|
| |
Electrical Stimulation And Pain Modulation
 Adobe Reader Version
Andersen E. and Dafny N. (1983)
An ascending serotonergic pain modulation pathway from the dorsal raphe nucleus
to the parafascicularis nucleus of the thalamus. Brain Res. 269, 57-67.
Abstract: Three types of spontaneously active neurons were found in the
parafascicularis (PF) nucleus of the thalamus of the rat: slow firing units
(0.5-10 spikes/s), bursting units (2-5 spikes/burst in 10-20 ms, one burst every
1-2 s) and fast firing units (15-40 spikes/s). A similar population of neurons
was found in the PF of rats treated with 5,7-dihydroxytryptamine (5,7-DHT), a
serotonin neurotoxin. Noxious tail pinch (TP) caused 68% of the PF neurons to
increase their firing rates to 242% of their initial baseline activity, while
non-noxious touch stimulation failed to induce a response. In the
5,7-DHT-treated rats, TP caused 85% of the neurons in the PF to increase their
firing rates to 581% of their initial baseline activity and 22% of the neurons
increased their firing in response to touching the tail. Both the number of
cells responding (P less than 0.05) and the percentage increase (P less than
0.001) were statistically greater in serotonin- depleted rats than in controls.
This indicates that serotonin (5-HT) has a tonic inhibitory influence on
responses to both noxious and non- noxious sensory stimuli. In control rats,
electrical stimulation of the dorsal raphe nucleus (DR) decreased the firing
rates of PF neurons. In contrast, the same DR stimulation induced an increase in
PF firing rates during stimulation in serotonin-depleted rats and this increase
in firing rates remained several seconds after cessation of stimulation. This
indicates that the DR may use at least two different neurotransmitters in its
projections to forebrain structures. In control rats, the TP stimulation induced
an increase in firing rates of rates of PF neurons while DR stimulation
attenuated the excitation induced by TP stimulation. In serotonin-depleted rats,
DR stimulation and TP both caused an increase in firing rates. This effect was
not additive indicating that there may be a serotonergic projection from the DR
to the PF which modifies responses to somatosensory stimuli. The inhibitory
effects elicited by electrical stimulation were limited to the immediate area of
the DR. Stimulation of the adjacent reticular formation 1 mm lateral to the DR
produced the opposite effect, an increase in firing rate often accompanied by
driven spike activity in the PF
Andersen E. (1986)
Periaqueductal gray and cerebral cortex modulate responses of medial thalamic
neurons to noxious stimulation. Brain Res. 375, 30-36.
Abstract: The response of medial thalamic neurons to noxious peripheral
stimulation were studied with intracellular recording methods in the cat.
Electrical stimulation of the contralateral forepaw produced an EPSP-IPSP
sequence followed by rebound excitation in these medial thalamic neurons. Action
potentials appeared with the initial EPSP or with the rebound excitation. The
mean latency to onset was 15 ms for the EPSP and 33 ms for IPSP. In contrast,
electrical stimulation of the PAG or of the pericruciate cerebral cortex
produced large IPSPs in the medial thalamic neurons. When PAG or cortex
stimulation were paired with noxious stimulation, both the PAG and cortex
responses predominated over the noxious response. This shows that the PAG and
the cerebral cortex have the capabilities of influencing the responses of the
medial thalamus to noxious stimulation. The medial thalamus is part of the relay
system which sends information about noxious stimulation to the cerebral cortex
where the noxious information reaches conscious awareness, so influencing the
message at the level of the medial thalamus would probably alter the conscious
perception of pain. The data suggest the existence of an ascending pain
modulation system from the midbrain to the thalamus and also suggests a
mechanism of cortical control over pain perception
Carr K.D. and Bak T.H. (1988)
Medial thalamic injection of opioid agonists: mu-agonist increases while
kappa-agonist decreases stimulus thresholds for pain and reward. Brain Res. 441,
173-184.
Abstract: Selective agonists for mu- and kappa-opioid receptor types were
infused, bilaterally, into the intralaminar central lateral nucleus of the rat.
