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Biomedical subjects

C J Woolf

Publications and source records attributed to C J Woolf.

At least 145 records · Page 8Linked to original sources

Morphine-sensitive and morphine-insensitive actions of C-fibre input on the rat spinal cord.

A dose-dependent differential action of morphine on the hamstring flexor withdrawal reflex recorded in flexor alpha-motoneurones has been found in the decerebrate-spinal rat. At low doses (0.5 mg/kg) morphine pretreatment reduces the prolonged heterosynaptic facilitation of the reflex that follows brief (20 s) C-primary afferent fibre conditioning stimuli, without modifying the activation of the motoneurones by C-fibre input or noxious peripheral stimuli. Moderate doses (5 mg/kg) of morphine are required to suppress the C-fibre-induced excitability increase once it is established by the conditioning stimulus buy only very high doses (20 mg/kg) reduce the direct reflex activation of the flexor motoneurones by either C-fibre input or noxious stimuli. The relevance of these findings to the antinociceptive and analgesic actions of morphine are discussed.

Animals↗

The brief and the prolonged facilitatory effects of unmyelinated afferent input on the rat spinal cord are independently influenced by peripheral nerve section.

Single C-fibre strength stimuli applied to the sciatic nerve in the decerebrate spinal rat evoke three separate bursts of activity in posterior biceps/semitendinosus flexor alpha motorneurones which are associated with the arrival in the spinal cord of volleys in the A-beta, A-delta and C-afferent fibres. Repetitive stimulation of the sciatic nerve at 1 Hz for 20 s generates a progressive wind-up of response and an after-discharge lasting up to 10 s. Twelve to fourteen days after section of the sciatic nerve, stimuli applied central to the section evoke a larger than normal response in the posterior biceps/semitendinosus flexor motorneurones and repetitive stimulation (1 Hz, 20 s) produces an after-discharge which is four times longer than that produced by stimulation of the intact nerve. In addition to the direct excitatory effects of sciatic nerve stimulation on the flexor motorneurones which lasts for seconds, conditioning stimuli to the sciatic nerve at C-fibre strength (1 Hz, 20 s) produce a facilitation of the flexor reflex evoked by a standard pressure stimulus to the ipsilateral and contralateral toes which lasts for 70 min. However, although the direct excitatory effects of stimulating a sectioned sciatic nerve on the posterior biceps/semitendinosus flexor motorneurones are exaggerated, the facilitation of the cutaneous flexion reflex evoked by stimulating sectioned sciatic nerves (1 Hz, 20 s) only lasts for 17 min. These results show that the mechanism which produces the rapid effects of sciatic nerve stimulation on the flexor reflex circuit can be separated from the mechanism which produces the prolonged facilitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Relative effectiveness of C primary afferent fibers of different origins in evoking a prolonged facilitation of the flexor reflex in the rat.

Changes in the excitability of the hamstring flexor withdrawal reflex produced by conditioning stimuli applied to C-afferent fibers of different origins have been examined in the decerebrate spinal rat. In the absence of conditioning stimuli, the flexor reflex elicited by a standard suprathreshold mechanical stimulus to the toes is stable when tested repeatedly for hours. Three categories of conditioning stimuli have been used in an attempt to modify the excitability of the flexor reflex; electrical stimulation of a cutaneous (sural) nerve or a muscle (gastrocnemius-soleus) nerve at C-fiber strength; the application of mustard oil, a chemical irritant that activates chemosensitive C-afferents, to the skin or injected intramuscularly and intraarticularly; and the indirect activation of high-threshold muscle afferents by fused tetanic contractions of the tibial muscles. Conditioning stimuli of an intensity sufficient to activate C-afferent fibers result in a heterosynaptic facilitation of the flexor motoneuronal response to the standard test input, which lasts from 3 min to more than 3 hr, depending on the stimulus and the C-afferents activated. Pretreatment of the sciatic nerve with the C-fiber neurotoxin capsaicin abolishes all the postconditioning facilitations, which is an indication that it is likely that it is C-afferents that are primarily responsible for the facilitatory effects of the conditioning stimuli, although some A delta afferents may contribute. Capsaicin pretreatment does not modify the reflex response to the test stimulus. The most prolonged increase in the excitability of the flexor reflex resulted from intraarticular injections of 5 microliter mustard oil. Using the subsequent injection of lignocaine intraarticulary, it was found that the prolonged facilitation of the reflex is triggered by the afferent input generated by the conditioning stimulus and does not require an ongoing input for its maintenance. These results indicate that there is a spectrum of central changes in the stimulus response relations of the spinal cord resulting from the activation of C-fibers of different origins. The prolonged duration of some of these changes means that the peripheral activation of C-afferents will modify the functional response of the spinal cord to other inputs applied long after the conditioning input, and this may be responsible for some of the sensory and motor alterations found after peripheral tissue injury.

