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Central Control of Nociception

Walter Zieglgänsberger

10.1002/cphy.cp010411

Source: Supplement 4: Handbook of Physiology, The Nervous System, Intrinsic Regulatory Systems of the Brain

Originally published: 1986

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Pain and Its Measurement
2 Primary Afferent System
2.1 Fiber Systems Signaling Sensory Pain From Skin, Muscle, and Viscera
2.2 Neurotransmitters in Primary Afferent Fibers
3 Neuronal Circuitry Mediating Nociception
3.1 Spinofugal Projection Systems and Intrinsic Spinal Circuitry
4 Neurotransmitters and Integration of Nociceptive Information
4.1 Amino Acid Neurotransmitters
4.2 Monoamines
4.3 Neuropeptides
5 Opioid‐Induced Analgesia
5.1 Opioid Actions on Central Neurons Signaling Sensory Pain
5.2 Mode of Action of Opioids
5.3 Actions of Naloxone
6 Pain Modulation Triggered by Peripheral Mechanisms
6.1 Activation of Low‐Threshold Receptors
6.2 Acupuncture
6.3 Transcutaneous Nerve Stimulation
6.4 Activation of High‐Threshold Receptors
6.5 Stress‐Induced Analgesia
6.6 Analgesia Evoked by Hypnosis
7 Pain Modulation Triggered by Central Stimulation
7.1 Dorsal Column Stimulation
7.2 Stimulation of Descending Pathways
7.3 Monoaminergic System and Stimulus‐Produced Analgesia
7.4 Opioid‐Induced and Stimulus‐Produced Analgesia
8 Epilogue
Figure 1. Figure 1.

Conceptual model of sensory, motivational, and central control determinants of pain. Output of T (transmission) cells of gate control system projects to sensory‐discriminative system and motivational‐affective system. Central control trigger is represented by line running from large‐fiber system to central control processes; these, in turn, project back to gate control system and to sensory‐discriminative and motivational‐affective systems. All 3 systems interact and project to motor system.

From Melzack 483
Figure 2. Figure 2.

Schematic illustration of different peptide systems in spinal cord of rat. At least 4 different types of neurons can be recognized. 1: Peptide neurons descend from brain, terminating in various parts of gray matter. Dotted lines, hypothetical projection. 2: Primary sensory neurons, with cell bodies in spinal ganglia, terminate in dorsal horn. 3: Local spinal interneurons or propriospinal neurons, with cell bodies in dorsal horn or in other parts of gray matter (not shown), terminate in dorsal horn. 4: Neurons in sympathetic lateral column (or in parasympathetic intermediolateral column) project out from spinal cord to periphery. Note that coexistence of peptides with classic transmitters, such as catecholamines and 5‐HT, is not indicated here. Abbreviations denote peptide against which antiserum was raised: ANG II, angiotensin II; APP, avian pancreatic polypeptide; CCK, cholecystokinin; ENK, enkephalin; NT, neurotensin; SOM, somatostatin; SP, substance P; TRH, thyrotropin‐releasing hormone; VIP, vasoactive intestinal polypeptide.

From Hökfelt et al. 340
Figure 3. Figure 3.

A: schematic indicating location of Rexed's laminae from segment L7 of cat spinal cord. B: course and destination of afferent fibers from dorsal root to dorsal horn. Afferent fibers: 1, muscle spindle afferent; 2, hair afferent; 3, touch corpuscle afferent; 4, Aδ‐afferent; 5, C afferent.

A adapted from Rexed 593; B from Wall 706
Figure 4. Figure 4.

Spinothalamic tract cell in primate with wide‐dynamic‐range receptive field. Cell was located in lateral portion of neck of dorsal horn (A). Receptive field included area sensitive to low‐intensity mechanical stimuli (black area in B), surrounded by area requiring higher‐intensity stimuli (hatched area). Cell was excited by hair movement (C), pressure (D), and pinch (E). Pinch was most effective stimulus. Temperature changes from 35°C to 50°C (F) and from 20°C to 10°C (G) excited cell. Lower traces in F and G are records of temperature at thermode‐skin interface. Time scale applies to C‐G.

From Chung et al. 145
Figure 5. Figure 5.

