Biomedical subjects

E M McLachlan

Publications and source records attributed to E M McLachlan.

At least 19 recordsLinked to original sources

PubMed2003

Transmission of signals through sympathetic ganglia--modulation, integration or simply distribution?

AIM: On structural grounds, synaptic transmission in sympathetic ganglia is potentially complex with extensive divergence and convergence between preganglionic and postganglionic neurones. In this review, the focus is on what constitutes a functional synapse in sympathetic ganglia and how intracellular recordings have enabled us to identify how the transmission process operates in vivo. RESULTS: Only one or two suprathreshold or 'strong' inputs are involved in activating each postganglionic neurone. The functional significance of the subthreshold or 'weak' inputs remains obscure. The strong inputs, and sometimes the weak ones as well, respond in the same way during reflexes. The expansion of ineffective weak connections enables the rapid restoration of functional control after lesions that damage preganglionic neurones. These novel connections may generate erroneous reflex responses after spinal injury. Postganglionic discharge in vivo consists of the summed firing of the strong preganglionic inputs limited, at high preganglionic discharge rates, by the properties of the afterhyperpolarization. CONCLUSION: Preganglionic signals are distributed widely through paravertebral ganglia with little modification.

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PubMed2002

Macrophage and lymphocyte invasion of dorsal root ganglia after peripheral nerve lesions in the rat.

The distribution of major histocompatibility complex class II (MHC II)-positive non-neuronal cells and T-lymphocytes was examined immunohistochemically in dorsal root ganglia (DRGs) up to 12 weeks following transection of one sciatic or lumbar spinal nerve in adult rats. Unlike within the brain, MHC II immunopositive (+) and T-cells are normally present within DRGs. After nerve transection, MHC II+ cell density increased (by about four times after each lesion) in DRGs projecting into lesioned nerves. Subsequently the number declined after sciatic but not spinal nerve transection. MHC II+ cells did not contain glial markers, even when these were up-regulated after the lesions. Initially, MHC II+ cells lay outside the satellite glia but, by 11 weeks, they had moved through them to lie against the somata. T-cells invaded the lesioned DRGs earlier than the MHC II+ cells. They achieved greater numbers after spinal (30 x control) than after sciatic (12 x control) nerve transection. They also increased in undamaged ganglia adjacent to the spinal nerve injury. T-cell density progressively declined after spinal but not sciatic nerve transection. Both cell types appeared to invade the DRGs initially through blood vessels and the meninges, particularly near the subarachnoid angle. At later stages, occasional neurones had dense aggregations of T-cell receptor+ and MHC II+ cells associated with them. We conclude that the magnitude and time course of changes in MHC II expression and T-cell numbers in lesioned DRGs differ from the responses within motor nuclei after axotomy. The influx of inflammatory cells may contribute to neurone survival in the short term. Their long-term presence has implications for patients. These cells have the potential to release excitatory cytokines that may generate ectopic impulse activity in sensory neurones after nerve injury and so may play a role in the generation of chronic neuropathic pain.

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PubMed2001

Correlation between electrophysiology and morphology of three groups of neuron in the dorsal commissural nucleus of lumbosacral spinal cord of mature rats studied in vitro.

The dorsal commissural nucleus (DCN) in the lumbosacral spinal cord receives afferent inputs from the pelvic organs via pudendal and pelvic nerves. Electrophysiological and morphological properties of neurons in the DCN of L6-S1 were examined using whole-cell recordings with biocytin-filled electrodes in transverse slices of mature rat spinal cord. Neurons were categorized into three groups according to their discharge in response to suprathreshold depolarizing pulses; neurons with tonic (19/42) and phasic (13/42) firing patterns, and neurons (10/42) that fired in bursts arising from a Ca(2+)-dependent hump. The predominantly fusiform somata of neurons labeled during recording (n = 31) had on average 3.1 primary dendrites, 7.5 terminating dendritic branches, 3.1 axon collaterals, and 14.2 axon terminations per neuron. The groups were morphologically distinct on the basis of their dendritic branching patterns. Phasic neurons (n = 10) had the most elaborate dendritic branching and the largest numbers of axon collaterals. All tonic neurons (n = 11) had axons/collaterals projecting to the intermediolateral area but none to the funiculi, suggesting that they function as interneurons in local autonomic reflexes. Many axons/collaterals of all phasic neurons lay within the DCN, suggesting that they integrate segmental and descending inputs. Seven of 10 neurons with Ca(2+)-dependent humps had axons/collaterals extending into one of the funiculi, suggesting that they project intersegmentally or to the brain. Ca(2+) hump neurons also had more axons/collaterals within the DCN and fewer in the intermediolateral area than tonic neurons. This correlation between firing pattern and morphology is an important step toward defining the cellular pathways regulating pelvic function.

