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V Chapman

Publications and source records attributed to V Chapman.

At least 55 records · Page 3Linked to original sources
PubMed1996

Concomitant administration of morphine and an N-methyl-D-aspartate receptor antagonist profoundly reduces inflammatory evoked spinal c-Fos expression.

BACKGROUND: After intraplantar injection of carrageenin, peripheral inflammation and spinal c-Fos expression are extensive, with the latter being sensitive to both large doses of morphine or N-methyl-D-aspartate receptor antagonism. The authors investigated the effects of coadministered morphine and (+)-HA966, a functional antagonist at the glycine site of the N-methyl-D-aspartate receptor, on the two parameters. METHODS: The effects of morphine, (+)-HA966 and coadministration of morphine and (+)-HA966 on spinal c-Fos expression in segments L4-L5 of the spinal cord and peripheral edema, induced at 1.5 h and 3 h after intraplantar carrageenin (6 mg/150 microliters) were studied. RESULTS: Previous coadministration of 0.3 mg/kg systemic morphine and 2.5 mg/kg subcutaneous (+)-HA966 significantly reduced c-Fos expression induced 1.5 h, but not 3 h, after carrageenin administration. However, coadministration of a larger dose of morphine (3 mg/kg) with (+)-HA966 (2.5 mg/kg) reduced c-Fos expression at 3 h after carrageenin administration, in a partially naloxone-reversible manner. CONCLUSIONS: Concurrent mu-opioid receptor activation and N-methyl-D-aspartate receptor antagonism reduces nociceptive transmission at the level of the spinal cord, as shown by the reduction of carrageenin-evoked c-Fos expression.

Analgesics, Opioid↗
PubMed1996

Inhibitory action of nociceptin on spinal dorsal horn neurones of the rat, in vivo.

Intrathecally administered nociceptin (5, 50, 225 micrograms) dose-relatedly inhibited the C-fibre evoked wind-up and post-discharge of dorsal horn neurones, but not the baseline C-fibre evoked responses. Spinal naloxone 50 micrograms, but not 10 micrograms, reversed the effects of nociceptin. Thus the antinociceptive role of nociceptin in the spinal cord differs from that of classical opioids.

Animals↗
PubMed1996

Physiological contributions of neurokinin 1 receptor activation, and interactions with NMDA receptors, to inflammatory-evoked spinal c-Fos expression.