Viscerosomatic convergence in spinothalamic neuron of monkey (T12 segment, lamina V). A: responses to squeezing skin of flank, distension of urinary bladder (60‐ml volume injected rapidly), and manual compression of exposed ipsilateral testicle. B: summation of responses to distension of bladder (80 cm H2O) and squeezing skin of flank. C: reversed sequence of B.

From Milne et al. 495
Figure 6. Figure 6.

Reciprocal sensory interaction. Scheme to illustrate possible interactions among dorsal horn and substantia gelatinosa neurons, leading to reciprocal interaction between afferent inputs from mechanoreceptors and nociceptors. SG, substantia gelatinosa neurons as classified by Cervero et al. 836; 1, 2, 3, and Th, classes of dorsal horn neurons according to Cervero et al. 119.

From Iggo 356
Figure 7. Figure 7.

Summary diagram of terminal and perikaryal immunoreactivity of glutamate decarboxylase (GAD) and peptide‐containing interneurons. ENK, enkephalin; SUB P, substance P; SOM, somatostatin; APP, avian pancreatic polypeptide; NT, neurotensin; 5‐HT, 5‐hydroxytryptamine. Perikarya with proximal dendritic segments illustrated against background of stipple, which indicates distribution of intrinsic peptide or GAD + terminals.

From Hunt et al. 353
Figure 8. Figure 8.

Diagram of neural systems important in pain and pain modulation. Small‐diameter nociceptive afferents (S) and larger‐diameter nonnociceptive fibers (L) activate spinal mechanisms leading to generation of impulses ascending to higher centers. Neurons in ventrobasal thalamus [ventralis posterolateralis shown here (VPL)] receive input from fibers of dorsal column‐medial lemniscal system 1 and from that portion of ventrolateral spinal cord 2 forming spinothalamic tract. Projection of these neurons to somatosensory (som sens) cortex provides basis for discriminative aspects of somesthesis, possibly including pain. Other fibers ascending from ventrolateral spinal cord 3 send projections into brain stem reticular formation (RF) and to medial thalamus. Ascending reticular formation fibers also project to medial thalamus and hypothalamus (hyp), where they may influence limbic forebrain mechanisms subserving motivational and affective components of pain. Both discriminative and motivational‐affective systems are modulated by descending pathways 3 acting at thalamic, brain stem, and spinal levels.

Adapted from Casey 112
Figure 9. Figure 9.

Responses of high‐threshold somatosensory area I cortical neuron (monkey) to mechanical and thermal stimuli. A: receptive field location was confined to glabrous skin of hallux. B: location of recording site was identified to be in layer 4 at junction between areas 3b and 1. C: peristimulus time histogram of responses to graded series of mechanical stimuli. D: film records of action potentials before (upper trace) and during (lower trace) noxious heat pulse from 35°C to 50°C. E: peristimulus time histogram of response to noxious heat pulse (time course of temperature indicated above abscissa). Bin width was 1 s for all peristimulus time histograms.

From Kenshalo and Isensee 395
Figure 10. Figure 10.

Schematic illustration of sections through rostral medulla of rat and cat. Several structures are indicated, each of which probably exerts control of spinal nociceptors: NRM; nucleus reticularis gigantocellularis (Rgc); nucleus reticularis gigantocellularis pars α (Rgc α); nucleus reticularis magnocellularis (Rmc); probable rat analog, nucleus reticularis paragigantocellularis (Rpg); and more lateral nucleus reticularis paragigantocellularis lateralis (Rpgl). Serotonin‐containing neurons are found in NRM and in Rpgl but not in Rmc or Rpg.

From Basbaum and Fields 39
Figure 11. Figure 11.

Effect of intravenous morphine on wide‐dynamic‐range neuron in dorsal horn of rat. Poststimulus histogram [50 trials; time base (TB), 5 ms] of responses induced by stimulation of sural nerve (16 V; pulse duration, 1 ms). First component related to Aα‐input is truncated; only discharges related to Aδ‐ and C‐fiber inputs are considered. Length between nerve‐stimulating electrodes and recording site in cord was 18 cm.

From LeBars et al. 431
Figure 12. Figure 12.

