discriminate differences among suprathreshold stimuli, are relatively unaffected by aging.

Sensory modulation of auditory stimuli in children with autism and receptive developmental language disorder: event-related brain potential evidence.

Three groups of age- and PIQ-matched children (Autism, Receptive Developmental Language Disorder, and normal controls) participated in two event-related brain potential (ERP) experiments. Each of these experiments was aimed at evaluating whether either of the two clinical groups of children demonstrated abnormalities in two auditory ERP components, N1 and P2, which are known to be dependent on stimulus characteristics (frequency, intensity, and probability), and believed to be generated within primary and secondary cortex. Results of Experiment 1 provide partial support for the idea that both clinical groups failed to fully process changes in stimulus intensity as indexed by the N1 component. Results are discussed in reference to potential abnormalities in serotonergic regulation of auditory cortex.

Perception of voicing for syllable-initial stops at different intensities: Does synchrony capture signal voiceless stop consonants?

In response to stop consonants with longer F1-cutback duration, the dominant synchronization of mid- and high-CF chinchilla auditory-nerve fibers changes from frequencies near F2 to frequencies near F1 at onset of voicing [D. G. Sinex and L. P. McDonald, J. Acoust. Soc. Am. 85, 1995-2004 (1989)]. If this change in neural synchronization is perceptually relevant for human listeners, then it may be predicted that changes in stimulus intensity and changes in the frequency difference between lower (F1) and higher (F2/F3) stimulus components should both affect perception of voicing. In a series of experiments, multiple continua of synthesized CVs varying in F1 cutback of the consonantal portion were played to listeners at levels ranging from 40 to 80 dB SPL. Across experiments, the frequency difference between F1 and F2 was manipulated by changing the onset frequency of F1 or F2. Subjects labeled more initial stops as voiceless as a function of increasing stimulus level and of decreasing frequency difference between F1 and F2. There was also an interaction between stimulus intensity and the frequency difference between F1 and F2 such that the effect of intensity was greater for smaller differences. These effects were reliable across a number of synthetic F1-cutback series, and the effect of intensity extended to a digitally edited series of hybrid CVs in which F1-cutback was varied by cross splicing naturally produced /da/ and /ta/. The effect of overall stimulus intensity was not affected by amplitude of prevocalic aspiration energy or by the presence or absence of release bursts. The results provide evidence for the perceptual significance of synchrony encoding of voicing for stop consonants.

Prepulse inhibition of the acoustic startle reflex using visual and auditory prepulses: disruption by apomorphine

The amplitude of the acoustic startle reflex can be reduced reliably when preceded at short intervals by a weak stimulus (prepulse) which itself does not elicit startle. The magnitude of this prepulse inhibition effect is attenuated by several dopamine agonists, such as apomorphine, especially when there is a relatively small difference between the intensity of the prepulse and the intensity of the background noise over which the prepulse is superimposed. One goal of the present experiment was to test the generality of this disruptive effect of apomorphine on prepulse inhibition by using either an auditory prepulse that included both a change in intensity and a change in frequency relative to the background noise or a visual prepulse stimulus. Apomorphine reduced auditory prepulse inhibition when induced by a small change in stimulus intensity, but not when induced by a change in both intensity and frequency. Apomorphine consistently reduced visual prepulse inhibition with a complete blockade at 100-ms test interval. However, it did not fully block the usual reduction in startle onset latency or even attenuate the increase in startle amplitude when a visual prepulse was presented 5, 10 or 15 ms before the startle stimulus. Consistent with conclusions from other laboratories using auditory prepulse inhibition, these data suggest that apomorphine did not prevent the animal from detecting prepulse presentation under conditions where the drug completely blocked prepulse inhibition. Moreover, they indicate that the blockade of prepulse inhibition by apomorphine was independent of prepulse modality, adding generality to the original finding. Visual prepulse inhibition may be a useful alternative procedure for evaluating the effects of drugs on this attentional process.

Thalamic VPM nucleus in the behaving monkey. III. Effects of reversible inactivation by lidocaine on thermal and mechanical discrimination.