1. Intraplantar injection of formalin (5%, 100 microliters in saline) was associated with a high level of spinal c-Fos immunoreactivity and a peripheral paw and ankle edema, as assessed at 3 h after formalin administration. For the two experimental series, the control number of formalin-evoked Fos-like immunoreactive (Fos-LI) neurons were 174 +/- 6 and 193 +/- 18 (means +/- SE) Fos-LI neurons per 40-microns section of the lumbar segment L4-L5 of the rat spinal cord. For both series of experiments, Fos-LI neurons were located predominantly in the superficial (I-II; 40 and 44% of the total number of Fos-LI neurons for the two experimental series) and deep (V-VI; 37 and 40% of the total number of Fos-LI neurons for the two experimental series) laminae of the dorsal horn of the spinal cord. The small number of remaining Fos-LI neurons were located in the nucleus proprius (laminae III-IV) and the ventral horn. 2. Prior intravenous administration of RP67580 (0.05, 0.5, and 1.5 mg/kg), a selective neurokinin 1 (NK1) receptor antagonist, dose-relatedly reduced the total number of formalin evoked Fos-LI neurons (88 +/- 5%, 80 +/- 4%, P < 0.01 and 64 +/- 4%, P < 0.0001, of the control number of formalin-evoked Fos-LI neurons). Laminar analysis of the regional effect of RP67580 on formalin-evoked Fos-LI neurons illustrated that the number of superficial and deep laminae Fos-LI neurons were attenuated to a similar extent by RP67580. 3. Prior intravenous administration of RP68651 (1.5 mg/kg), the inactive isomer of RP67580, produced only a small reduction in the total number of formalin-evoked Fos-LI neurons (84 +/- 5% of the control number of formalin-evoked Fos-LI neurons (P < 0.05). The effect of RP68651 on the number of formalin-evoked Fos-LI neurons was significantly smaller (P < 0.01) than the effect of the equivalent concentration of RP67580, the active isomer. 4. Prior coadministration of intravenous RP67580 (0.5 mg/kg) and subcutaneous (+)-HA966 (2.5 mg/kg), an antagonist at the glycine site of the N-methyl-D-aspartate (NMDA) receptor, significantly reduced the number of formalin-evoked Fos-LI neurons (64 +/- 4% of the control number of formalin-evoked Fos-LI neurons, P < 0.01). The attenuating effect of coadministered RP67580 and (+)-HA966 was significantly greater than the effect of RP67580 alone (P < 0.01) and the effect of (+)-HA966 alone (P < 0.05). Laminar analysis illustrated that coadministered RP67580 and (+)-HA966 reduced the number of formalin-evoked Fos-LI neurons in the superficial and deep laminae to a similar extent. 5. Intraplantar injection of formalin was associated with a peripheral paw (0.92 +/- 0.02 cm) and ankle (0.92 +/- 0.02 cm) edema, as compared with the paw (0.46 +/- 0.02 cm) and ankle (0.67 +/- 0.14 cm) diameters of saline-stimulated rats. Neither prior administration of intravenous RP67580 (0.05, 0.5, and 1.5 mg/kg) or RP68651 (1.5 mg/kg) or prior coadministration of RP67580) (0.5 mg/kg) and (+)-HA966 (2.5 mg/kg) influenced the extent of the paw or ankle-edema at 3 h after intraplantar injection of formalin. 6. Our results illustrate that NK1-receptor activation contributes to inflammatory-evoked spinal c-Fos expression and thus supports the current contention that NK1-receptor activation, and by inference SP, plays a role in spinal nociceptive processing. The second part of our study suggests that the previously reported NK1/NMDA-receptor interactions contribute to formalin-evoked spinal c-Fos expression and consequently may contribute to the longer term spinal neuroplasticity associated with inflammatory nociceptive processing.

Analgesics↗
PubMed1996

To what extent do spinal interactions between an alpha-2 adrenoceptor agonist and a mu opioid agonist influence noxiously evoked c-Fos expression in the rat? A pharmacological study.

Three hours after the intraplantar injection of carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was observed in both superficial and deep laminae of the dorsal horn segments L4 and L5 of the spinal cord. Systemic medetomidine, an alpha-2 adrenoceptor agonist (12.5, 25 or 75 micrograms/kg i.v.), dose-dependently reduced the number of superficial and deep Fos-LI neurons; 75 micrograms/kg produced a 66 +/- 4% and a 90 +/- 4% reduction of superficial and deep Fos-LI neurons, respectively, P < .0001 for both. In addition, systemic medetomidine dose-relatedly reduced the carrageenin-evoked paw and ankle edema; medetomidine 75 micrograms/kg resulted in a 70 +/- 3% reduction of paw edema and in a blockade of the development of ankle edema. The effects of medetomidine were blocked by systemic atipamezole (75 micrograms/kg, i.v.), which, when injected alone, had no effect on the number of Fos-LI neurons or the peripheral edema. Co-administration of a low dose of medetomidine (12.5 micrograms/kg i.v.) with an ineffective dose of morphine (1.5 micrograms/kg i.v.) strongly decreased the number of superficial and deep Fos-LI neurons (40 +/- 5%, P < .0001 and 62 +/- 11%, P < .0001 reduction as compared with control group) without altering the effects of medetomidine on the peripheral edema. Both atipamezole and a combined injection of atipamezole and naloxone blocked the effects of medetomidine plus morphine on both the total number of Fos-LI neurons (86 +/- 11% and 86 +/- 6% of control, respectively) and carrageenin inflammation (87 +/- 6%, P < .05 and 84 +/- 3%, P < .05 of control for the paw edema; 75 +/- 8%, P < .01 and 81 +/- 7%, P < .05 of control for the ankle edema, respectively). Naloxone alone blocked the effects of the co-administered agonists on the total number of Fos-Li neurons (91 +/- 6% of the control carrageenin group) without influencing the effect on the peripheral edema. Our results demonstrate, for the first time, that co-administration of alpha-2 adrenoceptor and mu opioid agonists substantially reduces inflammatory evoked expression of c-Fos, one of the long-term consequences of sustained nociceptive processing.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1995