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PubMed2001

Long-term changes in the distribution of galanin in dorsal root ganglia after sciatic or spinal nerve transection in rats.

The neuropeptide galanin is upregulated in primary afferent and sympathetic neurones and might be involved in the development of sympathetic perineuronal baskets ("rings") following nerve injury. Galanin, calcitonin gene-related peptide and tyrosine hydroxylase have been examined immunohistochemically in dorsal root ganglia and associated roots at times up to one year after transection of either sciatic or L5 spinal nerves in adult rats. Small diameter somata containing calcitonin gene-related peptide (with or without galanin) were reduced in number, whereas galanin (and, at later times, calcitonin gene-related peptide) appeared in medium to large diameter cells after both types of lesion. Galanin also appeared in axons in grey rami and somata in lumbar paravertebral ganglia. Within dorsal root ganglia, galanin-positive axons formed perineuronal rings of two types: (i) smooth coiled axons surrounded small (< 30 microm diameter) somata from which they probably arose; these were rare after 12 weeks, particularly after a spinal nerve lesion; and (ii) varicose terminals encircled medium to large galanin-positive somata; some arose from brightly immunofluorescent somata nearby and took nearly a year to disappear. About 30% of varicose galanin-positive rings had associated calcitonin gene-related peptide-positive terminals (partly colocalized) whereas nearly 45% had associated tyrosine hydroxylase-positive terminals (partly colocalized). Synaptophysin was present in swollen axons and in some varicosities of all types. We conclude that, after peripheral nerve lesions, varicose perineuronal rings around large diameter dorsal root ganglion cells may be formed by axotomized primary afferent neurones (some containing calcitonin gene-related peptide) and sympathetic neurones, both of which contain upregulated galanin. Exocytosis from the varicosities may modify the excitability of mechanosensitive somata. Small galanin-positive somata disappear over several months after both lesions as calcitonin gene-related peptide reappears in medium to large neurones.

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PubMed2000

Distinct sprouting responses of sympathetic and peptidergic sensory axons proximal to a sciatic nerve transection in guinea pigs and rats.

Sprouting of sympathetic and peptidergic sensory neurones proximal to nerve lesions may reflect upregulation of growth factors around damaged dorsal root ganglion (DRG) cells. Axons containing noradrenaline or calcitonin gene-related peptide were visualized in DRGs and spinal roots of guinea pigs and rats. After sciatic transection in rats, varicose terminals of both types appeared around large DRG somata. These neurones were surrounded by proliferated satellite cells expressing glial fibrillary acidic protein (GFAP) and p75. This did not occur in guinea pigs. Instead, sympathetic axons grew through the DRG and centrally along the dorsal roots (which contained p75-positive glia), avoiding the DRG somata. Thus the glial reaction to peripheral injury differs between species such that, in guinea pigs, the environment in the spinal roots rather than in the DRGs favours sympathetic sprouting.

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PubMed2000

Distinct mechanisms for activation of Cl- and K+ currents by Ca2+ from different sources in mouse sympathetic neurones.

We have investigated the roles of different voltage-dependent Ca2+ channels in the activation of the Cl- and K+ channels responsible for the afterdepolarization (ADP) and slow afterhyperpolarization (AHP) in sympathetic neurones of the isolated mouse superior cervical ganglion in vitro. The ADP and its associated Ca2+-activated Cl- current were markedly decreased by omega-agatoxin IVA (40-200 nM) and nifedipine (1-10 microM), but not by omega-conotoxin GVIA (300 nM). In contrast, the AHP and the apamin-sensitive Ca2+-activated K+ current that underlies this potential were blocked by omega-conotoxin GVIA, but were not affected by omega-agatoxin IVA and were only slightly reduced by nifedipine. Ryanodine (20 microM) reduced the Ca2+-activated Cl- current following an action potential by 75% but on average did not affect the Ca2+-activated K+ current. Evidence that R-type channels provide a proportion of the Ca2+ activating both types of Ca2+-dependent channel was obtained. We conclude that Ca2+ entering through L- and P-type Ca2+ channels preferentially activates the Cl- current responsible for the ADP in mouse sympathetic neurones, predominantly via Ca2+-induced Ca2+ release, whereas the Ca2+ that activates the K+ channels responsible for the AHP enters predominantly through N-type channels. The data can be explained by the selective association of each type of Ca2+ channel with particular intracellular mechanisms for activating other membrane channels, one indirect and the other direct, probably located at discrete sites on the soma and dendrites.