Afferent Pathways↗

Mapping increased glycogen phosphorylase activity in dorsal root ganglia and in the spinal cord following peripheral stimuli.

A histochemical technique has been used to map the distribution and the relative proportion of the active and inactive form of the enzyme glycogen phosphorylase in the primary afferent cell bodies of lumbar dorsal root ganglia and within the lumbar spinal cord of the rat. The glycogen phosphorylase was found to be present in large and small diameter primary afferent cell bodies and in the grey matter of the spinal cord, except in lamina 2. Most of the glycogen phosphorylase in control rats was in the inactive form. Peripheral innocuous mechanical and thermal stimuli failed to alter the activity of glycogen phosphorylase in the lumbar spinal cord, but noxious mechanical, chemical, and thermal stimuli when applied to the hindlimb of decerebrate rats increased the enzyme activity in the ipsilateral dorsal horn within 10 minutes. The number of primary afferent cell bodies with active glycogen phosphorylase also increased. These changes are likely to be due to the conversion of the inactive "b" form of the enzyme to the active "a" form under the influence of a calcium or cyclic AMP activated phosphorylase b kinase. Pentobarbitone anaesthesia diminished but did not completely suppress the noxious stimulus-evoked glycogen phosphorylase activity changes. Graded electrical stimulation of the sciatic nerve was performed to simulate the effects of the peripheral noxious stimuli in a controlled fashion. Stimulation at a strength that activated only large myelinated afferents produced no greater effect on the distribution of the active form of the enzyme in the dorsal horn than that produced by exposure of the nerve, but stimulation of the thin myelinated A-delta afferents and unmyelinated C-fibres produced a widespread increase in glycogen phosphorylase activity in the spinal cord and in the L4 dorsal root ganglion. The increased activity could be detected after stimulation for as short a period of time as 5 minutes. The mechanisms underlying the stimulus-evoked increase in glycogen phosphorylase activity in the spinal cord and dorsal root ganglia are not yet known, nor have we positively established which elements in the spinal cord, neurones, or glia are responsible for the changes in the glycogen phosphorylase activity. Nevertheless, it is clear that the neural activity generated by certain types of high threshold input is associated with the activation of glycogen phosphorylase, and this may be a useful tool for studying the spatial distribution of some activity-related changes in the nervous system.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

The somatotopic organization of primary afferent terminals in the superficial laminae of the dorsal horn of the rat spinal cord.

Transganglionic transport of wheatgerm agglutinin conjugated horse-radish peroxidase (WGA-HRP) was used to reveal the central distribution of terminals of primary afferent fibers from peripheral nerves innervating the hind leg of the rat. In separate experiments the sizes and locations of cutaneous peripheral receptive fields were determined by electrophysiological recording techniques for each of the nerves that had been labeled with WGA-HRP. By using digital image analysis, the sizes and positions of the peripheral receptive fields were correlated with the areas of superficial dorsal horn occupied by terminals of primary afferents from each of these receptive fields. Data were obtained from the posterior cutaneous nerve of the thigh, lateral sural, sural, saphenous, superficial peroneal, and tibial nerves. The subdivisions of the sciatic nerve, the sural, lateral sural, superficial peroneal, and tibial nerves each projected to a separate and distinct region of the superficial dorsal horn and collectively formed a "U"-shaped zone of terminal labeling extending from lumbar spinal segments L2 to the caudal portions of L5. The gap in the "U" extended from L2 to the L3-4 boundary and was occupied by terminals from the saphenous nerve. Collectively, all primary afferents supplying the hindlimb occupied the medial 3/4 of the superficial dorsal horn with terminals from the tibial nerve lying most medially and occupying the largest of all the terminal fields. Afferents from the superficial peroneal lay in a zone between the medially situated tibial zone and the more laterally placed sural zone. Afferents from the posterior cutaneous nerve were located most caudally and laterally. Terminal fields from the posterior cutaneous and saphenous nerves differed from the others in having split representations caused presumably by their proximity to the mid-axial line of the limb. Comparisons between the peripheral and the central representations of each nerve revealed that 1 mm2 of surface area of the superficial dorsal horn serves approximately 600-900 mm2 of hairy skin and roughly 300 mm2 of glabrous skin. The vast majority of terminal labeling observed in the dorsal horn was found in the marginal layer and substantia gelatinosa, suggesting that small diameter afferents have an orderly somatotopic arrangement in which each portion of the skin surface is innervated by afferent fibers that terminate in preferred localities within the dorsal horn.