When is the maximal effect of pre-administered systemic morphine on carrageenin evoked spinal c-Fos expression in the rat?

This study evaluated, in awake rats, the time course of the expression of c-Fos in spinal cord neurons, in the L4-L5 segments, at various time points after intraplantar carrageenin (0.5 h, 1 h, 1.5 h, 2 h and 2.5 h). In addition, the effects of pre-administered morphine (3 mg/kg, i.v.) on the c-Fos expression, at the various time points, were studied. Very few Fos-like immunoreactive (Fos-LI) neurons were observed 0.5 h after carrageenin. However, spinal c-Fos expression increased initially (at 1 h), in the superficial laminae (I-II) of the spinal dorsal horn, and incrementally increased both in the superficial and deep (V-VI) laminae at later time points after carrageenin. Systemic morphine did not significantly decrease the number of superficial Fos-LI neurons observed 1 h after carrageenin, whereas it significantly reduced the number of superficial Fos-LI neurons induced at 1.5 h and 2 h after carrageenin (58 +/- 3% and 57 +/- 10% reduction, P < 0.001, respectively). In addition, morphine reduced the number of deep Fos-LI neurons at 1.5 h and 2 h after carrageenin (86 +/- 4%, P < 0.01 and 82 +/- 8%, P < 0.001 reduction as compared to control carrageenin expression, respectively). In contrast, morphine was less efficacious in decreasing the number of Fos-LI neurons observed in the superficial and deep laminae at 2.5 h after carrageenin (34 +/- 6% and 59 +/- 6% reduction, P < 0.001, respectively). Thus, the peak effect of pre-administered morphine on carrageenin evoked c-Fos expression was observed 1.5 h and 2 h after intraplantar carrageenin, with a weaker effect observed at 2.5 h after carrageenin. The pharmacokinetic complications between the time course of the antinociceptive effects of morphine and c-Fos expression is discussed. These results clearly demonstrate that studies of c-Fos expression with pharmacological investigations should take into consideration this finding since one delay after the stimulation does not give a full indication of the full potential of the drug tested.

Analgesics, Opioid↗
PubMed1995

Time-related roles of excitatory amino acid receptors during persistent noxiously evoked responses of rat dorsal horn neurones.

The responses of convergent dorsal horn neurones to peripheral injection of formalin (5% formaldehyde, 50 microliters volume) were recorded extracellularly in the halothane anaesthetized rat. The control response of dorsal horn neurones to formalin was biphasic, with a first phase from 0-10 min and the second inflammatory phase from 10-60 min. Pre-administered intrathecal CNQX (5, 50 and 500 micrograms), 5 min before formalin injection, significantly reduced both the first phase (40 +/- 22, 52 +/- 20 and 40 +/- 28% inhibition, respectively, P < 0.05) and the second phase of the formalin response (40 +/- 20% inhibition, P < 0.05, 93 +/- 4% inhibition, P < 0.0001 and 65 +/- 17% inhibition, P < 0.05, respectively). Post-administered CNQX, administered 5 min after the peripheral injection of formalin, was less efficacious, as compared to pre-administered CNQX, at reducing the second phase of the formalin response. The lowest dose of post-administered CNQX (5 micrograms) facilitated the second phase of the response (47 +/- 19% facilitation, P < 0.05), and the higher dose (50 micrograms) produced smaller inhibitions of the response (42 +/- 10% inhibition, P < 0.05) than those observed with pre-administration of the same dose. However, the highest dose of CNQX (500 micrograms) studied produced similar inhibitions of the second phase of the formalin response, irrespective of the timing of administration. Intrathecal administration of 7-chlorokynurenate (7CK, 0.25-2.5 micrograms), a functional antagonist at the glycine site of the NMDA receptor, did not alter the first phase of the formalin response. The second phase of the formalin response was significantly inhibited, and to a similar extent, by both pre- and post-administration of 2.5 micrograms of 7CK (67 +/- 10% and 56 +/- 7% inhibition respectively, P < 0.05 for both). Overall, our results clearly demonstrate differential time-related roles of different transmitter systems in the induction and maintenance of inflammatory evoked persistent pain responses, and such events may become increasingly relevant to the control of pain in the clinic.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1995

