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M Pedemonte

Publications and source records attributed to M Pedemonte.

28 records · Page 2Linked to original sources

Temperature dependence of two-tone rate suppression in the northern leopard frog, Rana pipiens pipiens.

The existence region of two-tone rate suppression in frog low-frequency auditory-nerve fibers was found to include a suppressive region below a fiber's characteristic frequency, contrary to previous reports. In response to 3 degrees C rise in core temperature, the area and the best suppressive frequency (BSF) of the low-side suppressive region significantly increased. Increasing core temperature of the frog by 6 degrees C resulted in significant changes in the high-side suppressive region: Its area decreased, and its BSF and best suppressive threshold (BST) increased. Constant-temperature control trials were designed to partially simulate the relative movement of the probe tone within the excitatory tuning curve which occurred during temperature shifts. Lowering the probe tone by 0.5 oct had no effect on the low-side suppressive region, but significantly increased the area and lowered the BSF and BST of the high-side suppressive region. Temperature shifts in the frog appear to have a differential effect on the low-side and high-side suppressive areas of low-frequency auditory-nerve fibers. Moreover, excitation and suppression also respond differentially to temperature shifts.

Acoustic Stimulation↗

Effects of sleep on the responses of single cells in the lateral superior olive.

The effects of behavioral shifts on auditory lateral superior olive neurons were analyzed in guinea-pigs during the sleep-waking cycle with single unit extracellular recordings at the unit characteristic frequency and with low sound intensity. Shifts in the number of spikes in response to pure tones and in spontaneous firing proved to be closely related to waking, slow wave and paradoxical sleep. All of the recorded lateral superior olive (LSO) auditory neurons showed sleep-related firing shifts. Moreover, changes in the pattern of discharge over time were observed in 15% of the LSO cells on passing from waking to sleep. Sleep may determine either an increase or a decrease of the firing number in response to sound. The most important change observed in decreasing firing units was the near-absence of units responding to sound in the paradoxical sleep phase during the last 40 ms of the response. The waking cues for binaural detection, studied with our experimental paradigm, disappeared during slow wave sleep. We thus conclude that the binaural function of some lateral superior olive neurons (11.5%) was impaired during this sleep period in the present experimental conditions. Auditory efferent pathways are postulated to impinge on the auditory processing at LSO nucleus level during the sleep-waking cycle. Thus, auditory unitary activity appears to be dependent on both incoming information, and a CNS descending action closely related to the waking and sleep periods. Functional interactions between pontine sleep-related groups of neurons and auditory system units are suggested.

Acoustic Stimulation↗

Single unit activity in the guinea-pig cochlear nucleus during sleep and wakefulness.

The effects of waking and sleep on the response properties of auditory units in the ventral cochlear nucleus (CN) were explored by using extracellular recordings in chronic guinea-pigs. Significant increases and decreases in firing rate were detected in two neuronal groups, a) the "sound-responding" and b) the "spontaneous" (units that do not show responses to any acoustic stimuli controlled by the experimenter). The "spontaneous" may be considered as belonging to the auditory system because the corresponding units showed a suppression of their discharge when the receptor was destroyed. The auditory CN units were characterized by their PSTH in response to tones at their characteristic frequency and also by the changes in firing rate and probability of discharge evaluated during periods of waking, slow wave and paradoxical sleep. The CNS performs functions dependent on sensory inputs during wakefulness and sleep phases. By studying the auditory input at the level of the ventral CN with constant sound stimuli, it was shown that, in addition to the firing rate shifts, some units presented changes in the temporal probability of discharge, implying central actions on the corresponding neurons. The mean latency of the responses, however, did not show significant changes throughout the sleep-waking cycle. The auditory efferent pathways are postulated to modulate the auditory input at CN level during different animal states. The probability of firing and the changes in the temporal pattern, as shown by the PSTH, are thus dependent on both the auditory input and the functional brain state related to the sleep-waking cycle.

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A search for a mesencephalic periaqueductal gray-cochlear nucleus connection.

Horseradish peroxidase placed into the ventral mesencephalic periaqueductal gray (PAG) and in the lateral superior olivary complex region demonstrated indirect paths towards the cochlear nucleus (CN). Because no direct connections could be observed, a pathway throughout the auditory efferent system was proposed. The results suggest three possibilities: 1) The PAG is connected to the lateral superior peri-olivary complex synapsing with known efferent fibers that reach the CN; 2) Neurons located at the dorsal PAG were demonstrated to be connected to the inferior colliculus (IC). The possibility of synapses with known neurons that run from IC to the CN is postulated; 3) Neurons in the trapezoid body, which are partially associated with a system that communicates with the CN, are also connected to and from the PAG. The present results anatomically support an extracellular study (1) describing PAG actions on CN units.

Animals↗

Periaqueductal gray influence on anteroventral cochlear nucleus unitary activity and naloxone effects.