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PubMed2000

Ultrastructure of substance P-immunoreactive terminals and their relation to vascular smooth muscle cells of rat small mesenteric arteries.

Mesenteric arteries of the rat are surrounded by a plexus of primary afferent nerve terminals which contain both substance P (SP) and calcitonin gene-related peptide (CGRP). The ultrastructural arrangement of the innervation was studied in second-order branches of the rat mesenteric artery using immunohistochemical labelling with antibodies against SP. The structure and distribution of SP-immunoreactive (SP+) and SP-negative (SP-, i.e., virtually all noradrenergic) axons and their terminals within the adventitia of the artery have been determined. Sixteen percent of axons and 22% of varicosities in the perivascular plexus were SP+. Most of the SP+ varicosities lay between 0.4 and 2 microm from the smooth muscle cells, whereas most SP- varicosities lay much closer to the vessel (i.e., <1 microm). SP+ varicosities typically contained the same number and size of small synaptic vesicles and mitochondria as SP- varicosities, but there were more large dense-cored vesicles in the SP+ varicosities. Unlike SP- varicosities, the peptidergic varicosities did not show clustering of synaptic vesicles toward one part of the axon membrane, and none of them formed junctions with the smooth muscle cells. Close relationships between SP+ and SP- varicosities lacked any detectable structural specialization. The arrangement of SP+ (primary afferent) terminals and their association with vascular smooth muscle cells indicates that peptide released from afferent terminals must diffuse further than noradrenaline from sympathetic terminals to reach the vascular smooth muscle.

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PubMed2000

Diversity of channels involved in Ca(2+) activation of K(+) channels during the prolonged AHP in guinea-pig sympathetic neurons.

The types of Ca(2+)-dependent K(+) channel involved in the prolonged afterhyperpolarization (AHP) in a subgroup of sympathetic neurons have been investigated in guinea pig celiac ganglia in vitro. The conductance underlying the prolonged AHP (gKCa2) was reduced to a variable extent in 100 nM apamin, an antagonist of SK-type Ca(2+)-dependent K(+) channels, and by about 55% in 20 nM iberiotoxin, an antagonist of BK-type Ca(2+)-dependent K(+) channels. The reductions in gKCa2 amplitude by apamin and iberiotoxin were not additive, and a resistant component with an amplitude of nearly 50% of control remained. These data imply that, as well as apamin- and iberiotoxin-sensitive channels, other unknown Ca(2+)-dependent K(+) channels participate in gKCa2. The resistant component of gKCa2 was not abolished by 0.5-10 mM tetraethylammonium, 1 mM 4-aminopyridine, or 5 mM glibenclamide. We also investigated which voltage-gated channels admitted Ca(2+) for the generation of gKCa2. Blockade of Ca(2+) entry through L-type Ca(2+) channels has previously been shown to reduce gKCa2 by about 40%. Blockade of N-type Ca(2+) channels (with 100 nM omega-conotoxin GVIA) and P-type Ca(2+) channels (with 40 nM omega-agatoxin IVA) each reduced the amplitude of gKCa2 by about 35%. Thus Ca(2+) influx through multiple types of voltage-gated Ca(2+) channel can activate the intracellular mechanisms that generate gKCa2. The slow time course of gKCa2 may be explained if activation of multiple K(+) channels results from Ca(2+) influx triggering a kinetically invariant release of Ca(2+) from intracellular stores located close to the membrane.

4-Aminopyridine↗

PubMed1999

Changes in the action potential in sensory neurones after peripheral axotomy in vivo.