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Injury-induced plasticity of the flexor reflex in chronic decerebrate rats.

The hindlimb-flexor-withdrawal reflex elicited by stimulation of the skin of the hindpaw has been examined in chronic decerebrate rats. This flexor reflex manifests as a typical phasic avoidance response when measured either behaviourally in the decerebrate rat or electrophysiologically in the decerebrate-spinal preparation. Once the threshold of the cutaneous flexor-reflex afferents in the skin have been exceeded a brief burst of activity with only a short afterdischarge occurs in the flexor motoneurones. The response to sustained stimuli adapts rapidly. In the absence of any treatment to the hindlimb the threshold, duration and responsiveness of the reflex remains stable when tested repeatedly. Thermal or chemical stimuli of sufficient intensity to produce tissue injury and prolonged local inflammation in a hindpaw of the chronic decerebrate rat result in marked and long-lasting (several weeks) alterations in the ipsilateral withdrawal reflex. The mechanical threshold necessary to elicit the reflex by stimulation of the hindpaw falls so that light touch or brush can now elicit a response instead of the firm pressure or pinch required pre-injury. Suprathreshold stimuli to the inflamed skin generate a sustained oscillating pattern of flexion in contrast to the brief flicking movement found in control animals. Electromyographic recordings from the hamstring flexor muscles ipsilateral to the inflamed hindpaw show decreased mechanothresholds, increased spontaneous activity, prolonged afterdischarges to brief stimuli and a slowly adapting tonic response to sustained stimulation. Populations of single cutaneous mechanoreceptive C-primary afferents recorded both from untreated decerebrate rats and from rats with an inflamed hindpaw are indistinguishable in terms of their response properties. There is no difference in threshold, spontaneous activity or afterdischarge between the two populations. The possible mechanisms responsible for the conversion of the high threshold phasic flexor reflex into a low threshold tonic reflex are discussed as are the possible implications for sensory disorders that accompany chronic injury in man.

Animals↗

Cutaneous receptive field and morphological properties of hamstring flexor alpha-motoneurones in the rat.

Intracellular recordings have been made from twenty antidromically identified posterior biceps femoris/semitendinosus (p.b.s.t.) hamstring flexor alpha-motoneurones in the decerebrate-spinal rat. The hamstring motoneurones had either low or no spontaneous background activity. In nineteen of the twenty cells high-frequency phasic responses could be elicited by stimulation of the ipsilateral hind paw with firm pressure or pinch. There was no response to light touch or brush. Contralateral cutaneous mechanoreceptive fields with higher thresholds and weaker responses were present in 70% of the motoneurones. Noxious heating of the ipsilateral hind paw produced excitatory responses in six of eight cells tested and two of these cells also responded to heating of the contralateral hind paw. Stimulation of the ipsilateral sural nerve at graded strengths that successively activated A beta, A delta and C afferents produced excitatory post-synaptic potentials (e.p.s.p.s) at progressively longer latencies in the motoneurones. The C-fibre induced e.p.s.p. lasted up to 200 ms. Horseradish peroxidase was injected into ten motoneurones and in seven cases full reconstructions of dendritic field, cell body and axon could be made. In agreement with previous reports from studies in the cat, the dendritic fields of rat motoneurones are very extensive in the rostrocaudal, mediolateral and dorsoventral planes. The general pattern of dendritic branching for each motoneurone in this functionally homogeneous population was uniformly organized. Three major spatial orientations were always present: a rostrocaudally restricted series of dendrites emerging from the cell body and directed dorsolaterally towards the dorsolateral funiculus with branches in the lateral dorsal horn, a laterally, and a ventromedially directed series of branches arranged obliquely in the ventral horn, both of which were distributed rostrocaudally for equal distances from the cell body. Many of these dendritic branches terminated within the lateral and ventral white columns. Although the sizes of the rat flexor motoneurones' somas (51 +/- 4.9 micron, S.E., n = 10) were similar to those of cat lumbosacral alpha-motoneurones, the tip-to-tip rostrocaudal extent of their dendritic fields (1130 +/- 34 micron, S.E., n = 7) was half that reported in the cat. These results are discussed in terms of the organization of the cutaneous flexor withdrawal reflex in the rat.