The effect of periaqueductal gray (PAG) electrical stimulation on the response properties of auditory and 'spontaneously' firing units (abolished when the cochlea is destroyed) in the anteroventral cochlear nucleus (AVCN) was explored using extracellular recordings in acute guinea-pigs. Significant increases and decreases in firing rate were detected in both neuronal groups: only 4% of the sound-responding units were insensitive to PAG stimulation while the 'spontaneous' units showed significantly smaller changes in firing rate in response to PAG stimulation. The auditory AVCN neurons were categorized both by their sound post stimulus time (PST) histograms at their characteristic frequency (CF) and the changes in the probability of discharge after PAG stimulation while the tone burst was maintained constant. PAG was implicated in pain input modulation through enkephalin actions. Because enkephalins have been also observed at the CN level, a pharmacological approach administering naloxone was carried out. We observed that 1) naloxone abolished the unit discharge shifts observed after PAG stimulation and 2) when the drug was injected without PAG stimulation, it produced changes in the firing, increasing or decreasing, and shifts in the probability of discharge versus time, even in cases in which the firing rate was not altered. An involvement of the auditory efferent pathways to CN is postulated and a possible enkephalinergic factor is suggested as a modulator of the auditory input at this level. The probability of discharge observed in the PSTH at the AVCN is dependent on the auditory input plus the central efferent action to its neurons.

Acoustic Stimulation↗

Correlative changes of auditory nerve and microphonic potentials throughout sleep.

Gross cochlear potentials in response to alternating clicks and pure tone bursts were recorded in guinea-pigs with chronically implanted electrodes in the round window during sleep and the awake state. A significant increase in both averaged potentials, the compound auditory nerve action potential (cAP) and cochlear microphonics (CM) occurred in slow wave sleep (SWS) with a subsequent diminution in paradoxical sleep (PS) periods. The cAP, CM, amplitude and area averages were similar during quiet wakefulness and in PS. Moreover, as an episode of PS progressed, the recorded potentials continued to decrease. On the other hand, increased averaged values were again observed during a subsequent episode of SWS. An involvement of the efferent olivo-cochlear bundle is postulated, first, because it is the only known pathway connecting the CNS and the auditory periphery and, second, because several key pre-receptor variables (middle ear muscles and ossicles and sound-source ear relation) were either abolished or altered dramatically.

Acoustic Stimulation↗

Differential effects of benzodiazepines on cochlear and auditory nerve responses.

The influence exerted by chlordiazepoxide or midazolam upon auditory nerve compound action potential (cAP) and cochlear microphonic (CM) has been analyzed in chronic as well as in acutely prepared guinea pigs. Pre-receptorial variables were carefully controlled. The benzodiazepines dissociated the cochlear recorded potentials, increasing the cAP amplitude, in response to clicks, and decreasing the CM area, produced by a coherent pure tone pip. Both responses were dose related. A direct effect upon the cochlea was eliminated by local infusion of the drugs. It was also demonstrated to be a specific benzodiazepinic action because the use of an antagonist, Ro 15-1788, abolished the effect. Benzodiazepines could have increased the GABAergic activity at the pontine origins of the olivo-cochlear bundle or in the reticulo-cochlear fibers. These are the only central pathways that could be responsible for the effects obtained at the cochlea or auditory nerve levels. We suggest that this is the cause of the withdrawal of inhibitory tonus from the primary afferent fibers mediated by the efferent system (lateral superior olive), as may occur during dishabituation. It may also be the cause of the CM decrement, but the effect in this case would be exerted mainly through another set of efferent fibers (trapezoid body nucleus).

Action Potentials↗

Reciprocal actions between sensory signals and sleep.

To the best of our knowledge, there is no simple way to induce neural networks to shift from waking mode into sleeping mode. Our best guess is that a whole group of neurons would be involved and that the process would develop in a period of time and a sequence which are mostly unknown. The quasi-total sensory deprivation elicits a new behavioral state called somnolence. Auditory stimulation as well as total auditory deprivation alter sleep architecture. Auditory units exhibiting firing shifts on passing to sleep (augmenting or diminishing) are postulated to be locked to sleep-related networks. Those ( approximately 50%) that did not change during sleep are postulated to continue informing the brain as in wakefulness. A rhythmic functional plasticity of involved networks is postulated. A number of auditory and visual cells have demonstrated a firing phase locking to the hippocampal theta rhythm. This phase locking occurs both during wakefulness and sleep phases. The theta rhythm may act as an organizer of sensory information in visual and auditory systems, in all behavioral states adding a temporal dimension to the sensory processing. Sensory information from the environment and body continuously modulates the central nervous system activity, over which sleep phenomenology must develop. It also produces a basal tonus during wakefulness and sleep, determining changes in the networks that contribute to sleep development and maintenance and, eventually, it also leads to sleep interruption.

Acoustic Stimulation↗