Ratemeter recording of wide‐dynamic‐range neuron displaying depressant response to microiontophoretic application of Met‐enkephalin (M‐Enk). Depressant effect of M‐Enk on this spontaneously active neuron was antagonized by prior iontophoretic application of naloxone. Recordings are continuous, and drug applications are indicated by horizontal bars; ejection currents (subscripts) are given in nanoamperes (10−9 A).

Adapted from Zieglgänsberger and Tulloch 804
Figure 13. Figure 13.

Schematic diagram illustrating hypothesized (enkephalinergic) control mechanism of neurons in substantia gelatinosa over multimodal neurons involved in somatosensory perception. Small bipolar (enkephalinergic) neuron impinges together with afferent large‐ and small‐diameter fibers on dendrites of laminae 4 and 5 cells carrying opiate receptors (dots). Inhibitory interneurons (IN) have postulated to make C‐fiber input to bipolar neurons inhibitory (see ref. 836). Descending pathways can act directly, e.g., via noradrenergic, dopaminergic, or serotonergic pathways, on neurons of spinothalamic system (L4 and L5) or via enkephalinergic neurons in substantia gelatinosa (only this part of descending influence would be sensitive to opiate antagonist naloxone). Presynaptic contact is marked with question mark. +, ‐ Represent excitatory and inhibitory influences. SOM indicates possibility of primary afferent inhibition by somatostatin. This inhibitory‐acting neuropeptide was demonstrated in primary afferent small‐caliber fibers (see ref. 335).

Adapted from Zieglgänsberger and Tulloch 804
Figure 14. Figure 14.

Different types of descending inhibitory influences in dorsal horn. A: encoding of intensity of noxious skin heating in single dorsal horn neuron as affected by stimulation in periaqueductal gray (PAG) and mesencephalic lateral reticular formation (LRF). B: location of stimulation sites in midbrain.

From Carstens et al. 104
Figure 15. Figure 15.

Increased spontaneous firing and enhanced nociceptive responses of lamina V neuron after naloxone administration. Neuron was excited by alternately heating glabrous skin of left hindpaw above 45°C and deflecting adjacent hairs by a moving air jet. Responses remained enhanced for >20 min after administration of naloxone, 0.5 mg/kg iv.

From Duggan and Johnson 194
Figure 16. Figure 16.

Increased reflexes and excitatory postsynaptic potentials (EPSPs) recorded in motoneuron after administration of naloxone, 0.1 mg/kg iv. Reflexes were recorded in S1 ventral root. Intracellular records were obtained with 1.2 M potassium citrate‐containing electrode. A: responses to electrical stimulation combined medial and lateral gastrocnemius nerves (MLG) with stimulus strength 1.5 times threshold for fastest‐conducting fibers. On reflex records, arrow marks timing of nerve stimulus. On intracellular records, stimulus coincided with the trailing edge of 2‐mV calibration pulse. After naloxone, neuron fired to each nerve stimulus. Upward arrow indicates that upper part of each action potential was clipped by amplifier gain used to record the much smaller EPSP. B: responses to stimulation of tibial nerve with stimulus 3 times threshold for fastest‐conducting fibers. Timing of stimulus as outlined in A.

From Duggan 186
Figure 17. Figure 17.

Effects of diffuse noxious inhibitory control evoked from various parts of body by noxious pinch (period of pinch arrowed) on response of convergent neuron to regular light stroking (dots) applied every 10 s.

From LeBars et al. 427
Figure 18. Figure 18.

A: inhibition of responses of wide‐dynamic‐range spinothalamic tract cell of monkey to stimulation of A‐ or C‐fibers of sural nerve by descending volleys initiated by stimulation in nucleus raphe magnus (NRM). Histograms in A and C show control responses to stimulation of A‐ and C‐fibers, respectively. Inset in C is C‐fiber volley recorded from sural nerve. Stimulation in NRM during times shown by bars in B and D (150‐μA pulses at 333 Hz) inhibited responses. E shows location of stimulating electrode in sagittal section at midline of brain stem.

From Gerhart et al. 249
Figure 19. Figure 19.