Action Potentials↗

Neurogenic extravasation and substance P levels are low in muscle as compared to skin the rat hindlimb.

Activation of cutaneous chemosensitive afferents results in the release of substances which increase the permeability of the microcirculation, producing inflammation. That this inflammation is neurogenic is readily demonstrated by antidromic electrical stimulation of afferent fibres. In the present study we have used the technique of dye extravasation to compare both qualitatively and quantitatively neurogenic extravasation skin and skeletal muscle. Plasma extravasation has been found to occur in skeletal muscle after stimulation but only at less than 10% of the levels seen in skin. We have also found that the levels of the C-fibre markers substance P and fluoride-resistant acid phosphatase are greatly reduced in muscle compared with skin nerves. These results show that there are substantial differences in the population of C-fibres supplying muscle compared with those supplying skin.

Animals↗

The cutaneous contribution to the hamstring flexor reflex in the rat: an electrophysiological and anatomical study.

The location and properties of the cutaneous receptive fields responsible for detecting the flexor withdrawal reflex in the posterior head of biceps femoris (pBF) and semitendinosus (ST) components of the hamstring muscle have been examined in unanaesthetized decerebrate rats, spinalized at T10-T11. Single alpha-motoneurone efferents were recorded from the nerve to pBF and the principal head of ST and their responses to ipsi- and contralateral hindlimb skin stimulation investigated. The efferents to both muscles characteristically had a low or absent background discharge and they all had mechanoreceptive fields on the ipsilateral foot. The mechanical threshold of these fields was high with no response to light touch or brush. Fifty-four percent of these units also had a smaller and weaker contralateral mechanoreceptive field. The only apparent difference between ST and pBF efferents was that more ST efferents had contralateral fields than pBF units. Noxious, hot and cold thermal stimuli applied to the ipsilateral foot activated 56% of the efferents. Mustard oil, a chemical irritant, produced a long-lasting flexor response when applied to the ipsilateral foot. The responses of these efferents to stimulation of A beta, A delta and C cutaneous afferents in the sural nerve were also studied. Short latency reflexes were elicited in all efferents by A beta inputs, longer latency reflexes were elicited in 64% by A delta inputs and very long latency responses with long afterdischarges were found in 73% of the units to C inputs. Retrograde labelling of the hamstring motoneurones with WGA-HRP indicated that they lay in ventrolateral lamina IX extending from the caudal portion of the third lumbar segment to the junction of the 5th and 6th lumbar segments. Transganglionic labelling of small diameter primary afferent terminals in the dorsal horn of cutaneous nerves innervating the foot revealed that the longitudinal distribution corresponded closely with that of the hamstring motor nucleus. The flex-or reflex in the spinal rat provides a useful model therefore, for studying how the input in nociceptive afferents is processed and transformed within the spinal cord, to produce appropriate outputs.

Afferent Pathways↗

A selective effect of naloxone on heterosynaptic C-fibre-mediated inhibitions in the rat dorsal horn.

The effect of naloxone on C-primary afferent-mediated inhibitions of C-fibre-evoked activity in deep dorsal horn neurons has been examined in decerebrate-spinal rats. The same C-afferents that evoke activity in a given neurone can inhibit that C-evoked activity (homosynaptic inhibition), and C-afferent input can also inhibit the activity evoked in dorsal horn neurones by other C-afferents (heterosynaptic inhibition). Naloxone was found to selectively reverse heterosynaptic C-mediated inhibitions without affecting homosynaptic inhibitions. In several neurones the heterosynaptic inhibitions were completely abolished by naloxone. These results show that homo- and heterosynaptic C-mediated inhibitions operate by different mechanisms and that, at least in some neurones, endogenous opioids are likely to be the major inhibitory transmitters involved in producing the heterosynaptic inhibition of the activity evoked by one C-input by another C-input.

Afferent Pathways↗

Axotomy increases glycogen phosphorylase activity in motoneurones.