Following nerve injury, modified somatic ion channels may underlie ectopic activity in axotomized A-type neurones in dorsal root ganglia (DRGs) leading to abnormal pain signalling. Using intracellular microelectrodes both in vivo and in vitro, action potentials (APs) were recorded in rat DRG neurones classified by axonal conduction velocity. After lesions to L5 spinal or sciatic nerves, APs in both A alpha/beta and A delta cells were wider, and those in A alpha/beta neurones more frequently showed inflections during repolarization, than APs in cells in undamaged ganglia. AP amplitudes and dV/dt(max) were not significantly altered by axotomy. These results confirm previous observations in intact ganglia in vitro but differ from those reported for dissociated neurones using patch recording techniques.

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PubMed1999

Calcium channel subtypes differ at two types of cholinergic synapse in lumbar sympathetic neurones of guinea-pigs.

1. The involvement of different presynaptic Ca2+ channels in transmission at 'weak' (subthreshold) and 'strong' (suprathreshold) synapses was investigated in guinea-pig paravertebral ganglia isolated in vitro. Selective Ca2+ channel antagonists were used to block excitatory synaptic currents evoked by stimulating single preganglionic axons. 2. The N-type Ca2+ channel blocker, omega-conotoxin GVIA (100 nM), reduced peak synaptic conductance by similar amounts at weak synapses (by 39 +/- 6 %) and strong synapses (34 +/- 6 %). 3. The P-type Ca2+ channel blocker, omega-agatoxin IVA (40 nM), significantly reduced transmitter release at weak synapses (by 42 +/- 6 %) but had only a small effect at strong synapses (reduced by 6 +/- 2 %). 4. Blockers of Q-, L- or T-type Ca2+ channels had no significant effects on peak synaptic conductance at either type of synapse. 5. We conclude that the two functionally distinct types of preganglionic terminal in sympathetic ganglia which synapse on the same neurone differ in their expression of particular types of voltage-dependent Ca2+ channels. Both types utilize N-type channels and channels resistant to blockade by specific antagonists, but Ca2+ entry through P-type channels makes a substantial contribution to acetylcholine release only at weak synapses.

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PubMed1999

Satellite-cell-derived nerve growth factor and neurotrophin-3 are involved in noradrenergic sprouting in the dorsal root ganglia following peripheral nerve injury in the rat.

Injury to a peripheral nerve induces in the dorsal root ganglia (DRG) sprouting of sympathetic and peptidergic terminals around large-diameter sensory neurons that project in the damaged nerve. This pathological change may be implicated in the chronic pain syndromes seen in some patients with peripheral nerve injury. The mechanisms underlying the sprouting are not known. Using in situ hybridization and immunohistochemical techniques, we have now found that nerve growth factor (NGF) and neurotrophin-3 (NT3) synthesis is upregulated in satellite cells surrounding neurons in lesioned DRG as early as 48 h after nerve injury. This response lasts for at least 2 months. Quantitative analysis showed that the levels of mRNAs for NT3 and NGF increased in ipsilateral but not contralateral DRG after nerve injury. Noradrenergic sprouting around the axotomized neurons was associated with p75-immunoreactive satellite cells. Further, antibodies specific to NGF or NT3, delivered by an osmotic mini-pump to the DRG via the lesioned L5 spinal nerve, significantly reduced noradrenergic sprouting. These results implicate satellite cell-derived neurotrophins in the induction of sympathetic sprouting following peripheral nerve injury.

Animals↗

PubMed1999

Electrophysiological roles of L-type channels in different classes of guinea pig sympathetic neuron.

