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E H Chudler

Publications and source records attributed to E H Chudler.

25 records · Page 2Linked to original sources
PubMed1988

SI nociceptive neurons participate in the encoding process by which monkeys perceive the intensity of noxious thermal stimulation.

The activity of primary somatosensory (SI) cortical nociceptive neurons was recorded while the monkeys performed a psychophysical task in which they detected small increases in skin temperature superimposed on noxious levels of thermal stimulation. The detection latency to these stimuli, expressed as detection speed, was used as a measure of the perceived intensity of sensation. Two-thirds of the neurons that responded to noxious thermal stimulation increased their discharge in response to graded increases in stimulus intensity. The remaining neurons responded to noxious thermal stimulation, but did not grade their response with the intensity of the stimulus. The response of SI nociceptive neurons that encode the intensity of noxious thermal stimulation was significantly correlated with the monkey's detection speed. We conclude that SI nociceptive neurons are involved in the encoding process by which monkeys perceive the intensity of noxious thermal stimulation.

Afferent Pathways↗
PubMed1986

Cortical nociceptive responses and behavioral correlates in the monkey.

Experiments were performed to characterize cerebral cortical activity and pain behavior elicited by electrical stimulation of the tooth pulp in unanesthetized monkeys. Four monkeys were trained on two different operant paradigms: two on a simple escape task and two on an appetitive tolerance-escape task. All monkeys were implanted with bipolar stimulating electrodes in the right maxillary canine tooth and subdural recording electrodes over the left primary (SI) and/or secondary (SII) somatosensory cortices. Subdural tooth pulp-evoked potentials (TPEPs) recorded over the SII consisted of components P1 (27.5 ms), N1 (40.3 ms), P2 (84.0 ms), N2 (163.5 ms), P3 (295.3 ms), and N3 (468.0 ms). The long latency component (P3-N3) was found exclusively over the SII and was elicited by high intensity stimulation. The appearance of component P3-N3 required the recruitment of A delta nerve fibers into the maxillary nerve compound action potential and was correlated with high frequencies of escape. Administration of morphine sulfate (4 mg/kg, i.m.) caused a contemporaneous reduction in escape frequency and in the amplitude of P3-N3 recorded over the SII. The relationships between TPEP amplitude, escape behavior and A delta nerve fiber activity strongly suggest that the SII is involved with nociception and pain behavior.

Animals↗
PubMed1985

Physiological properties of intradental mechanoreceptors.

A major role of tooth receptors in signaling overt or impending tissue damage (nociception) has been previously established by substantial evidence from mechanical, thermal and chemical stimulation of exposed dentin. We report evidence showing that some intradental receptors in canine teeth of the cat detect mechanical transients applied to intact enamel. This new finding suggests that dental innervation may play an important non-nociceptive role in oral function such as detecting tooth contact during mastication and swallowing.

Animals↗
PubMed1984

Origins of tooth pulp-evoked far-field and early near-field potentials in the cat.

Electrical stimulation of the mandibular canine tooth pulp in barbiturate-anesthetized cats activated myelinated A-beta-fibers in the inferior alveolar (dental) nerve and evoked a complex pattern of short-latency potentials that were recorded epidurally from the cortex. Three far-field components ( FFPs designated I, IIa,b, and IIIa,b) and two early near-field components ( ENFPs designated P1 and N1) were identified from computer-averaged potentials recorded over the contralateral lateral sigmoid gyrus or ipsilateral presylvian /anterior coronal gyri. Several corroborative lines of evidence indicated that tooth pulp-evoked FFPs and ENFPs originate from the following generator sources: I, inferior alveolar (dental) nerve/semilunar (gasserian) ganglion; IIa,b, trigeminal lemniscal fibers from the principal (main) sensory nucleus; IIIa,b, thalamocortical fibers from the thalamic ventral posteromedial nucleus; P1, N1, cytoarchitectural area 3 on the banks of the coronal or orbital sulcus. The latencies and waveforms of volume-conducted, surface-recorded potentials were not significantly different from those recorded at putative generator sites along the trigeminal lemniscal projection system. The short latencies and distribution of surface- and depth-recorded tooth pulp-evoked potentials suggested bilateral, trisynaptic paths from peripheral nerve to cortical neurons. Amplitude measurements of FFPs and ENFPs recorded at the cortical, epidural surface were compared to calculated values based on a mathematical model of two concentric spheres of inhomogeneous media in which a single equivalent dipole is radially oriented at some distance from the center. The morphology and distribution of FFPs and ENFPs are discussed in relationship to source geometry. Surface- and depth-recorded tooth pulp-evoked potentials had recovery functions that were covariant with rates of stimulation. In addition, stimulation of putative generator sites along the trigeminal lemniscal system reproduced portions of the tooth pulp-evoked surface-recorded potentials. Selective ablation of trigeminal cortical area 3 abolished ENFPs and lesions of lemniscal brain stem sites abolished FFPs . Disruption of extralemniscal brain stem sites had no effect on the surface-recorded evoked potentials examined. These findings and other supporting evidence from previous studies imply that the projection of fast-conducting tooth pulp input to the cortex may subserve a nonnociceptive modality and participate in sensorimotor integration.

Afferent Pathways↗
PubMed1981

Effects of naloxone and hypophysectomy on electroconvulsive shock-induced analgesia.

Powerful analgesia follows electroconvulsive shock in both hypophysectomized and sham-operated rats. Antagonism of this analgesia by naloxone implicates opioid peptides in its mediation, its occurrence in hypophysectomized animals implicating opioids of central nervous system rather than pituitary origin. Because naloxone only partially reduces electroconvulsive shock analgesia in hypophysectomized rats, the participation of another, non-opioid analgesia substrate also seems indicated.

Animals↗