1. The present study evaluates the necessity of the ventroposterior medial thalamic nucleus (VPM) for discrimination of the intensity of noxious heating, innocuous cooling, and innocuous tactile (airpuff) stimulation of the maxillary skin. 2. Two rhesus monkeys were trained to detect small differences (< 1.0 degrees C) in the intensity of noxious heat (near 46 degrees C) and innocuous cold (near 30 degrees C) as well as differences in the force of an airpuff applied to the skin over the maxilla. As a control the monkeys also detected small differences in the intensity of a white light. Lidocaine hydrochloride (2%) was microinjected into regions of thalamus where single-unit recordings had identified neuronal responses to the noxious heating and/or cooling stimuli. The effectiveness of the anesthetic blockade was monitored by multiunit recordings using microelectrodes positioned 1-3 mm from the orifice of the injection cannula. The monkey's ability to detect near-threshold changes in stimulus intensity was compared before and after each injection. 3. During six experimental sessions, single injections of 1-4 microliters lidocaine near the dorsomedial border of VPM did not significantly alter the monkey's ability to detect small changes in the intensity of noxious heat, cool, airpuff, or visual stimuli despite neurophysiological evidence that spontaneous neuronal activity was blocked within parts of VPM. 4. During three experiments, dual simultaneous microinjections of lidocaine (delivered through 2 microcannulae separated by approximately 1 mm) resulted in profound deficits in noxious heat discrimination, with lesser deficits in cool and airpuff discrimination; visual discrimination was never altered. Monitoring of adjacent microelectrodes revealed that although activity ventral to the injection sites was blocked, activity in medial thalamic nuclei, implicated in nociceptive processing, was probably not altered by these injections. 5. These data suggest that VPM is important for the perception of noxious and innocuous thermal stimuli as well as for the perception of tactile stimuli. However, considering the ineffectiveness of small single microinjections of lidocaine, it appears that some critical proportion of VPM must be inactivated to disrupt thermal or tactile discrimination, possibly because of overlapping receptive field properties of neurons in different areas of the nucleus.

Estrogen-sensitive neurons in the female rat ventral tegmental area: a dual route for the hormone action

1. Electrical stimulation of the ventral part of the midbrain central gray (CG) elicited antidromic action potentials in 136 neurons in the ventral tegmental area (VTA) of 23 urethan-anesthetized ovariectomized female rats. 2. Antidromic action potentials were positive-negative biphasic and completed mostly within 2.4 ms. Many had a notch in their initial positive deflection, at which antidromic potentials often failed to propagate into the neuronal soma. 3. The latency for antidromic activation ranged 1.0-10.5 ms, and the threshold was 100-1,700 microA. The relative refractory period was 0.8-2.8 ms. In 23 neurons (17%) gradual changes in stimulus intensity caused latency jumps, suggesting that their axons terminate or spread into branches in stimulation sites. 4. The parameters for antidromic activation were compared among 12 animals with a subcutaneous Silastic capsule of estrogen and 11 others with a blank capsule. Estrogen raised the mean threshold from 675 +/- 40 (SE) microA (n = 69) to 908 +/- 40 microA (n = 67). At the same time, estrogen significantly decreased the probability of the antidromic propagation from 63 to 41%. No changes were detected in the latency or the refractory period. 5. The probability distribution of the threshold was different in ovariectomized animals from that in estrogen-treated animals. Estrogen increased the number of cells with thresholds in the 1,300- to 1,500-microA range. 6. The probability of antidromic propagation was stable in each neuron to stimuli repeated at 1.0 Hz. Electrical stimulation of the preoptic area (POA) with a 30-s train of 50-microA pulses at 100 Hz increased the probability of antidromic propagation into the soma.(ABSTRACT TRUNCATED AT 250 WORDS)

Post-synaptic activity evoked in the rostral ventrolateral medullary neurones by stimulation of the defence areas of hypothalamus and midbrain in the rat

Neurones in the rostral ventrolateral medulla (RVLM) of the rat were recorded intracellularly ( n = 30) and extracellularly ( n = 91) in vivo. 91% of them had spontaneous activity with frequencies of 1.1 – 29.9 Hz. Onset latencies of the excitation induced by the stimulation of the hypothalamic and midbrain defence areas ranged from 1.5 to 44 ms and 2 to 60 ms respectively. There was no statistical difference between two groups. Excitation followed by inhibition or inhibition followed by excitation was observed in these processes. Excitatory postsynatic potentials (EPSPs) were summated by simultaneous stimulation of both sites and the onset latency was changed with the change of stimulus intensity. It is concluded that projections from the defence areas of hypothalamus and midbrain are relayed to RVLM neurones forming excitatory and inhibitory synapses; one mechanism of the effect summation caused by both sites is via EPSPs.