Inhibition of high‐threshold spinothalamic tract (STT) cell of monkey by stimulation in NRM. A: response of cell to electrical stimulation of skin and inhibition of this response after stimulation in NRM (10 50‐μA shocks at 333 Hz). Inhibition (as percentage of control response) increases with increasing stimulus strength (10 stimuli) (B) or with increasing numbers of stimulus pulses (100 μA) (C). D: location of STT cell. E: receptive field. F: location of stimulation electrode. RM, nucleus raphe magnus; VII, facial nucleus. G: time course of inhibition (stimulus‐train duration indicated by solid bar at bottom).

From Willis et al. 746
Figure 20. Figure 20.

Inhibitory postsynaptic potential (IPSP) evoked in spinothalamic neuron by NRM stimulation. Antidromic spike in A resulted from stimulation in contralateral ventral posterior lateral nucleus of thalamus. For this record, calibration bars at center bottom represent 20 mV and 2 ms. Spikes in B are background discharge of impaled cell. Stimulation at point indicated in inset in C inhibited background discharge. Stimulus‐train parameters for this and remaining records were 100‐ms train of 0.1‐ms pulses at 333 Hz and 200 μA. Calibrations: 20 mV, 20 ms. The IPSP in D was recorded with DC‐coupled amplifier. Hyperpolarization outlasted sweep, as shown by comparison with reference trace. The NRM‐train duration indicated by horizontal bar under record in this and following traces. Calibrations: 2 mV, 50 ms. E‐H: IPSP during passage of graded amounts of current through acetate‐filled microelectrode. I: field potential evoked by same NRM stimulus when micro‐electrode was just outside cell. Calibrations: 2 mV, 20 ms.

From Giesler et al. 255
Figure 21. Figure 21.

Schematic representation of system employed for superfusing in situ spinal cord of anesthetized rat. Polyethylene 10 (PE 10) catheter used for infusion is inserted through cisterna magna to caudal level of lumbar cord. Outflow cannula is placed into cisterna magna. Artificial cerebrospinal fluid is perfused at rate of 100 μl/min and collected by withdrawal syringe and iced sampling tubes. Modification of release from spinal cord is achieved in this schematic by placement of electrode into raphe magnus. In other experiments, microinjection cannulae were placed into periaqueductal gray.

From Yaksh and Hammond 766
Figure 22. Figure 22.

Release of serotonin and norepinephrine into spinal cord superfusates of 2 representative rats after electrical stimulation of nucleus raphe magnus. Left: sites of stimulation indicated on coronal sections of medulla by black circles. After collection of 25‐min sample of superfusate to determine basal efflux of serotonin and norepinephrine, raphe magnus was stimulated at 25 Hz with 0.5 ms square‐wave pulses of either 150 or 250 μA for 25 min. During stimulation, another sample of superfusate was collected to determine release of serotonin and norepinephrine evoked by raphe stimulation. Quantitation of amines was by high‐pressure liquid chromatography with electrochemical detection. Right: release of serotonin (5‐HT) and norepinephrine (NE) expressed as ng/ml superfusate under basal conditions (B; open bars) and during stimulation of raphe magnus (S; stippled bars).

From Yaksh and Hammond 766


Figure 1.

Conceptual model of sensory, motivational, and central control determinants of pain. Output of T (transmission) cells of gate control system projects to sensory‐discriminative system and motivational‐affective system. Central control trigger is represented by line running from large‐fiber system to central control processes; these, in turn, project back to gate control system and to sensory‐discriminative and motivational‐affective systems. All 3 systems interact and project to motor system.

From Melzack 483


Figure 2.

Schematic illustration of different peptide systems in spinal cord of rat. At least 4 different types of neurons can be recognized. 1: Peptide neurons descend from brain, terminating in various parts of gray matter. Dotted lines, hypothetical projection. 2: Primary sensory neurons, with cell bodies in spinal ganglia, terminate in dorsal horn. 3: Local spinal interneurons or propriospinal neurons, with cell bodies in dorsal horn or in other parts of gray matter (not shown), terminate in dorsal horn. 4: Neurons in sympathetic lateral column (or in parasympathetic intermediolateral column) project out from spinal cord to periphery. Note that coexistence of peptides with classic transmitters, such as catecholamines and 5‐HT, is not indicated here. Abbreviations denote peptide against which antiserum was raised: ANG II, angiotensin II; APP, avian pancreatic polypeptide; CCK, cholecystokinin; ENK, enkephalin; NT, neurotensin; SOM, somatostatin; SP, substance P; TRH, thyrotropin‐releasing hormone; VIP, vasoactive intestinal polypeptide.