The relative distribution of glycogen phosphorylase a and b in the lumbar spinal cord of the adult rat following either transection or crush of the sciatic nerve has been studied. The activity of the glycogen phosphorylase was measured histochemically by its capacity to convert glucose-1-phosphate to glycogen which was then stained with iodine. Prior to any treatment, the enzyme was largely in its inactive b form. Sciatic section and crush produced a transient (24 h) decrease in the amount of the active glycogen phosphorylase a in the sciatic motoneurone pool. Fourteen days post-transection, but not crush, a marked increase in the level of the active glycogen phosphorylase a form of the enzyme could be detected in the axotomised motoneurones which persisted for up to 6 weeks. No equivalent changes occurred in the axotomized dorsal root ganglion cells. Glycogen phosphorylase although normally present in neurones in its inactive b form can be converted to the active a form by calcium or adenosine 3':5'-phosphate. The substantial increase in the level of glycogen phosphorylase a in axotomized motoneurones may be a reflection of an increased calcium influx into these cells due to the development of abnormally hyperexcitable membranes and the appearance of dendritic spikes that is known to occur in these motoneurones.

Adenosine Monophosphate↗

Muscle but not cutaneous C-afferent input produces prolonged increases in the excitability of the flexion reflex in the rat.

Stimulation of cutaneous afferent fibres in the sural nerve and muscle afferent fibres in the gastrocnemius-soleus nerve at a strength that excites C axons produces a delayed and long-lasting burst of activity in posterior biceps femoris/semitendinosus flexor motoneurones. Following a 20 s stimulation at 1 Hz to the sural nerve the flexor motoneurones continue to fire for 20 s while a similar stimulus to gastrocnemius-soleus nerve results in an after-discharge lasting three times longer. Using stimuli to the sural and gastrocnemius-soleus nerves as conditioning stimuli (20 s, 1 Hz) changes in the excitability of the flexor reflex were measured by recording the discharge evoked by a test sural nerve stimulus or by a standard pinch to the ipsilateral and contralateral toes. Prior to any conditioning stimulus the flexor reflex remained stable for prolonged periods. Conditioning stimuli at strengths that activated large myelinated afferent fibres only, or large and small myelinated afferent fibres, failed to produce more than a very transient alteration in the reflex excitability. Conditioning stimuli at C-fibre strength to the sural nerve produced a marked increase in the excitability of the reflex for 10 min. C-fibre strength gastrocnemius-soleus nerve conditioning stimuli resulted in a similar increase in excitability followed by a second phase of facilitation peaking at 20-30 min and lasting for up to 90 min. The afferent barrage initiated by cutting the sural and gastrocnemius-soleus nerves resulted in similar patterns of reflex excitability increases with the muscle nerve resulting in a more prolonged effect than the cutaneous nerve. The results show that a brief C-afferent fibre input into the spinal cord can produce a prolonged increase in the excitability of the flexion reflex and that muscle C-afferent fibres evoke longer-lasting changes than cutaneous C fibres. The differences in the time course of the post-conditioning effects may be related to the well-described differences in the sensory consequences of injury to skin versus deep tissue.

Animals↗

Alterations in the structure, function, and chemistry of C fibers following local application of vinblastine to the sciatic nerve of the rat.

Vinblastine, a transport blocker, was applied locally to the sciatic nerve in rats. It was found to be a powerful neurotoxin with a dose-dependent action, destroying all afferents at doses of 5 X 10(-4)M, primarily C fibers at intermediate doses of 2.5 X 10(-4)M, and only at a critically low dose of 10(-4)M was a degeneration-free axon transport blockade, lasting for 4 to 5 days, produced. Such transport block failed to alter thermal responsiveness of the rats as measured behaviorally, by the flexor reflex, or by dorsal horn cell responses. It did, however, significantly reduce both the chemical sensitivity of the C afferents and their ability to produce neurogenic edema. This began 24 hr after treatment and lasted 4 to 5 days. Therefore, it is likely that these functions are dependent on the continuous transport of some compound to the axon terminals from the cell body. This low concentration of local vinblastine treatment also resulted in depletion of fluoride-resistant acid phosphatase from C fiber terminals in the dorsal horn of the spinal cord. Transmission from C fibers to second-order neurons in the spinal cord, however, was totally unaffected. Substance P levels in the spinal terminals was largely unaffected, although in 1 of 5 cases there was depletion. It appears, therefore, that some, but not all, retrograde changes in sensory neurons following peripheral nerve damage can be mimicked by blockade of axon transport. The effects following vinblastine treatment are compared to other peripheral nerve manipulations, such as cut, crush, and application of local capsaicin.