Suppression of Nociceptive Responses by Spinal Mu Opioid Agonists

To determine the influence of stimulation intensity on dose-response curves of three analgesics in halothane-anesthetized rats, continued immersion of the tail in 52.5 degrees C or 60 degrees C water for 15 s results first in a nociceptive reflex tail movement (tail flick = 2.8 +/- 0.4 s and 1.4 +/- 0.2 s, respectively), and a progressive increase in arterial blood pressure (delta BP = 21 +/- 1 and 24 +/- 1 mm Hg) and heart rate (delta HR = 27 +/- 2 and 32 +/- 2 beats/min). Intrathecally administered mu opioids, morphine (MOR), sufentanil (SUF), and [D-Ala2-N-Phe4,Gly-ol]-enkephalin (DAG), produced a dose-dependent inhibition of the tail flick and BP response with the relative activity being SUF = DAG > MOR. Although the magnitude of the response evoked by increasing stimulus intensity from 52.5 degrees C to 60 degrees C was increased only mildly (suggesting that both represented essentially supramaximal stimuli), this increase in stimulus intensity resulted in a significant rightward shift in the dose-response curves (decrease in apparent potency) of the three agonists, with the magnitude of the shift being MOR > SUF = DAG. Thus, the dose ratio (ED50 at 60 degrees C/ED50 at 52.5 degrees C) for these three analgesics given intrathecally on the tail flick and BP response was, respectively, 3.7 +/- 0.9 and 6500 +/- 465 for MOR; 0.5 +/- 0.9 and 2.4 +/- 0.9 for SUF; and 0.5 +/- 1.2 and 7.0 +/- 0.9 for DAG. Unlike SUF and DAG, with the 60 degrees C stimulus, the highest dose of MOR failed to abolish the BP and heart rate response. Previous work with an irreversible antagonist to define receptor occupancy requirements showed that the relative efficacy was SUF = DAG >> MOR. The present studies thus confirm the pharmacodynamically based prediction that for a given change in stimulus intensity, anesthetics with a high efficacy (DAG and SUF) show less shift in their dose response curves with a given increase in stimulus intensity than an agonist with low efficacy (MOR).

Perception of voicing in syllable-initial stops at different intensities: Does neural synchrony encode voice-onset?

In response to stop consonants differing in voice onset time (VOT), the dominant synchronization of mid-CF chinchilla auditory nerve fibers changes from the frequencyof F2 to the frequency of F1 at onset of voicing [D. G. Sinex and J. P. McDonald, J. Acoust. Soc. Am. 85, 1995–2004 (1987)]. If this change in neutral synchronization is perceptually relevant for human listeners, changes in stimulus intensity and changes in the frequency difference between F1 and F2 should both affect perception of voicing. In a series of experiments, several continua of synthesized CV’s varying in VOT were played to listeners at levels ranging from 40 to 80 dB SPL. The frequency difference between F1 and F2 was manipulated through the use of different places of articulation and different following vowels. Subjects labeled more CV’s as voiceless as a function of increasing stimulus level and of deceasing F1–F2 frequency difference. There was also an interaction between stimulus intensity and F1–F2 frequency difference such that the effect of intensity was greater for smaller F1–F2 differences. These effects were reliable across a number of synthetic VOT series, and the effect of intensity extended to a computer edited series of hybrid CV’s in which VOT was varied by cross-splicing a naturally produced /da/ and /ta/. The effect of overall stimulus intensity was not affected by amplitude of aspiration energy or by the presence or absence of release bursts. The results provide evidence for synchrony encoding of voicing for stop consonants. [Work supported by NIDCD/NIH Grant No. DC-00719.]

The spinal pharmacology of acutely and chronically administered opioids

Systematic studies on the pharmacology of the antinociceptive activity of spinally administered agents have emphasized the action in animal models of μ and δ opioid receptors. Importantly, aside from receptor selectivity, the opioid agonists differ in the property of efficacy. Agents with high efficacy (large receptor reserves) show smaller rightward shifts in their dose-response curves in the face of a given degree of opioid tolerance or when the stimulus intensity is elevated. With regard to loss of drug effect with long-term exposure (tolerance), multiple mechanisms may be considered, including changes in stimulus intensity, change in afferent processing, or changes in receptor number/coupling. Basic studies are providing insights into these several mechanisms.