From Hökfelt et al. 340


Figure 3.

A: schematic indicating location of Rexed's laminae from segment L7 of cat spinal cord. B: course and destination of afferent fibers from dorsal root to dorsal horn. Afferent fibers: 1, muscle spindle afferent; 2, hair afferent; 3, touch corpuscle afferent; 4, Aδ‐afferent; 5, C afferent.

A adapted from Rexed 593; B from Wall 706


Figure 4.

Spinothalamic tract cell in primate with wide‐dynamic‐range receptive field. Cell was located in lateral portion of neck of dorsal horn (A). Receptive field included area sensitive to low‐intensity mechanical stimuli (black area in B), surrounded by area requiring higher‐intensity stimuli (hatched area). Cell was excited by hair movement (C), pressure (D), and pinch (E). Pinch was most effective stimulus. Temperature changes from 35°C to 50°C (F) and from 20°C to 10°C (G) excited cell. Lower traces in F and G are records of temperature at thermode‐skin interface. Time scale applies to C‐G.

From Chung et al. 145


Figure 5.

Viscerosomatic convergence in spinothalamic neuron of monkey (T12 segment, lamina V). A: responses to squeezing skin of flank, distension of urinary bladder (60‐ml volume injected rapidly), and manual compression of exposed ipsilateral testicle. B: summation of responses to distension of bladder (80 cm H2O) and squeezing skin of flank. C: reversed sequence of B.

From Milne et al. 495


Figure 6.

Reciprocal sensory interaction. Scheme to illustrate possible interactions among dorsal horn and substantia gelatinosa neurons, leading to reciprocal interaction between afferent inputs from mechanoreceptors and nociceptors. SG, substantia gelatinosa neurons as classified by Cervero et al. 836; 1, 2, 3, and Th, classes of dorsal horn neurons according to Cervero et al. 119.

From Iggo 356


Figure 7.

Summary diagram of terminal and perikaryal immunoreactivity of glutamate decarboxylase (GAD) and peptide‐containing interneurons. ENK, enkephalin; SUB P, substance P; SOM, somatostatin; APP, avian pancreatic polypeptide; NT, neurotensin; 5‐HT, 5‐hydroxytryptamine. Perikarya with proximal dendritic segments illustrated against background of stipple, which indicates distribution of intrinsic peptide or GAD + terminals.

From Hunt et al. 353


Figure 8.

Diagram of neural systems important in pain and pain modulation. Small‐diameter nociceptive afferents (S) and larger‐diameter nonnociceptive fibers (L) activate spinal mechanisms leading to generation of impulses ascending to higher centers. Neurons in ventrobasal thalamus [ventralis posterolateralis shown here (VPL)] receive input from fibers of dorsal column‐medial lemniscal system 1 and from that portion of ventrolateral spinal cord 2 forming spinothalamic tract. Projection of these neurons to somatosensory (som sens) cortex provides basis for discriminative aspects of somesthesis, possibly including pain. Other fibers ascending from ventrolateral spinal cord 3 send projections into brain stem reticular formation (RF) and to medial thalamus. Ascending reticular formation fibers also project to medial thalamus and hypothalamus (hyp), where they may influence limbic forebrain mechanisms subserving motivational and affective components of pain. Both discriminative and motivational‐affective systems are modulated by descending pathways 3 acting at thalamic, brain stem, and spinal levels.

Adapted from Casey 112


Figure 9.

Responses of high‐threshold somatosensory area I cortical neuron (monkey) to mechanical and thermal stimuli. A: receptive field location was confined to glabrous skin of hallux. B: location of recording site was identified to be in layer 4 at junction between areas 3b and 1. C: peristimulus time histogram of responses to graded series of mechanical stimuli. D: film records of action potentials before (upper trace) and during (lower trace) noxious heat pulse from 35°C to 50°C. E: peristimulus time histogram of response to noxious heat pulse (time course of temperature indicated above abscissa). Bin width was 1 s for all peristimulus time histograms.

From Kenshalo and Isensee 395


Figure 10.