Subcataleptic doses of the mu-agonist, DAGO (0.25 and 1.0 microgram), elevated
tailshock threshold for eliciting pain vocalization and motor responses. The
hyperalgesic effect of U50,488 is not likely to be the result of antagonist
action at a mu 2-isoreceptor; the general mu-antagonist, naloxone, and its less
lipophilic quaternary analogue, both failed to produce a significant reduction
in pain thresholds. Paralleling their effects on pain, DAGO and U50,488 elevated
and reduced, respectively, lateral hypothalamic electrical stimulation threshold
for positive reinforcement. These results suggest that medial thalamic opioid
mechanisms are not exclusively involved in pain modulation but may generally
regulate the responsiveness of the organism to motivating stimuli. Moreover, mu-
and kappa-receptors may mediate opposite behavioral effects of opioid peptides
Chen Y., Wang Y., and Yin Q.
(1991) [The role of paraventricular nucleus of hypothalamus in acupuncture
analgesia in rats]. Zhen. Ci. Yan. Jiu. 16, 32-38.
Abstract: Recent evidence has indicated that vasopressin (VP) can increase the
pain threshold. It is not clear whether the paraventricular nucleus (PVN) of
hypothalamus, which is one of the main nuclei that secrete VP in brain, is
involved in the acupuncture analgesia (AA). The present study was designed to
examine the role of PVN in AA. Experiments were carried out on Wistar rats using
tail stimulation vocalization test to measure the pain threshold. The acupoints
"Renzhong" and "Chengjiang" were selected for electroacupuncture. Electrical
stimulation of PVN could increase significantly the pain threshold and enhance
the effect of AA. On the contrary, electrolytical lesion of PVN could decrease
the effect of AA obviously, which could be recovered by cerebroventricular
injection (ICV) of 300 ng of arginine VP. Pretreatment with AVP- antiserum (ICV)
could attenuate the effect of AA. These data indicated that PVN plays an
important role in pain modulation and in the effect of AA. This role might be
mediated by the VP-containing neurons in PVN
Chudler E.H. and Dong W.K.
(1995) The role of the basal ganglia in nociception and pain. Pain 60, 3-38.
Abstract: The involvement of the basal ganglia in motor functions has been well
studied. Recent neurophysiological, clinical and behavioral experiments indicate
that the basal ganglia also process non-noxious and noxious somatosensory
information. However, the functional significance of somatosensory information
processing within the basal ganglia is not well understood. This review explores
the role of the striatum, globus pallidus and substantia nigra in nociceptive
sensorimotor integration and suggests several roles of these basal ganglia
structures in nociception and pain. Electrophysiological experiments have
detailed the non-nociceptive and nociceptive response properties of basal
ganglia neurons. Most studies agree that some neurons within the basal ganglia
encode stimulus intensity. However, these neurons do not appear to encode
stimulus location since the receptive fields of these cells are large. Many
basal ganglia neurons responsive to somatosensory stimulation are activated
exclusively or differentially by noxious stimulation. Indirect techniques used
to measure neuronal activity (i.e., positron emission tomography and
2-deoxyglucose methods) also indicate that the basal ganglia are activated
differentially by noxious stimulation. Neuroanatomical experiments suggest
several pathways by which nociceptive information may reach the basal ganglia.
Neuroanatomical studies have also indicated that the basal ganglia are rich in
many different neuroactive chemicals that may be involved in the modulation of
nociceptive information. Microinjection of opiates, dopamine and gamma-aminobutyric
acid (GABA) into the basal ganglia have varied effects on pain behavior.
Administration of these neurochemicals into the basal ganglia affects
supraspinal pain behaviors more consistently than spinal reflexive behaviors.
The reduction of pain behavior following electrical stimulation of the
substantia nigra and caudate nucleus provides additional evidence for a role of
the basal ganglia in pain modulation. Some patients with basal ganglia disease
(e.g., Parkinson's disease, Huntington's disease) have alterations in pain
sensation in addition to motor abnormalities. Frequently, these patients have
intermittent pain that is difficult to localize. Collectively, these data
suggest that the basal ganglia may be involved in the (1) sensory-discriminative
dimension of pain, (2) affective dimension of pain, (3) cognitive dimension of
pain, (4) modulation of nociceptive information and (5) sensory gating of
nociceptive information to higher motor areas. Further experiments that
correlate neuronal discharge activity with stimulus intensity and escape
behavior in operantly conditioned animals are necessary to fully understand how
the basal ganglia are involved in nociceptive sensorimotor integration
Condes-Lara M. (1998) Different
direct pathways of locus coeruleus to medial prefrontal cortex and centrolateral
thalamic nucleus: electrical stimulation effects on the evoked responses to
nociceptive peripheral stimulation. Eur. J. Pain 2, 15-23.