Afferent Pathways↗

The properties of neurones recorded in the superficial dorsal horn of the rat spinal cord.

The physiological properties of neurones in the superficial laminae of the dorsal horn of the fourth and fifth lumbar segments of the rat spinal cord have been investigated in decerebrate spinal animals. Both extracellular recordings with platinum-plated tungsten microelectrodes (n = 72) and intracellular recordings with glass microelectrodes (N = 79) were made. Attempts were made to fill cells intracellularly with horseradish peroxidase or Lucifer Yellow. Thirty-seven percent of the intracellularly injected neurones were recovered after histological processing and their cell bodies found to be in lamina 1 or 2 and in the dorsal white matter overlying lamina 1. The dendritic spread of the stained neurones was maximal in the rostrocaudal plane with a restricted mediolateral spread. The physiological properties of the extracellularly recorded units, the intracellularly unidentified units, and the intracellularly stained units were the same. The neurones were characterized by low background activity and all had excitatory receptive fields on the lower limb. Some neurones responded only to low-threshold mechanical stimulation of the skin or only to noxious skin stimulation but the majority of units (58%) were wide-dynamic-range cells responding to both types of stimuli. Receptive field classification was made questionable, however, by the existence of cells (9%) that exhibited a spontaneous shift in the size of their receptive fields and in the type of stimulus that elicited a response. The neurones in the superficial dorsal horn commonly showed a marked inhibition to repeated cutaneous stimuli (27%) or a prolonged afterdischarge followed a single stimulus (20%). Afferent input from the sural nerve was found to be from A and C fibres in both extra-and intracellular recordings. A delta- and C-mediated excitations were most common although convergent inputs from A beta-fibres occurred in 40% of units. No correlation was found between cell structure or distribution of dendritic fields and physiological properties in our small sample of intracellularly stained cells. The morphology of the cells was highly diverse, as were the different receptive fields. There was, however, some correlation between the location of cell bodies and their responses. Neurones responding only to low-threshold stimuli were distributed either in the dorsal white matter or in inner lamina 2. Wide-dynamic-range cells were distributed throughout the superficial dorsal horn. These results suggest that neurones of different shapes and positions may subserve the same function and, conversely, that neurones of the same shape and position may subserve different functions.

Animals↗

Chronic peripheral nerve section diminishes the primary afferent A-fibre mediated inhibition of rat dorsal horn neurones.

The inhibitory effect of A-primary afferent activity on A- and C-evoked activity in dorsal horn convergent neurones has been investigated in the decerebrate spinal rat. A-afferent conditioning stimuli produce a powerful inhibition of the C-evoked activity in the majority of units recorded in lamina 5 but were almost without effect on the C-evoked activity in units recorded within the substantia gelatinosa (laminae 1 and 2). The ability of an A-volley to inhibit the response to a C-volley begins immediately after the arrival of the A-volley and lasts for 50-70 ms. Conditioning A-stimuli also inhibit the A-evoked activity of dorsal horn neurones, the inhibition lasting up to 125 ms. Unlike the effect of A-conditioning stimuli on C-responses, which was restricted to units in lamina 5, the A-volleys inhibited the response of both substantia gelatinosa and lamina 5 units. In rats with chronically sectioned sciatic nerves (7-14 days) both A on A and A on C inhibitions were significantly diminished in spite of intact afferent volleys and postsynaptic activity. In neurones activated by stimulation of the sectioned nerve, the A-conditioning stimuli either failed to produce an inhibition or produced a weak and shorter effect. These results are discussed in terms of the possible functional significance of A-afferent mediated inhibition.

Animals↗

Do opioid peptides mediate a presynaptic control of C-fibre transmission in the rat spinal cord?

A presynaptic inhibitory role for opioid peptides in the control of C-fibre-evoked activity in the dorsal horn has been investigated. The excitability of C-fibre terminals in the dorsal horn of decerebrate spinal rats was tested using intraspinal terminal stimulation and recording the size of the antidromic C wave from the dorsal roots. Naloxone (1-2 mg/kg) failed to alter the baseline terminal excitability of the C-fibres, but reduced the increase in terminal excitability produced by A-fibre afferent conditioning stimuli. The inhibition of postsynaptic C-evoked activity in lamina 5 cells produced by A-afferent fibre conditioning stimuli was also reduced by naloxone. This effect may reflect the reversal of an opioid-mediated presynaptic inhibition, although blockade of a direct postsynaptic inhibitory action could also be involved.

Animals↗