Reflex responses in active muscles elicited by stimulation of low-threshold afferents from the human foot.

1. Reflex responses were elicited in muscles that act at the ankle by electrical stimulation of low-threshold afferents from the foot in human subjects who were reclining supine. During steady voluntary contractions, stimulus trains (5 pulses at 300 Hz) were delivered at two intensities to the sural nerve (1.2-4.0 times sensory threshold) or to the posterior tibial nerve (1.1-3.0 times motor threshold for the intrinsic muscles of the foot). Electromyographic (EMG) recordings were made from tibialis anterior (TA), peroneus longus (PL), soleus (SOL), medial gastrocnemius (MG), and lateral gastrocnemius (LG) muscles by the use of intramuscular wire electrodes. 2. As assessed by averages of rectified EMG, stimulation of the sural or posterior tibial nerves at nonpainful levels evoked a complex oscillation with onset latencies as early as 40 ms and lasting up to 200 ms in each muscle. The most common initial responses in TA were a decrease in EMG activity at an onset latency of 54 ms for sural stimuli, and an increase at an onset latency of 49 ms for posterior tibial stimuli. The response of PL to stimulation of the two nerves began with a strong facilitation of 44 ms (sural) and 49 ms (posterior tibial). With SOL, stimulation of both nerves produced early inhibition beginning at 45 and 50 ms, respectively. With both LG and MG, sural stimuli produced an early facilitation at 52-53 ms. However, posterior tibial stimuli produced different initial responses in these two muscles: facilitation in LG at 50 ms and inhibition in MG at 51 ms. 3. Perstimulus time histograms of the discharge of 61 single motor units revealed generally similar reflex responses as in multiunit EMG. However, different reflex components were not equally apparent in the responses of different single motor units: an individual motor unit could respond slightly differently with a change in stimulus intensity or background contraction level. The multiunit EMG record represents a global average that does not necessarily depict the precise pattern of all motor units contributing to the average. 4. When subjects stood erect without support and with eyes closed, reflex patterns were seen only in active muscles, and the patterns were similar to those in the reclining posture. 5. It is concluded that afferents from mechanoreceptors in the sole of the foot have multisynaptic reflex connections with the motoneuron pools innervating the muscles that act at the ankle. When the muscles are active in standing or walking, cutaneous feedback may play a role in modulating motoneuron output and thereby contribute to stabilization of stance and gait.

Effects of stimulus intensity on posterior tibial nerve somatosensory evoked potentials.

Relationships between stimulus intensity and peak latencies and amplitudes in posterior tibial nerve somatosensory evoked potential patterns were evaluated in ten healthy subjects. Eight intermediate latency peaks between 30 and 125 milliseconds (ms) after stimulus onset and seven amplitudes were analyzed. In general, there was a decrease in latency with each increase in stimulus intensity over a five step intensity range between 5 and 19 milliamps (mA) for most peaks. Similarly, increases in amplitudes generally occurred with increases in stimulus intensity for most peaks. Later peaks N105 and P115 as well as amplitudes P90-N105 and N105-P115 were least sensitive to stimulus intensity changes. The greatest changes in peak latency and amplitude occurred as stimulus intensity was increased from 7 to 11 mA. Beyond 11 mA relatively little change was observed in either peak latencies or amplitudes. Under anesthesia, by contrast, there was no stimulus intensity-peak latency interaction and beyond 11 mA there were decreases in amplitudes. Possible reasons for these findings are discussed.

The Psychophysical Attributes of Heat-Induced Pain and Their Relationships to Neural Mechanisms

During the last two decades there has been a proliferation of studies evaluating the psychophysical and neural attributes of heat-induced pain. Experiments using radiant and contact heat-induced pain have produced different observations thereby broadening our appreciation of the importance of acknowledging how a noxious heat stimulus is delivered; moreover manipulations of stimulus parameters have now provided a foundation for understanding the underlying neural mechanisms of heat-induced pain and their biological significance. The psychophysical attributes of heat-induced pain include highly reliable thresholds for most body regions, minimal adaptation to maintained noxious stimuli, an exquisite sensitivity to small changes in stimulus intensity, slow temporal summation for some types of heat-induced pain (i.e., second pain) but not for others (i.e., first pain), spatial summation---especially for suprathreshold noxious temperatures---and the perceived spread of pain well beyond the actual body area stimulated (i.e., radiation). The present body of information indicates that the pain system is optimally adapted for conveying precise information about intensity, and is less concerned with other stimulus features, such as spatial patterns or boundaries.