Abstract: Projections from the locus coeruleus (LC) to the centrolateral
thalamus (Cl) and the medial prefrontal cortex (PfCx) were studied using
orthodromic and antidromic stimulation techniques. The LC is a major
noradrenergic source in the central nervous system, and its descending
projections provide an important source of pain suppression at spinal level.
Previously, the author has described a cortico-thalamic loop involved in pain
modulation. The present paper reports on a study of the participation of LC as
part of an ascending pain-control system acting on the cortico-thalamic
loop.Rats were anaesthetized with halothane, and single unit recordings were
made in LC using glass micropipettes. Stainless steel electrodes were placed in
cortex and thalamus for electrical stimulation.Stimulation in PfCx or Cl
produces antidromic responses in neurons in LC. The latencies, conduction
velocity and location of neurons in LC projecting to PfCx or Cl structures are
described. Separate projections to both structures have significantly different
conducting velocities, arriving earlier at Cl (mean conduction velocities 0.27
and standard deviation +/-0.06 m/s) and then at PfCx (mean conduction velocities
0.20+/- 0.04 m/s). The presence of orthodromic responses suggests reciprocal
connections. The paper also describes the suppression of spontaneous and
nociceptive- evoked activity in the PfCx and Cl following electrical stimulation
in LC.It is proposed that the LC innervation could be associated with an
ascending noradrenergic system acting upon a Cl-PfCx pain-modulation mechanism.
Copyright 1998 European Federation of Chapters of the International Association
for the Study of Pain
Dafny N., Dong W.Q., Prieto-Gomez
C., Reyes-Vazquez C., Stanford J., and Qiao J.T. (1996) Lateral hypothalamus:
site involved in pain modulation. Neuroscience 70, 449-460.
Abstract: The present study is an attempt to examine the neuronal circuitry of a
supraspinal site engaged in pain modulation. Five physiological measures were
postulated as the criteria for defining a central nervous system site engaged in
the circuitry of pain modulation. The lateral hypothalamus met these five
measures: (i) 81% of the lateral hypothalamus neurons (247/304) responded to
noxious stimuli using a single cell recording procedure; (ii) stimulation of the
periaqueductal gray-dorsal raphe area or the habenula modulated 98% and 87% of
the lateral hypothalamus noxious-evoked activity; (iii) microiontophoretically
applied morphine modulated 77% of the lateral hypothalamus noxious evoked
activity; (iv) electrical stimulation of the lateral hypothalamus produced
behavioral analgesia proportional to the stimulus intensity as assessed by the
tail flick assay; and (v) morphine application into the lateral hypothalamus
produced behavioral analgesia in a dose-response manner using the tail flick
assay. In conclusion, the lateral hypothalamus can be considered one of the pain
modulation sites
Dong W.Q., Qiao J.T., Skolnick
M., and Dafny N. (1991) Focal dorsal raphe stimulation and pinnal electrical
stimulation modulate spontaneous and noxious evoked responses in thalamic
neurons. Int. J. Neurosci. 57, 123-140.
Abstract: This study investigated the nocieceptive responses of single neurons
within the nucleus parafascicularis (PF) thalami of the rat following two modes
of electrical stimulation known to induce analgesia. It was found that both
focal electrical dorsal raphe stimulation (DRS) and bilateral pinnal (ear)
electrical stimulation (PES) converge on the same PF neurons, affecting both the
spontaneous discharges and the noxious evoked responses toward these neurons.
