- Email: [email protected]
Processing of nociceptive information in the dorsal horn: Difference between noci-specific (NS) and wide dynamic range (WDR) neurones
PROCESSING OF NOCICEPTIVE INFORMATION IN THE DORSAL HORN: DIFFERENCE BETWEEN NOCI-SPECIFIC (NS) AND WIDE DYNAMIC RANGE (WDR) NEURONES.
ACC
Hall
C
Chairnun: D. Le Bars, INSERM, Unite 161, Paris, France Participanfs: Gj grvero, De t.. of Physiology, Univ. of Bristol Med. School, Bristol, U Wlllls, Mparme Biomedical Institute, Galveston, TX, USA
The role of NS and WDR neurones in the processing of nociceptive information is widely accepted although many questions remain unsolved. Some problems relate to the way in which neurones are sampled and to the criteria of classification: both sampling and criteria of classification appear highly “laboratory sensitive” and will determine the view of any articular research groups as to the functional role of the two types of cells. The existence of sub-classes of R S and WDR neurones further increases the difficulties. Regarding the properties of NS/WDR neurones, several issues will be approached: - Location within the dorsal horn Size of the receptive fields Capacities of discrimination between nociceptive and nonnociceptive information - Encoding ca acities of the intensity of nociceptive stimuli Visceral an dpmuscular in uts Change of receptive fiel B properties following a noxious stimulus Modulation by tonic descending inhibition Modulation by stimulation of supras inal structures Modulation by Diffuse Noxious Inhi g itory Controls Modulation by segmental and propriospinal mechanisms Susceptibility to pharmacological agents Funiculi in which ascending axons travel - Supraspinal target Properties clearly diverging will be emphasized so as to facilitate the discrimination between these two neuronal classes. In this respect, contributions of the audience will be welcome.
PAIN FROM MYELINATED AFFERENTS
ri
Chaimmn:
W.J. Roberts, Neurological Sciences Institute, Good Samaritan Hosp. and Medical Center, Portland, OR, USA Participants:
I
ACC
Hall
D
Ii
S.A. Lynch_,Neurobiology and Anesthesiology Branch, National Institute of Dental Research - NIH, Bethesda, MD, USA U. Lindblom, Dept. of Neurology, Karolinska Sjukhuset, Stockholm Sweden Neuropathic pain results from central responses to activity in primary afferent fibers, and it is commonly assumed that the fibers that elicit pain innervate nociceptors. There is good experim.ental evidence to support this view for acute induced pain in humans. However, the physiological basis for persistent pains is more complex. Evidence from both human and animal studies indicates that activity in large myelinated (A-beta) afferents, which normally subserve sensations of touch and pressure, are responsible at least in part for the pain evoked by non-noxious stimuli in some individuals with persistent spontaneous pain. The participants will review theories and evidence relating to pain from A-beta afferents. The consistency of findings will be examined from studies of humans and experimental animals with adequate mechanical stimulation, electrical stimulation, and selective nerve fiber blocks. Physiological mechanisms will be discussed, as will the conditions under which such pain exists and the neurological signs and methods for diagnosis.
1
ACC
Hall
C
Chairnun: D. Le Bars, INSERM, Unite 161, Paris, France Participanfs: Gj grvero, De t.. of Physiology, Univ. of Bristol Med. School, Bristol, U Wlllls, Mparme Biomedical Institute, Galveston, TX, USA
The role of NS and WDR neurones in the processing of nociceptive information is widely accepted although many questions remain unsolved. Some problems relate to the way in which neurones are sampled and to the criteria of classification: both sampling and criteria of classification appear highly “laboratory sensitive” and will determine the view of any articular research groups as to the functional role of the two types of cells. The existence of sub-classes of R S and WDR neurones further increases the difficulties. Regarding the properties of NS/WDR neurones, several issues will be approached: - Location within the dorsal horn Size of the receptive fields Capacities of discrimination between nociceptive and nonnociceptive information - Encoding ca acities of the intensity of nociceptive stimuli Visceral an dpmuscular in uts Change of receptive fiel B properties following a noxious stimulus Modulation by tonic descending inhibition Modulation by stimulation of supras inal structures Modulation by Diffuse Noxious Inhi g itory Controls Modulation by segmental and propriospinal mechanisms Susceptibility to pharmacological agents Funiculi in which ascending axons travel - Supraspinal target Properties clearly diverging will be emphasized so as to facilitate the discrimination between these two neuronal classes. In this respect, contributions of the audience will be welcome.
PAIN FROM MYELINATED AFFERENTS
ri
Chaimmn:
W.J. Roberts, Neurological Sciences Institute, Good Samaritan Hosp. and Medical Center, Portland, OR, USA Participants:
I
ACC
Hall
D
Ii
S.A. Lynch_,Neurobiology and Anesthesiology Branch, National Institute of Dental Research - NIH, Bethesda, MD, USA U. Lindblom, Dept. of Neurology, Karolinska Sjukhuset, Stockholm Sweden Neuropathic pain results from central responses to activity in primary afferent fibers, and it is commonly assumed that the fibers that elicit pain innervate nociceptors. There is good experim.ental evidence to support this view for acute induced pain in humans. However, the physiological basis for persistent pains is more complex. Evidence from both human and animal studies indicates that activity in large myelinated (A-beta) afferents, which normally subserve sensations of touch and pressure, are responsible at least in part for the pain evoked by non-noxious stimuli in some individuals with persistent spontaneous pain. The participants will review theories and evidence relating to pain from A-beta afferents. The consistency of findings will be examined from studies of humans and experimental animals with adequate mechanical stimulation, electrical stimulation, and selective nerve fiber blocks. Physiological mechanisms will be discussed, as will the conditions under which such pain exists and the neurological signs and methods for diagnosis.
1