Low-frequency component of the gerbil brainstem response: Response characteristics and anesthesia effects

The auditory brainstem response (ABR) was recorded with epidural electrodes in awake and anesthetized gerbils. Low- and high-frequency components of the ABR were separated by analog filters and compared as functions of stimulus intensity, frequency, repetition rate, and effects of anesthesia. In response to 0.5 kHz tone bursts, thresholds of the low-frequency component (LF-ABR) were significantly lower than that of the most prominent peak of the high-frequency components (wave P4). At both 2 and 4 kHz, thresholds of the LF-ABR and wave P4 were not significantly different. Changes in stimulus intensity over a 70 dB range produced similar changes in peak amplitudes and latencies for the LF-ABR and P4. However, while the amplitude of the LF-ABR was inversely related to stimulus frequency, the amplitude of P4 was reduced at 0.5 kHz, as compared to 2 and 4 kHz. Increases in stimulus rate from 7 to 100 bursts/s produced little change in the amplitude of the LF-ABR. At rates of 80 and 100 bursts/s, the LF-ABR was sinusoidal in appearance due to the proximity of successively generated potentials. In contrast, the amplitude of P4 varied inversely with stimulus rate between 20 and 100 bursts/s. Administration of ketamine and xylazine produced minor changes in the amplitudes and latencies of both the LF-ABR and wave P4. The response characteristics of the gerbil LF-ABR are similar to those of the low-frequency component of the ABR in humans and cats. The LF-ABR provides an estimate of hearing threshold at low frequencies (0.5 kHz) as well as higher frequencies (2–4 kHz). A major advantage to the LF-ABR is that it can be recorded at high stimulation rates in awake and anesthetized animals, thus providing an efficient measure of auditory function.

Encoding of a spectrally-complex communication sound in the bullfrog's auditory nerve

1. A population study of eighth nerve responses in the bullfrog, Rana catesbeiana, was undertaken to analyze how the eighth nerve codes the complex spectral and temporal structure of the species-specific advertisement call over a biologically-realistic range of intensities. Synthetic advertisement calls were generated by Fourier synthesis and presented to individual eighth nerve fibers of anesthetized bullfrogs. Fiber responses were analyzed by calculating rate responses based on post-stimulus-time (PST) histograms and temporal responses based on Fourier transforms of period histograms. 2. At stimulus intensities of 70 and 80 dB SPL, normalized rate responses provide a fairly good representation of the complex spectral structure of the stimulus, particularly in the low- and mid-frequency range. At higher intensities, rate responses saturate, and very little of the spectral structure of the complex stimulus can be seen in the profile of rate responses of the population. 3. Both AP and BP fibers phase-lock strongly to the fundamental (100 Hz) of the complex stimulus. These effects are relatively resistant to changes in stimulus intensity. Only a small number of fibers synchronize to the low-frequency spectral energy in the stimulus. The underlying spectral complexity of the stimulus is not accurately reflected in the timing of fiber firing, presumably because firing is 'captured' by the fundamental frequency. 4. Plots of average localized synchronized rate (ALSR), which combine both spectral and temporal information, show a similar, low-pass shape at all stimulus intensities. ALSR plots do not generally provide an accurate representation of the structure of the advertisement call. 5. The data suggest that anuran peripheral auditory fibers may be particularly sensitive to the amplitude envelope of sounds.

Acetylcholine modifies neuronal acoustic rate‐level functions in guinea pig auditory cortex by an muscarinic receptors