The effects of different stimulus current intensity, frequency and pulse
duration were also examined. It was found that for both DRS and PES at pulse
frequency of 10 Hz and current amplitude of 10 microA are the optimal parameters
to modulate both the spontaneous and the noxious evoked responses. These stimuli
produced prolonged effects related to the duration of stimulation. The external
(PES) low current stimulation which was delivered below the sensory threshold
was as effective in modulating noxious responses as the invasive DRS in intact
animals and in animals with bilateral dorsolateral-funiculus ablation. It was
observed that dorsal lateral funiculus ablation (DLFx) did not modify the DRS
and the PES effects. These observations further support the existence of an
ascending pain modulation pathway
Ennis M., Behbehani M., Shipley
M.T., Van Bockstaele E.J., and Aston-Jones G. (1991) Projections from the
periaqueductal gray to the rostromedial pericoerulear region and nucleus locus
coeruleus: anatomic and physiologic studies. J. Comp Neurol. 306, 480-494.
Abstract: Previous studies showed that the nucleus locus coeruleus (LC) receives
two major afferent inputs from 1) nucleus paragigantocellularis and 2) nucleus
prepositus hypoglossi, both in the rostral medulla. Recent reports suggested
that the midbrain periaqueductal gray (PAG) projects to the rostromedial
pericoerulear area and LC. Since the PAG is a major site for control of central
antinociception, and since descending noradrenergic fibers have been implicated
in pain modulation, we have investigated in detail the functional anatomy of
projections from PAG to the dorsolateral pontine tegmentum. A combined
anatomical and electrophysiological approach was used to assess the organization
and synaptic influence of PAG on neurons in the rostromedial pericoerulear
region and in LC proper. Injections of the tracer wheatgerm agglutinin
conjugated to horseradish peroxidase encompassing LC proper and the rostromedial
pericoerulear area retrogradely labeled neurons in PAG located lateral and
ventrolateral to the cerebral aqueduct; injections restricted to LC proper did
not consistently label PAG neurons. Deposits of the anterograde axonal tracer
Phaseolus vulgaris leucoagglutinin into this same region of PAG labeled axons
that robustly innervated the zone rostral and medial to LC. Only sparse fibers
were observed in LC proper. Consistent with these results, focal electrical
stimulation of LC antidromically activated only a few PAG neurons (6 of 100);
all of these driven cells were located lateral and ventrolateral to the cerebral
aqueduct. The majority of neurons in the rostromedial pericoerulear area were
robustly activated by single pulse stimulation of PAG. In contrast, single pulse
electrical stimulation of lateral PAG produced weak to moderate synaptic
activation of some LC neurons; stimulation of ventrolateral PAG produced
predominant inhibition of LC discharge, perhaps through recurrent collaterals
subsequent to antidromic activation of neighboring LC cells. Taken together,
these results indicate that PAG strongly innervates the region rostral and
medial to LC, including Barrington's nucleus, but only weakly innervates LC
proper. Although recent studies indicate that the dendrites of LC neurons ramify
heavily and selectively in the rostromedial pericoerulear region, the results of
the present physiological studies suggest that PAG preferentially targets
rostromedial pericoerulear neurons rather than LC dendrites
Fardin V., Oliveras J.L., and
Besson J.M. (1984) A reinvestigation of the analgesic effects induced by
stimulation of the periaqueductal gray matter in the rat. II. Differential
characteristics of the analgesia induced by ventral and dorsal PAG stimulation.
Brain Res. 306, 125-139.
Abstract: This study consists of a detailed analysis of the analgesic effects
induced by stimulation of the various parts of the periaqueductal gray matter (PAG)
in the freely moving rat. In order to characterize the analgesia, two criteria
are considered: (1) the evaluation of the degree of analgesia and behavioral
side effects evoked during central stimulation; and (2) the presence of
post-effects. Central stimulation (50 Hz sine waves) was delivered via bipolar
concentric electrodes and analgesia was quantified by the change in the
vocalization threshold induced by electrical stimulation of the tail. Within the
ventral PAG, the vocalization threshold increased gradually with the intensity
of the central stimulation, the degree of analgesia generally being powerful.