The electrophysiological consequences of blocking Ca(2+) entry through L-type Ca(2+) channels have been examined in phasic (Ph), tonic (T), and long-afterhyperpolarizing (LAH) neurons of intact guinea pig sympathetic ganglia isolated in vitro. Block of Ca(2+) entry with Co(2+) or Cd(2+) depolarized T and LAH neurons, reduced action potential (AP) amplitude in Ph and LAH neurons, and increased AP half-width in Ph neurons. The afterhyperpolarization (AHP) and underlying Ca(2+)-dependent K(+) conductances (gKCa1 and gKCa2) were reduced markedly in all classes. Addition of 10 microM nifedipine increased input resistance in LAH neurons, raised AP threshold in Ph and LAH neurons, and caused a small increase in AP half-width in Ph neurons. AHP amplitude and the amplitude and decay time constant of gKCa1 were reduced by nifedipine in all classes; the slower conductance, gKCa2, which underlies the prolonged AHP in LAH neurons, was reduced by 40%. Surprisingly, AHP half-width was lengthened by nifedipine in a proportion of neurons in all classes; despite this, neuron excitability was increased during a maintained depolarization. Nifedipine's effects on AHP half-width were not mimicked by 2 mM Cs(+) or 2 mM anthracene-9-carboxylic acid, a blocker of Cl(-) channels, and it did not modify transient outward currents of the A or D types. The effects of 100 microM Ni(2+) differed from those of nifedipine. Thus in Ph neurons, Ca(2+) entry through L-type channels during a single action potential contributes to activation of K(+) conductances involved in both the AP and AHP, whereas in T and LAH neurons, it acts only on gKCa1 and gKCa2. These results differ from the results in rat superior cervical ganglion neurons, in which L-type channels are selectively coupled to BK channels, and in hippocampal neurons, in which L-type channels are selectively coupled to SK channels. We conclude that the sources of Ca(2+) for activating the various Ca(2+)-activated K(+) conductances are distinct in different types of neuron.

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PubMed1999

Synaptic responses evoked by lower urinary tract stimulation in superior cervical ganglion cells in the rat.

PURPOSE: Stimulation of afferent neurons from the urinary tract can evoke powerful cardiovascular reflexes in animals and in humans. Here we tested whether and to what extent postganglionic sympathetic neurons projecting to the head and neck are involved in these reflexes. MATERIALS AND METHODS: In adult anesthetized female Wistar rats, reflex changes in synaptic activity elicited from the lower urinary tract were recorded in neurons of the superior cervical ganglion using intracellular recording techniques. RESULTS: Gentle movements of the urethral cannula and/or slow injections of 0.3 to 0.6 ml. saline into the bladder modified synaptic activity in 75% of neurons tested: 11/15 neurons tested showed reflexes to urethral stimulation (8 excitatory, 3 inhibitory) and 8/12 neurons responded to bladder distension (5 excitatory, 3 inhibitory). Five neurons showed a reciprocal response pattern to the two stimuli. Suprathreshold and subthreshold inputs to a given cell mostly showed the same type of response. There was no evidence that urinary tract stimulation recruited preganglionic inputs that did not have ongoing activity prior to the stimulus. CONCLUSIONS: Reflexes from the lower urinary tract clearly reached sympathetic neurons located in remote segments. The response incidence in the population studied suggests that most sympathetic neurons involved in cardiovascular regulation participate in these reflexes. The different reflex patterns probably occur in neurons with different functional targets in the head and neck.

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PubMed1998

The role of N-type Ca2+ channels in regulating excitability of guinea-pig sympathetic neurones.

Ca2+ entry through voltage-gated channels activated during the action potential modifies neuronal excitability by activating several types of K+ channel. We have determined the effects of Ca2+ influx through N-type Ca2+ channels in sympathetic paravertebral neurones of the guinea-pig, using the specific antagonist, omega-conotoxin GVIA. Blockade of large conductance (BK) Ca2(+)-activated K+ channels slowed action potential repolarization but did not affect the peak amplitude of the conductance (gKCal) underlying the afterhyperpolarization. Blockade of small conductance (SK) Ca2(+)-activated K+ channels decreased gKCal but did not affect action potential repolarization. Blockade of N-type Ca2+ channels slowed action potential repolarization and reduced the peak amplitude of gKCa1. We conclude that Ca2+ entry via N-type channels activates both BK and SK channels in guinea-pig sympathetic neurones. This differs from our previous observations in rat sympathetic neurones.

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PubMed1998

Tetrodotoxin-resistant impulses in single nociceptor nerve terminals in guinea-pig cornea.

1. Extracellular recording techniques have been used to study nerve impulses in single sensory nerve terminals in guinea-pig cornea isolated in vitro. 2. Nerve impulses occurred spontaneously and were evoked by electrical stimulation of the ciliary nerves. 3. The nerve impulses were identified as originating in polymodal receptors, mechano-receptors or 'cold' receptors. All three types are believed to be nociceptors. 4. Tetrodotoxin (TTX, 1 microM) blocked nerve impulses evoked by electrical stimulation of the ciliary nerves. However, ongoing and/or naturally evoked nerve impulses persisted in the presence of TTX in all three types of receptors. Lignocaine (lidocaine; 1 mM) blocked all electrical activity. 5. TTX-resistant sodium channels therefore play a major role in generating the action potentials that signal pain to the brain.