Cholinergic modification of neuronal responsiveness in auditory cortex includes alteration of spontaneous and tone-evoked neuronal discharge. Previously it was suggested that the effects of acetylcholine (ACh) and muscarinic agonists on neuronal discharge resembled those due to increases in the intensity of acoustic stimuli (Ashe et al. 1989). To determine the relationship between neuronal modifications due to ACh acting at muscarinic receptors and those due to changes in stimulus intensity, we determined acoustic rate-level functions for neurons in the auditory cortex of barbiturate-anesthetized guinea pigs before, during and after administration of ACh. ACh facilitated acoustic rate-level functions in 82% of the cells tested. In addition, during ACh administration 66% of neurons responded to stimuli that were previously subthreshold, that is, ACh decreased the response threshold. Cholinergic facilitation of rate-level functions was attenuated by the general muscarinic antagonist atropine. The nature of the muscarinic receptors involved in the actions of ACh was further examined by presenting single tones before, during, and after administration of ACh and specific muscarinic receptor subtype antagonists, either pirenzepine (M1) or gallamine (M2). ACh-induced facilitation of spontaneous and tone evoked neuronal discharge was antagonized by pirenzepine, but not by gallamine, suggesting the involvement of the M1 muscarinic receptor subtype. These data indicate that ACh can facilitate stimulus-evoked responses and decrease response thresholds for neurons in auditory cortex, possibly via activation of M1 muscarinic receptors. Such effects of ACh acting at muscarinic receptors could underly cholinergic regulation of information processing in the auditory cortex.

Brain-stem auditory evoked potentials in squirrel monkey ( Saimiri sciureus)

To more fully characterize brain-stem auditory evoked potentials (BAEPs) in non-human primates, BAEPs were recorded from chronically implanted epidural electrodes in 10 squirrel monkeys ( Saimiri sciureus). The effects of stimulus intensity, repetition rate, and anesthesia (ketamine 20 mg/kg i.m.) on peak latencies and inter-peak intervals were evaluated. Monkey wave forms consisted of approximately 7 peaks (I–VII), each exhibiting similar latencies across sessions, with later peaks exhibiting greater variability. In some subjects, additional peaks (IIa, IIIa) and slow potentials were recorded. The slow potentials provided a substratum for peaks IV through VII. As with human, monkey peaks exhibited systematic changes in latency with changes in stimulus intensity or repetition rate. These shifts included significant decreases in latency with increasing intensity for peaks I–IV and increases in latency with increases in repetition rate for peaks III, V, and VI. Inter-peak intervals were similar to those observed in human. Furthermore, ketamine anesthesia significantly delayed the latencies of most peaks (except I, V, and VII). Some differences between monkey and human BAEPs were evident in the relative amplitude of specific peaks. For example, peak V is typically most prominent in human, while this was true for peak III in monkey. The similarities between unanesthetized monkey and human inter-peak intervals suggest that the times required for impulses to reach particular brain-stem areas are conserved across primate species that vary in brain size. This supports the hypothesis that comparably numbered BAEP peaks in monkey and human index homologous processes. The data also suggest that the differences between animal and human BAEPs commonly reported may result from the use of anesthetics. In summary, unanesthetized monkey BAEPs resemble human BAEPs in morphology, number of peaks, polarity, latency variability, inter-peak intervals, slow potentials superimposed on the high-frequency peaks, and variations in morphology, amplitude, and resolution of peaks as a function of recording site. Thus, unanesthetized monkey BAEPs may be an excellent model for investigating the neural substrates of human BAEP or for determining species differences in acoustic processing among primates.

Physiological and anatomical studies of the interactions between Purkinje cells and basket cells in the cat's cerebellar cortex: evidence for a unitary relationship

Intracellular recordings have been obtained from neurons in lobule V of the cat's vermis, which were identified as basket cells following intracellular injections of HRP. Stimulation of the inferior cerebellar peduncle or peripheral nerves elicited an initial depolarizing and subsequent hyperpolarizing response. Neither potential could be graded with changes in stimulus intensity; both displayed all-or-none properties at threshold levels of stimulation. The depolarization and hyperpolarization were confirmed as an excitatory postsynaptic potential and an inhibitory postsynaptic potential (IPSP), respectively, on the basis of their response to intracellular injections of hyperpolarizing and depolarizing currents into the cell body. A possible source of the unitary IPSP is the Purkinje cell, via its recurrent axonal collaterals. To test this hypothesis, an electron microscopic analysis was carried out to define the synaptic relationships between the recurrent collaterals of an HRP-filled Purkinje cell and 3 basket cells. Serial section analysis reveals that collaterals from a single Purkinje cell contact several basket cells, but each basket cell received somatic input from only one Purkinje cell. These data provide an anatomical substrate for the unitary IPSP observed during intracellular recording from basket cells. The unitary nature of the Purkinje cell-basket cell interaction indicates that a very limited population of cortical neurons may be involved in local circuits that integrate afferent information in the cerebellar cortex.