There was no relationship between the strength of the analgesic effects and the
motor disturbances also produced by stimulation of this region. Antinociceptive
effects generally disappeared when the stimulation ceased. Only when the
intensity of the stimulation was strong enough to induce very powerful analgesic
effects were post-stimulation analgesic effects noticed. Within the dorsal and
dorsolateral PAG as well as in the ventral region just surrounding the aqueduct,
analgesia appeared suddenly, was generally less pronounced and was always
concomitant with strong aversive reactions. In contrast with the analgesia from
the ventral PAG, marked post-effects were observed. These latter characteristics
were also obtained from stimulation of regions located outside the PAG (colliculi,
intercollicular commissure and tectum adjacent to the dorsolateral PAG) although
these zones were not extensively studied. By consideration of various data in
the literature, it is concluded from this study, which clearly distinguishes
stimulation-produced-analgesia (SPA) from ventral PAG versus dorsal PAG, that
analgesia induced from this midbrain area involves at least two different
neuronal substrates. Whilst the ventral PAG seems to be more preferentially
involved in pain modulation, the authenticity of 'analgesia' triggered by
stimulation of aversive regions (which are widely spread over the PAG) is
questioned and proposals to explain the simultaneous appearance of analgesic
effects and aversion are considered
Herz A. and Millan M. (1989)
[Participation of opioids and opioid receptors in antinociception at various
levels of the nervous system]. Farmakol. Toksikol. 52, 5-12.
Abstract: At the cerebral level, studies employing several experimental
approaches point to an essential role of beta-endorphin in analgesia, induced by
electrical stimulation of the periaqueductal grey of the midbrain. Tolerance and
cross-tolerance studies suggest that mu-opioid receptors mediate this effect.
The significance of s
Herz A. and Millan M.J. (1990)
Opioids and opioid receptors mediating antinociception at various levels of the
neuraxis. Physiol Bohemoslov. 39, 395-401.
Abstract: One of the central issues in present experimental pain research is to
establish the identity, location, and mechanism of action of various opioids (opioid
peptides and alkaloids) and multiple opioid receptors in the modulation of
nociceptive processes. At the cerebral level, studies employing several
experimental approaches point to an essential role of beta-endorphin in
analgesia, induced by electrical stimulation of the periaqueductal grey of the
midbrain. Tolerance and cross- tolerance studies suggest that mu-opioid
receptors mediate this effect. The significance of d
Ignelzi R.J. and Nyquist J.K.
(1979) Excitability changes in peripheral nerve fibers after repetitive
electrical stimulation. Implications in pain modulation. J. Neurosurg. 51,
824-833.
Abstract: The Melzack-Wall gate control theory has been invoked to explain the
peripheral analgesia resulting from repetitive electrical stimulation of
peripheral nerve. This model emphasizes presynaptic inhibitory interactions
among afferent fiber terminals in the spinal cord. An alternative explanation,
that of velocity change in peripheral nerve fiber conduction, has been suggested
by compound action potential studies from our laboratory. The present study was
designed to extend this work, and to investigate the single fiber changes
subsequent to brief (5- to 20-minute) periods of repetitive, high frequency (180
to 200/sec) electrical stimulation through an implantable peripheral nerve cuff
device of the type used clinically for pain relief. Most fibers, regardless of
their diameter (estimated from conduction velocity), show one or more of the
following characteristics: a transient slowing of conduction velocity, an
increase in electrical threshold and/or a decrease in response probability
following a period of repetitive electrical stimulation. This supports the
hypothesis that there are changes in direct peripheral nerve fiber excitability
occurring under conditions simulating clinical electroanalgesia
Ignelzi R.J. and Atkinson J.H.
(1980) Pain and its modulation. Part 2. efferent mechanisms. Neurosurgery 6,
584-590.
Abstract: Recent studies of central nervous system effects on pain and on its
efferent modulation have created new theories and have led to direct clinical
applications that may in time eclipse more classical interventions. In this
review electrical stimulation analgesia is presented as a paradigm of how basic
science work has been applied clinically to produce some of the most exciting
advances in recent years in the treatment of chronic pain. Opiate receptors and
analgesia are presented in relationship to the descending inhibitory systems
used in electroanalgesia. Neuromodulators and neurotransmitters important in
pain modulation through complex inhibitory and excitatory pathways are
discussed, with the roles of B-endorphin, enkephalin, serotonin, and other
important biogenic amines being stressed. The neuropharmacology of pain as it is
currently understood clinically suggests that psychotropic interventions may be
quite useful in treating difficult pain problems
Krainick J.U. and Thoden U.