7-Nitro-indazole, a selective inhibitor of neuronal nitric oxide synthase, reduces formalin evoked c-Fos expression in dorsal horn neurons of the rat spinal cord.

The effect of intravenous 7-nitro-indazole (7NI), a selective inhibitor of neuronal nitric oxide synthase, on intraplantar formalin evoked spinal expression of c-Fos was studied. The spinal expression of c-Fos in the superficial laminae of the dorsal horn was not significantly altered by 7NI. In contrast formalin evoked c-Fos expression in the deep laminae was reduced by 15 mg/kg of 7NI (42 +/- 8% reduction of control, P < 0.05). Formalin evoked inflammation was not influenced by 7NI. Our results implicate a functional relationship between c-Fos expression and nitric oxide, at the spinal level, under inflammatory conditions.

Animals↗
PubMed1995

Carrageenan oedema and spinal Fos-LI neurones are reduced by piroxicam in the rat.

Intraplantar carrageenan induced a peripheral oedema and c-Fos like immunoreactivity (Fos-LI) in L4-L5 segments in the dorsal horn (DH) of the rat spinal cord. The total number of carrageenan evoked Fos-LI neurones was 153 +/- 10 per section, with a predominant localization in the superficial and deep laminae of the DH (46 +/- 4% and 32 +/- 2%, respectively). Pre-administered piroxicam (1, 2.5 and 5 mg kg-1, p.o.) dose-dependently reduced the number of Fos-LI neurones in both the superficial and deep laminae of DH, with effects being significantly strongest on the deep laminae Fos-LI neurones. The effects of piroxicam on the number of spinal Fos-LI neurones and on ankle oedema were positively correlated.

Animals↗
PubMed1995

Concurrent reduction of inflammation and spinal Fos-LI neurons by systemic diclofenac in the rat.

Intraplantar carrageenan induced a peripheral inflammation and c-Fos like immunoreactivity (Fos-LI) in the dorsal horn, L4-L5 segments, of the rat spinal cord. The total number of control carrageenan evoked Fos-LI neurons was 126 +/- 6 per section, which were predominately located in the superficial and deep laminae (41 +/- 2% and 39 +/- 2% of the total number of Fos-LI neurons per section) of the dorsal horn. Pre-administered diclofenac (3, 6, 9 mg/kg i.v.) dose dependently reduced the number of Fos-LI neurons, with effects being strongest on the deep laminae Fos-LI neurons. The effects of diclofenac (9 mg/kg) on the number of Fos-LI neurons (68 +/- 2% reduction) and inflamed ankle (72 +/- 7% reduction) and paw (49 +/- 6% reduction) diameters, were positively correlated.

Animals↗
PubMed1995

Cholecystokinin B receptor antagonism enhances the ability of a low dose of morphine to reduce c-Fos expression in the spinal cord of the rat.