Schematic illustration of sections through rostral medulla of rat and cat. Several structures are indicated, each of which probably exerts control of spinal nociceptors: NRM; nucleus reticularis gigantocellularis (Rgc); nucleus reticularis gigantocellularis pars α (Rgc α); nucleus reticularis magnocellularis (Rmc); probable rat analog, nucleus reticularis paragigantocellularis (Rpg); and more lateral nucleus reticularis paragigantocellularis lateralis (Rpgl). Serotonin‐containing neurons are found in NRM and in Rpgl but not in Rmc or Rpg.

From Basbaum and Fields 39


Figure 11.

Effect of intravenous morphine on wide‐dynamic‐range neuron in dorsal horn of rat. Poststimulus histogram [50 trials; time base (TB), 5 ms] of responses induced by stimulation of sural nerve (16 V; pulse duration, 1 ms). First component related to Aα‐input is truncated; only discharges related to Aδ‐ and C‐fiber inputs are considered. Length between nerve‐stimulating electrodes and recording site in cord was 18 cm.

From LeBars et al. 431


Figure 12.

Ratemeter recording of wide‐dynamic‐range neuron displaying depressant response to microiontophoretic application of Met‐enkephalin (M‐Enk). Depressant effect of M‐Enk on this spontaneously active neuron was antagonized by prior iontophoretic application of naloxone. Recordings are continuous, and drug applications are indicated by horizontal bars; ejection currents (subscripts) are given in nanoamperes (10−9 A).

Adapted from Zieglgänsberger and Tulloch 804


Figure 13.

Schematic diagram illustrating hypothesized (enkephalinergic) control mechanism of neurons in substantia gelatinosa over multimodal neurons involved in somatosensory perception. Small bipolar (enkephalinergic) neuron impinges together with afferent large‐ and small‐diameter fibers on dendrites of laminae 4 and 5 cells carrying opiate receptors (dots). Inhibitory interneurons (IN) have postulated to make C‐fiber input to bipolar neurons inhibitory (see ref. 836). Descending pathways can act directly, e.g., via noradrenergic, dopaminergic, or serotonergic pathways, on neurons of spinothalamic system (L4 and L5) or via enkephalinergic neurons in substantia gelatinosa (only this part of descending influence would be sensitive to opiate antagonist naloxone). Presynaptic contact is marked with question mark. +, ‐ Represent excitatory and inhibitory influences. SOM indicates possibility of primary afferent inhibition by somatostatin. This inhibitory‐acting neuropeptide was demonstrated in primary afferent small‐caliber fibers (see ref. 335).

Adapted from Zieglgänsberger and Tulloch 804


Figure 14.

Different types of descending inhibitory influences in dorsal horn. A: encoding of intensity of noxious skin heating in single dorsal horn neuron as affected by stimulation in periaqueductal gray (PAG) and mesencephalic lateral reticular formation (LRF). B: location of stimulation sites in midbrain.

From Carstens et al. 104


Figure 15.

Increased spontaneous firing and enhanced nociceptive responses of lamina V neuron after naloxone administration. Neuron was excited by alternately heating glabrous skin of left hindpaw above 45°C and deflecting adjacent hairs by a moving air jet. Responses remained enhanced for >20 min after administration of naloxone, 0.5 mg/kg iv.

From Duggan and Johnson 194


Figure 16.

Increased reflexes and excitatory postsynaptic potentials (EPSPs) recorded in motoneuron after administration of naloxone, 0.1 mg/kg iv. Reflexes were recorded in S1 ventral root. Intracellular records were obtained with 1.2 M potassium citrate‐containing electrode. A: responses to electrical stimulation combined medial and lateral gastrocnemius nerves (MLG) with stimulus strength 1.5 times threshold for fastest‐conducting fibers. On reflex records, arrow marks timing of nerve stimulus. On intracellular records, stimulus coincided with the trailing edge of 2‐mV calibration pulse. After naloxone, neuron fired to each nerve stimulus. Upward arrow indicates that upper part of each action potential was clipped by amplifier gain used to record the much smaller EPSP. B: responses to stimulation of tibial nerve with stimulus 3 times threshold for fastest‐conducting fibers. Timing of stimulus as outlined in A.

From Duggan 186


Figure 17.