(1976) [Methods of pain modulation by electrical stimulation (author's transl)].
Langenbecks Arch. Chir 342, 75-81.
Abstract: Different methods of modulating pain by electrical stimulation are
described: (1) Nondestructive transcutaneous nerve stimulation is recommended
for neurogenic pain syndromes prior to other procedures (success rate about
30%); (2) The implantation of electrodes on the dorsal columns yields good
effects in 65% after careful selection; (3) First results with implantations in
deep brain structures are discussed
Landau B. and Levy R.M. (1993)
Neuromodulation techniques for medically refractory chronic pain. Annu. Rev.
Med. 44, 279-287.
Abstract: Advances in our knowledge of the physiology of pain transmission and
modulation have created new surgical options for the control of chronic pain.
The pain modulation network can be activated by administration of spinal opiates
or by electrical stimulation of the nervous system with transcutaneous,
peripheral nerve, spinal cord, and deep brain stimulation. The theoretical basis
and the clinical applications of neurostimulation for the treatment of medically
intractable chronic pain are reviewed
Moyanova S. and Ta L. (1988)
Dorsal raphe stimulation modulates responses of substantia nigra, pars
reticulata neurons to painful stimulation. Acta Physiol Pharmacol. Bulg. 14,
24-32.
Abstract: There are but few data that substantia nigra neurons are involved in
the pain-processing mechanisms in the CNS. In contrast, a great deal of evidence
suggests a participation of the dorsal raphe nucleus (RD) in these processes.
The purpose of the present study was to examine the effects of painful
stimulation (suprathreshold electrical stimulation of the peroneal nerve--NP) on
the extracellular activity of neurons of substantia nigra, pars reticulata (SNR)
in cats, and to determine if a train of stimuli applied to RD could affect the
responses of SNR neurons to this type of painful stimulation. The majority of
SNR neurons (83.3%) responded to NP-stimulation either with an increase or with
a decrease in the firing rate. The RD-stimulation when applied simultaneously or
just before the NP-stimulation reduced or even eliminated the increase in the
firing rate caused by pain irrespective of the ability of RD-stimulation applied
proviously alone to reduce or not the spontaneous activity of the SNR neurons.
In cells which responded with inhibition to NP- and RD-stimulations when applied
alone, RD-stimulation applied just before NP-stimulation slightly prolonged the
NP-induced inhibition. The results indicate that in addition to the descending
pain modulation pathway from the dorsal raphe nucleus to the spinal cord, which
pathway is well established, there may be an ascending one to some supraspinal
structures, the substantia nigra being one of them
Vignocchi G., Murri L., Rossi
B., Rosa C., and Ghione S. (1989) Correlation between pain thresholds and
polysynaptic components of blink reflex in essential arterial hypertension.
Funct. Neurol. 4, 59-61.
Abstract: An interaction between pain modulation and arterial pressure control
has been proposed on the basis of experimental data in man and animal. Eight
hypertensive patients and eight normotensive volunteers were investigated by
electrical stimulation of the first trigeminal branch and dental pulp, to
evaluate nociceptive sensation and reflex responses. A significant threshold
increase of pain sensation and R2, R3 polysynaptic components of the blink
reflex, has been found in hypertensive patients
Walker J.M., Huang S.M.,
Strangman N.M., Tsou K., and Sanudo-Pena M.C. (1999) Pain modulation by release
of the endogenous cannabinoid anandamide. Proc. Natl. Acad. Sci. U. S. A 96,
12198-12203.
Abstract: Synthetic cannabinoids produce behavioral analgesia and suppress pain
neurotransmission, raising the possibility that endogenous cannabinoids serve
naturally to modulate pain. Here, the development of a sensitive method for
measuring cannabinoids by atmospheric pressure-chemical ionization mass
spectrometry permitted measurement of the release of the endogenous cannabinoid
anandamide in the periaqueductal gray (PAG) by in vivo microdialysis in the rat.