Three hours after intraplantar carrageenin (6 mg/150 microliters) Fos-like immunoreactivity was predominantly observed in the superficial and deep laminae of the L4-L5 segments of the dorsal horn of the spinal cord in the rat. The total number of Fos-like immunoreactive neurons was equally divided between the superficial (laminae I-II) and deep laminae (laminae V-VI), 99 +/- 3 and 102 +/- 7 Fos-like immunoreactive neurons per section, respectively. In the absence of carrageenin stimulation a negligible number of Fos-like immunoreactive neurons were observed. Pre-administered systemic morphine (0.3 mg/kg) did not significantly influence the total number of Fos-like immunoreactive neurons 3 h after carrageenin. However, pre-administration of a higher dose of morphine (3 mg/kg) significantly reduced the total number of Fos-like immunoreactive neurons (28 +/- 8% reduction, P < 0.001, as compared with control carrageenin Fos-like immunoreactive expression), with this effect being equally divided between the superficial and deep laminae (29 +/- 5 and 29 +/- 6% reduction, respectively, P < 0.001, as compared with control carrageenin Fos-like immunoreactive expression, for both). Pre-administration of the selective cholecystokinin B receptor antagonist, L-365-260 (0.2 mg/kg), alone did not influence the total number of Fos-like immunoreactive neurons 3 h after carrageenin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Different chromosomal localization of the Clcn4 gene in Mus spretus and C57BL/6J mice.

We report the unprecedented finding of a gene with a different map position in two mouse strains. The Clcn4 gene was found to map to the X chromosome in the wild Mediterrean mouse, Mus spretus but to chromosome 7 in the inbred strain of laboratory mouse C57BL/6J. These data indicate that a recent evolutionary rearrangement occurred on the mouse sex chromosomes, very close to the pseudoautosomal region. Our data provide molecular evidence for a major divergence near the pseudoautosomal region, consistent with the hypothesis that hybrid sterility in these species results from abnormal pairing of sex chromosomes during male meiosis.

Amino Acid Sequence↗
PubMed1995

Comparative analysis of mouse NotI linking clones with mouse and human genomic sequences and transcripts.

NotI cleavage sites are frequently associated with CpG islands that identify the 5' regulatory sites of functional genes in the genome. Therefore we analyzed a sample of 22 NotI linking clones prepared from mouse brain DNA, to determine whether these mouse NotI site associated clones could be used for comparative analysis of mouse and human genomes by cross-reaction with both mouse and human genomic DNA and RNA in Southern and Northern hybridization. We further examined whether we could establish the identity of these clones with known genes by comparing the nucleotide sequences surrounding the NotI site with the GenBank database. We observed that 70% of the clones cross-hybridized with human DNA and that 4 of 11 tested clones (36%) detected a transcript in human HeLa cells RNA whereas 73% clones (8/11) detected transcripts in mouse RNAs from one or more organs. Single pass sequence analysis was successful on 16 of 19 clones. The GC content in these sequence was very high (48.8% to 73.8%) suggesting that 12 of 16 sequenced clones contained a CpG island. Three out of 19 clones showed significant similarity with previously analyzed mouse gene sequences in GenBank, including the mouse rRNA gene family, cathepsin and the scip POU-domain genes. In addition, two sequences showed significant similarity to the human and rabbit protein phosphatase 2A-beta subunit and the human transforming growth factor-beta. Thus, 5 of 16 clones showed homology with identified genes. These results and the recent work of using RLGS methods for genetic mapping indicate that NotI linking clones can be used to efficiently cross reference a comparative analysis of the mouse and human genomic maps.

Animals↗
PubMed1995

Reduction of carrageenin oedema and the associated c-Fos expression in the rat lumbar spinal cord by nitric oxide synthase inhibitor.