Effects of diffuse noxious inhibitory control evoked from various parts of body by noxious pinch (period of pinch arrowed) on response of convergent neuron to regular light stroking (dots) applied every 10 s.

From LeBars et al. 427


Figure 18.

A: inhibition of responses of wide‐dynamic‐range spinothalamic tract cell of monkey to stimulation of A‐ or C‐fibers of sural nerve by descending volleys initiated by stimulation in nucleus raphe magnus (NRM). Histograms in A and C show control responses to stimulation of A‐ and C‐fibers, respectively. Inset in C is C‐fiber volley recorded from sural nerve. Stimulation in NRM during times shown by bars in B and D (150‐μA pulses at 333 Hz) inhibited responses. E shows location of stimulating electrode in sagittal section at midline of brain stem.

From Gerhart et al. 249


Figure 19.

Inhibition of high‐threshold spinothalamic tract (STT) cell of monkey by stimulation in NRM. A: response of cell to electrical stimulation of skin and inhibition of this response after stimulation in NRM (10 50‐μA shocks at 333 Hz). Inhibition (as percentage of control response) increases with increasing stimulus strength (10 stimuli) (B) or with increasing numbers of stimulus pulses (100 μA) (C). D: location of STT cell. E: receptive field. F: location of stimulation electrode. RM, nucleus raphe magnus; VII, facial nucleus. G: time course of inhibition (stimulus‐train duration indicated by solid bar at bottom).

From Willis et al. 746


Figure 20.

Inhibitory postsynaptic potential (IPSP) evoked in spinothalamic neuron by NRM stimulation. Antidromic spike in A resulted from stimulation in contralateral ventral posterior lateral nucleus of thalamus. For this record, calibration bars at center bottom represent 20 mV and 2 ms. Spikes in B are background discharge of impaled cell. Stimulation at point indicated in inset in C inhibited background discharge. Stimulus‐train parameters for this and remaining records were 100‐ms train of 0.1‐ms pulses at 333 Hz and 200 μA. Calibrations: 20 mV, 20 ms. The IPSP in D was recorded with DC‐coupled amplifier. Hyperpolarization outlasted sweep, as shown by comparison with reference trace. The NRM‐train duration indicated by horizontal bar under record in this and following traces. Calibrations: 2 mV, 50 ms. E‐H: IPSP during passage of graded amounts of current through acetate‐filled microelectrode. I: field potential evoked by same NRM stimulus when micro‐electrode was just outside cell. Calibrations: 2 mV, 20 ms.

From Giesler et al. 255


Figure 21.

Schematic representation of system employed for superfusing in situ spinal cord of anesthetized rat. Polyethylene 10 (PE 10) catheter used for infusion is inserted through cisterna magna to caudal level of lumbar cord. Outflow cannula is placed into cisterna magna. Artificial cerebrospinal fluid is perfused at rate of 100 μl/min and collected by withdrawal syringe and iced sampling tubes. Modification of release from spinal cord is achieved in this schematic by placement of electrode into raphe magnus. In other experiments, microinjection cannulae were placed into periaqueductal gray.

From Yaksh and Hammond 766


Figure 22.

Release of serotonin and norepinephrine into spinal cord superfusates of 2 representative rats after electrical stimulation of nucleus raphe magnus. Left: sites of stimulation indicated on coronal sections of medulla by black circles. After collection of 25‐min sample of superfusate to determine basal efflux of serotonin and norepinephrine, raphe magnus was stimulated at 25 Hz with 0.5 ms square‐wave pulses of either 150 or 250 μA for 25 min. During stimulation, another sample of superfusate was collected to determine release of serotonin and norepinephrine evoked by raphe stimulation. Quantitation of amines was by high‐pressure liquid chromatography with electrochemical detection. Right: release of serotonin (5‐HT) and norepinephrine (NE) expressed as ng/ml superfusate under basal conditions (B; open bars) and during stimulation of raphe magnus (S; stippled bars).

From Yaksh and Hammond 766
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Article Title: Central Control of Nociception
 

How to Cite

Walter Zieglgänsberger. Central Control of Nociception. Compr Physiol 2011, Supplement 4: Handbook of Physiology, The Nervous System, Intrinsic Regulatory Systems of the Brain: 581-645. First published in print 1986. doi: 10.1002/cphy.cp010411