Electrical stimulation of the dorsal and lateral PAG produced CB1 cannabinoid
receptor-mediated analgesia accompanied by a marked increase in the release of
anandamide in the PAG, suggesting that endogenous anandamide mediates the
behavioral analgesia. Furthermore, pain triggered by subcutaneous injections of
the chemical irritant formalin substantially increased the release of anandamide
in the PAG. These findings indicate that the endogenous cannabinoid anandamide
plays an important role in a cannabinergic pain-suppression system existing
within the dorsal and lateral PAG. The existence of a cannabinergic pain-modulatory
system may have relevance for the treatment of pain, particularly in instances
where opiates are ineffective
Xiong K. and Zheng P. (1990)
[The effect of the septal area in acupuncture analgesia]. Zhen. Ci. Yan. Jiu.
15, 1-5, 12.
Abstract: This review summarized some articles on the effect of the septal area
in acupuncture analgesia. The data showed that the pain threshold of animal was
increased when septal area was stimulated by electro- acupuncture, and that
electrical stimulation of septal area had a marked inhibitory effect on the pain
discharges of cells in parafascicular nucleus of thalamus, lateral habenular
nucleus, periaqueductal gray and dorsal raphe nucleus. The septal area play an
important role in acupuncture analgesia. The majority of the cholinergic neurons
in septal area are located in nucleus of the vertical limb of the diagonal band
(VDB); gamma-aminobutyric acid of septal area is mainly found in the diagonal
band nucleus(td); Dopamine is present in high levels in td and lateral septal
nucleus(S1) of septal area; The S1 contain high densities enkephalin-containing
neuronal cell bodies and terminals; In addition, substance P and norepinephrine
are also high levels in the septal area. These substance above-mentioned have a
relations with acupuncture analgesia of septal area. A large number of serotonin-containing
neurons are found in the raphe nuclei. The serotonin play an important role in
acupuncture analgesia. The serotonin-containing neurons in dorsal raphe nucleus
project to S1. The fiber connections of the raphe nuclei with the td are
reciprocation. The periaqueductal gray is a important structure on pain
modulation. It projects to septal area and receives the fibers from S1. A number
of adrenergic neurons are located within the locus coeruleus. The locus
coeruleus participate pain modulation and acupuncture analgesia. The neuro-anatomy
study demonstrated that locus coeruleus projects to septal area.(ABSTRACT
TRUNCATED AT 250 WORDS)
Zemlan F.P. and Behbehani M.M.
(1988) Nucleus cuneiformis and pain modulation: anatomy and behavioral
pharmacology. Brain Res. 453, 89-102.
Abstract: The anatomical substrate and behavioral pharmacology of stimulation-
produced analgesia resulting from electrical stimulation of the
pontomesencephalic nucleus cuneiformis (NCF) was determined in the present
study. Maximum increase in nociceptive tail-flick latencies following NCF
stimulation occurred during the first 5 min post stimulation and decreased
afterwards. The increased reflex latency could be attenuated by prior treatment
with the narcotic antagonist, naloxone or the cholinergic antagonist,
scopolamine. The anatomical projections of NCF were identified in
autoradiographic and histochemical studies. Ipsilateral fibers coursed caudal
from the NCF injection site through the ventral pontine reticular formation to
innervate nucleus raphe magnus and the ipsilateral nucleus magnocellularis. At
rostral medullary levels fibers coursed dorsolateral to innervate the
ipsilateral nucleus reticularis parvocellularis. Descending contralateral fibers
crossed through the decussation of the superior cerebellar peduncle, then
coursed ventrolaterally projecting to the contralateral nucleus magnocellularis.
Two primary groups of ascending fibers were observed. The dorsally located group
ascended through the central tegmental tract projecting to the dorsal raphe,
ipsilateral periaqueductal gray, nucleus parafascicularis and centromedianus,
the intermediolateral and lateral thalamic nuclei. The ventral group coursed
ventrolateral from the injection site projecting to the substantia nigra, zona
compacta, ventral tegmental area of Tsai, zona incerta, Fields of Forel, lateral
hypothalamic nucleus and nucleus reuniens. These anatomic and behavioral data
suggest that NCF plays an important role in sensory/motor integration relevant
to pain transmission
Zhang S., Tang J.S., Yuan B.,
and Jia H. (1998) Inhibitory effects of electrical stimulation of ventrolateral
orbital cortex on the rat jaw-opening reflex. Brain Res. 813, 359-366.