1. Three hours after intraplantar carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was mainly observed in L4 and L5 segments of the dorsal horn. Both superficial (I-II) and deep laminae (V-VI) neurones were labelled. 2. We have studied the effect of systemic administration of a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) on carrageenin evoked c-Fos expression and thus the contribution of nitric oxide to this expression. 3. Pre-administration of L-NAME (10, 25, 50, 100 mg kg-1, i.v.) dose-dependently reduced the number of superificial and deep laminae Fos-LI neurones, 100 mg kg-1 produced a 63 +/- 2% and 72 +/- 4% reduction of Fos-LI neurones respectively, P < 0.0001 for both superficial and deep neurones. 4. Pre-administered L-NAME dose-relatedly reduced the carrageenin-evoked paw and ankle oedema, with 100 mg kg-1 of L-NAME resulting in a 74 +/- 2% and 103 +/- 2% reduction respectively. 5. Post-administration of L-NAME (10 mg kg-1, i.v.) reduced the number of superficial and deep laminae Fos-LI neurones (65 +/- 7% and 53 +/- 8% reduction respectively, P < 0.01 for both superficial and deep neurones). 6. Post-administered L-NAME reduced both the paw and ankle oedema (52 +/- 8% and 62 +/- 10% reduction respectively, P < 0.0001 for both paw and ankle). 7. Pre-administered D-NAME (100 mg kg-1, i.v.), the inactive isomer of L-NAME, produced a weak reduction of the number of superficial laminae Fos-LI neurones (26 +/- 8% reduction, P<0.05), without influencing the deep Fos-LI neurones (5 +/- 8% enhancement) or the oedema.8. Systemic L-arginine (1200 mg kg-1) did not reverse the reduction of the total number of Fos-LI neurones induced by 100mg kg-1 of L-NAME, or the effect of L-NAME on the paw and ankle oedema.9. Intraplantar L-arginine (30 mg) did not reverse the effect of L-NAME (100 mg kg-1) on the total number of Fos-LI neurones. However, the inhibitory effects of L-NAME on the paw and ankle oedema were partially reversed by intraplantar L-Arginine (34 +/- 9% and 45 +/- 11% reduction of carrageenin oedema respectively) with these effects being significant as compared to the effect of L-NAME alone(P<0.05 for both).10. There is a strong correlation between the reduction of the number of Fos-LI neurones and the oedema by L-NAME, clearly demonstrating a predominant role of peripheral NO in the development of one of the signs of carrageenin inflammation.

Amino Acid Oxidoreductases↗
PubMed1995

The contribution of NMDA receptor activation to spinal c-Fos expression in a model of inflammatory pain.

1. Intraplantar carrageenin (6 mg 150 microliters-1) evoked a high level of spinal c-Fos expression in the dorsal horn, of segments L4-L5 of the spinal cord, and an extensive peripheral oedema; both parameters were assessed 3 h after carrageenin. 2. Two series of experiments were performed, with the mean total number of Fos like-immunoreactive neurones (Fos-LI), after carrageenin, not being significantly different for the two series of experiments (266 +/- 17 and 332 +/- 31 Fos-LI neurones). For both series of experiments Fos-LI neurones were predominantly located in the superficial and deep laminae, only 10% of the total number of Fos-LI neurones were located in the nucleus proprius and 10% were located in the ventral horn. 3. Pre-administration of the N-methyl-D-aspartate (NMDA) receptor antagonist, (+)-HA966 (0.5 mg kg-1 and 2.5 mg kg-1, s.c.), 30 min before carrageenin, did not significantly influence the total number of Fos-LI neurones, as compared to control carrageenin expression. 4. Pre-administration of the highest dose of (+)-HA966 (10 mg kg-1) significantly reduced the number of deep laminae Fos-LI neurones (28 +/- 3% reduction of control number of Fos-LI neurones after carrageenin, P < or = 0.05), without influencing the number of superficial Fos-LI neurones. There was a tendency towards a reduction of the number of Fos-LI neurones in the nucleus proprius by the highest concentration of pre-administered (+)-HA966, (31 +/- 8% reduction), but this effect did not reach significance. 5. Pre-plus post-administered (+)-HA966 (0.5 mg kg-1), 30 min before and again 45 min afterintraplantar carrageenin, did not significantly influence the total number of Fos-LI neurones, as compared to control carrageenin expression.6. Pre- plus post-administration of 2.5 mg kg-1 (+)-HA966 significantly reduced the total number of Fos-LI neurones, as compared to control carrageenin expression. This effect was reflected by a significant reduction in the number of Fos-LI neurones in the nucleus proprius (36+/-7% reduction of control carrageenin c-Fos expression respectively, P<0.05).7. Pre-plus post-administration of 10 mg kg-1 of (+)-HA966 significantly reduced the number of Fos-LI neurones in the superficial laminae, nucleus proprius, deep laminae and ventral horn (33 +/-0.5%,55+/-6%, 40+/-4% and 51+/-4% reduction of control carrageenin c-Fos expression, respectively, P<0.05,for all areas).8. A single post-administration of (+)-HA966 (10 mg kg-1), 45 min after intraplantar carrageenin, did not significantly influence the number of Fos-LI neurones in the superficial, deep laminae or ventral horn, but significantly reduced the number of Fos-LI neurones in the nucleus proprius, as compared tocontrol carrageenin expression (39+-/8% reduction of control carrageenin c-Fos expression, P <0.05).9 None of the concentrations of (+)-HA966 studied, irrespective of the timing of administration,influenced the peripheral carrageenin oedema. Our results illustrate a contribution of central NMDA receptor activation to carrageenin-evoked spinal c-Fos expression. These results extend previous studies demonstrating the contribution of the NMDA receptor to central hyperalgesia and the expression of c-Fos.