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PubMed1998

Analysis of the periodicity of synaptic events in neurones in the superior cervical ganglion of anaesthetized rats.

1. The patterns of on-going synaptic events recorded intracellularly in neurones of superior cervical ganglia (SCG)of anaesthetized female rats were analysed by constructing inter-event interval histograms, autocorrelograms, ln-survivor curves and histograms triggered by the arterial pulse wave and by the intercostal EMG. 2. In 11/12 cells with on-going frequencies > 0.5 Hz, one or two inputs were strong (i.e. always suprathreshold). In five cells, action potentials also arose from synaptic potentials with amplitudes close to threshold. 3. Synaptic events in 5/11 neurones tested were phase-related to the arterial pressure wave (i.e. had cardiac rhythmicity, CR). 4. Synaptic events in 9/10 neurones tested (including all with CR) were phase-related to the intercostal EMG and/or their autocorrelograms showed peaks at multiples of the respiratory interval (i.e. had respiratory rhythmicity, RR). 5. The intervals between all synaptic events were exponentially distributed in 8/12 neurones although intervals between single strong events showed peaks related to the respiratory cycle. Bursts occurred only by chance. 6. Event patterns could be simulated by combining events from several respiration-modulated inputs with their timing distributed over nearly half the cycle. From the simulations, the mean number of active preganglionic inputs was estimated to be approximately 6 with mean discharge frequency approximately 0.4 Hz. 7. We conclude that, in the spontaneously breathing anaesthetized rat, most preganglionic neurones to the SCG fire with relatively low probability in relation to the respiratory cycle. Rhythms in a postganglionic neurone reflect the activity of its suprathreshold preganglionic inputs.

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PubMed1998

Axonal sprouts containing calcitonin gene-related peptide and substance P form pericellular baskets around large diameter neurons after sciatic nerve transection in the rat.

Trauma to a peripheral nerve is followed by anatomical remodelling proximal to the lesion, including sprouting of perivascular axons to form baskets of noradrenergic terminals ("rings") around large diameter primary afferent somata in the dorsal root ganglia containing lesioned neurons and sprouting of Abeta axons terminating deep in the dorsal horn into Lamina II. These abnormal structural associations may contribute to the changes in sensory processing that lead to neuropathic pain. The trigger for sprouting of sympathetic axons is probably a neurotrophin (such as nerve growth factor) concentrated locally. Nerve growth factor messenger RNA is known to be increased in dorsal root ganglia after sciatic nerve transection and increased local nerve growth factor elicits collateral sprouting of intact sympathetic terminals into adjacent denervated skin. Nociceptive terminals containing calcitonin gene-related peptide, with or without substance P, also sprout in response to raised concentrations of nerve growth factor. We have found that axons of small sensory neurons immunoreactive for these peptides also form rings around large diameter dorsal root ganglion cells of adult rats after sciatic nerve transection, concurrently with the development of rings of noradrenergic terminals.

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PubMed1998

Are there functional P2X receptors on cell bodies in intact dorsal root ganglia of rats?

P2X purinoceptors have been suggested to participate in transduction of painful stimuli in nociceptive neurons. In the current experiments, ATP (1-10 mM), alpha,beta-methylene-ATP (10-30 microM) and capsaicin (10 nM-1 microM) were applied to neurons impaled with high resistance microelectrodes in rat dorsal root ganglia (L4 and L5) isolated in vitro together with the sciatic nerve and dorsal roots. The agonists were either bath applied or focally applied using a picospritzer. GABA (100 microM) and 40-80 mM K+ solutions gave brisk responses when applied by either technique. Only three of 22 neurons with slowly conducting axons (C cells) showed evidence of P2X-purinoceptor-mediated responses. Only two of 13 cells which responded to capsaicin (putative nociceptors), and none of 29 cells with rapidly conducting axons (A cells), responded to the purinergic agonists. When acutely dissociated dorsal root ganglion cells were studied using patch-clamp techniques, all but four of 30 cells of all sizes responded with an inward current to either ATP or alpha,beta-methylene-ATP (both 100 microM). Our data suggest that few sensory cell bodies in intact dorsal root ganglia express functional purinoceptors.

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