Abstract: In previous studies, we have shown that electrically or chemically
evoked activation of the ventrolateral orbital cortex (VLO) depresses the rat
tail-flick (TF) reflex, and this antinociceptive effect is mediated by the
periaqueductal gray (PAG). The aim of the present study was to examine whether
electrical stimulation of the VLO could inhibit the rat jaw-opening reflex (JOR),
and to determine whether electrolytic lesions of the PAG could attenuate this
VLO-evoked inhibition. Unilateral electrical stimulation of the VLO
significantly depressed the JOR elicited by tooth pulp or facial skin stimuli,
with a mean threshold of 30.5+/-2.3 microA (n=22). Increasing stimulation
intensities from 30 to 80 microA resulted in greater reduction of the dEMG
amplitude from 22.9+/-5.0% to 69.7+/-3.7% of the baseline value (P<0.01, n=22).
The inhibitory effect appeared 50 ms after the beginning of VLO stimulation and
lasted about 150 ms, as determined by varying the conditioning-test (C-T) time
interval. Unilateral lateral or ventrolateral lesions of the PAG produced only a
small attenuation of the VLO-evoked inhibition of the JOR, but bilateral lesions
eliminated this inhibition. These findings suggest that the VLO plays an
important role in modulation of orofacial nociceptive inputs, and provide
further support for the hypothesis that the antinociceptive effect of VLO is
mediated by PAG leading to activation of a brainstem descending inhibitory
system and depression of nociceptive inputs at the trigeminal level. The role
played by VLO in pain modulation is discussed in association with the proposed
endogenous analgesic system consisting of medullary cord-Sm-VLO-PAG-medullary
cord
Zhang Y.Q., Tang J.S., Yuan B.,
and Jia H. (1995) Effects of thalamic nucleus submedius lesions on the tail
flick reflex inhibition evoked by hindlimb electrical stimulation in the rat.
Neuroreport 6, 1237-1240.
Abstract: Bilateral electrolytic lesions of the thalamic nucleus submedius (Sm)
facilitated the TF reflex and attenuated the antinociception evoked by hindlimb
electrical stimulation with high intensities in lightly anaesthetized rats.
However, the antinociception produced by low intensity hindlimb stimulation was
unchanged, except that the after- effect was reduced. The results show that the
Sm is probably involved in pain modulation and plays an important role in
mediation of the antinociception elicited by high intensity peripheral
stimulation
Zhang Y.Q.,
Tang J.S., Yuan B., and Jia H. (1997) Inhibitory effects of electrically evoked
activation of ventrolateral orbital cortex on the tail-flick reflex are mediated
by periaqueductal gray in rats. Pain 72, 127-135.
Abstract: The present study found in lightly anesthetized rats that the radiant
heat-evoked tail flick (TF) reflex was markedly inhibited by a unilateral
electrical stimulation (a 20 ms train of 0.2 ms, 100 Hz, 30- 100 microA pulses)
of the ventrolateral orbital cortex (VLO), with the tail flick latency (TFL)
being increased. The mean threshold of VLO stimulation for producing inhibition
of the TF reflex was 39.2 +/- 8.7 microA (n = 26), and this inhibitory effect
increased following increasing stimulation intensity from 40 to 70 microA. The
inhibition developed and remained during the stimulation and disappeared rapidly
after termination of the stimulation. When the VLO was stimulated at an
intensity of 100 microA in addition to the inhibition an after- facilitation of
the TF reflex (a decrease in TFL) was observed at 5-10 s after termination of
the stimulation. Bilateral electrolytic lesions of the lateral or ventrolateral
parts of the periaqueductal gray matter (PAG) dramatically reduced or eliminated
the VLO-evoked inhibition, and the after-facilitation as well. The difference
was significant between the TFL changes produced by VLO stimulation before and
after PAG lesion (P < 0.01). The results suggest that the antinociception
elicited by VLO stimulation is mediated by PAG, leading to activation of the
brainstem descending inhibitory system which depresses the nociceptive
transmission at the spinal level. The role played by VLO in pain modulation was
discussed in association with the proposed endogenous analgesic system
consisting of spinal cord-Sm-VLO-PAG-spinal cord
|