Animals↗
PubMed1994

Bi-directional effects of intrathecal NMDA and substance P on rat dorsal horn neuronal responses.

Intrathecal NMDA (5 ng) facilitated wind-up but not C-fibre evoked responses, whereas 50 ng facilitated C-fibre and A delta-fibre evoked responses but not wind-up of convergent dorsal horn neurones in the halothane anaesthetized rat. Higher doses of NMDA and SP (10-500 ng) were without effect. Co-administered SP (10 ng) with NMDA (5 ng) facilitated A delta-fibre evoked responses and wind-up. Excitatory amino acid and peptide interactions are discussed.

Animals↗
PubMed1994

Enhanced responses of rat dorsal horn neurons after UV irradiation of the hindpaw; roles of the NMDA receptor.

Recordings were made from nociceptive dorsal horn neurones in the anaesthetized rat 3 and 5 days after ultraviolet (UV) irradiation of the hindpaw. The electrically evoked A beta-fibre-evoked responses from the paw were enhanced and their thresholds were lowered. Spontaneous neuronal activity was increased but the C-fibre-evoked responses were unaltered. These enhanced responses, suggestive of allodynia, were reduced by N-methyl-D-aspartate receptor (NMDA) antagonism.

Action Potentials↗
PubMed1994

Mapping of the X-linked cataract (Xcat) mutation, the gene implicated in the Nance Horan syndrome, on the mouse X chromosome.

The Xcat mutation in the mouse, an X-linked inherited disorder, is characterized by the congenital onset of cataracts. The cataracts have morphologies similar to those of cataracts found in the human Nance Horan (X-linked cataract dental) syndrome, suggesting that Xcat is an animal model for Nance Horan. The Xcat mutation provides an opportunity to investigate, at the molecular level, the pathogenesis of cataract. As a first step to cloning the Xcat gene, we report the localization of the Xcat mutation with respect to known molecular markers on the mouse X chromosome. Back-cross progeny carrying the Xcat mutation were obtained from an interspecific cross. Genomic DNA from each mouse was subjected to Southern and PCR analysis to identify restriction fragment length polymorphisms and simple sequence length polymorphisms, respectively. Our results refine the location of Xcat to a 2-cM region, eliminate several genes from consideration as the Xcat mutation, identify molecular probes tightly linked with Xcat, and suggest candidate genes responsible for the Xcat phenotype.

Animals↗