Search PubMed⌕ Search

Biomedical subjects

R H Evans

Publications and source records attributed to R H Evans.

At least 37 records · Page 2Linked to original sources
PubMed1997

Organochlorine pesticides associated with ocular, nasal, or otic infection in the eastern box turtle (Terrapene carolina carolina).

From May 1987 to September 1994, 19 eastern box turtles (Terrapene carolina carolina) originating from scattered locations on Long Island, New York (USA) were presented with one or more of the following signs: listlessness, ocular and nasal discharge, conjunctivitis, blepharitis, and otitis media. Numerous species of bacteria and yeast were isolated by aerobic culture. Histopathologic findings confirmed chronic active bacterial infections. Toxicologic analyses of livers revealed elevated concentrations of chlordane metabolites in two diseased turtles. A third turtle liver contained residues of endosulfan sulfate. Immunosuppressive effects of low-level exposure to organochlorines, including chlordane and endosulfan, could be involved in the pathogenesis of the observed infections.

Animals↗
PubMed1996

Spontaneous coronary artery rupture and cardiac tamponade in Ehlers-Danlos syndrome type IV.

Spontaneous coronary artery rupture resulted in cardiac tamponade in a man with Ehlers-Danlos syndrome (type IV) presenting with acute onset of cardiac chest pain. Electrocardiograms suggested acute myocardial infarction. The haemopericardium was drained and angiography showed a ruptured distal branch of the left circumflex coronary artery. The patient remains well.

Adult↗
PubMed1996

Depression of glutamatergic transmission by nociceptin in the neonatal rat hemisected spinal cord preparation in vitro.

The present study explored the action of nociceptin, the putative endogenous ligand for the orphan opioid receptor (ORL1), on the rat hemisected spinal cord preparation. Electrical stimulation of a dorsal root evokes a glutamatergic population ventral root potential (DR-VRP) in the corresponding ventral root. Low intensity stimulation evokes two A fibre-mediated components; a compound action potential of motoneurones superimposed on a population e.p.s.p. (excitatory postsynaptic potential); at higher stimulus intensities sufficient to activate C fibres a more prolonged population e.p.s.p. is evoked. All three components were depressed by nociceptin in a concentration-dependent manner with IC50 values (s.e.mean) of 119 +/- 2 nM (n = 4), 241 +/- 3 nM (n = 4) and 32 +/- 2 nM (n = 4), respectively. The depressant actions of nociceptin (30 nM and 300 nM) were not reversed by the opioid antagonist naloxone (1 microM). Nociceptin (100 nM and 300 nM) had no effect on the afferent volleys in the dorsal root. Nociceptin therefore appears to be acting as an inhibitory peptide at the spinal level through a naloxone-insensitive opioid receptor.

Amino Acid Sequence↗
PubMed1995

Effect of raised Mg2+ on the antidromic activation of immature rat spinal motoneurones in vitro.

Currents elicited by electrical stimulation of the ventral root were recorded from motoneurones of the immature rat spinal cord in vitro using the patch pipette technique. Control medium contained Ca2+ (1.5 mM) and Mg2+ (0.75 mM). In nine preparations the mean amplitude of antidromic current responses was 5.12 +/- 0.41 nA. Raising Mg2+ (EC50 9.6 +/- 1.1 mM) to levels up to 50 mM produced an all-or-none maximal depression of the current responses by 69 +/- 1%. These levels of Mg2+ depressed currents elicited by depolarizing command steps by only 30% and compound action potentials recorded in ventral roots by only 17%. It is concluded that raised Mg2+ caused conduction block from the initial segment to the soma dendritic region of motoneurones. This non-synaptic depressant action of raised Mg2+ should be considered when raised Mg2+ is used in order to specifically block synaptic activity in vitro.

Action Potentials↗
PubMed1995

A comparison of the effects of selective metabotropic glutamate receptor agonists on synaptically evoked whole cell currents of rat spinal ventral horn neurones in vitro.

1. Whole cell synaptic currents were recorded under voltage clamp from a total of 54 ventral horn neurones held near to their resting potential by the patch clamp technique in immature rat spinal cord preparations in vitro. Twenty eight neurones were identified, by antidromic invasion from ventral roots, as motoneurones. Excitatory postsynaptic currents (e.p.s.cs) of peak amplitude -480 pA +/- 66 s.e. mean and -829 +/- 124 pA were evoked respectively from the unidentified ventral horn neurones and the motoneurones in response to maximal activation of the segmental dorsal root. 2. The e.p.s.cs were depressed reversibly by the metabotropic glutamate agonists 1S3S-1-aminocyclopentane-1,3-dicarboxylate (1S3S-ACPD) (EC50 17.1 microM +/- 0.3 s.e. mean, n = 14) and L-2-amino-4-phosphonobutanoate (L-AP4) (EC50 = 2.19 +/- 0.19 microM, n = 15). Since both agonists independently produced more than 90% depression it is likely that the receptors that mediate their effects are present on the same presynaptic terminals. 3. When the Mg2+ concentration was raised from 0.75 mM to 2.75 mM together with the addition of 50 microM D-2-amino-5-phosphonopentanoate (AP5), a treatment which would increase the proportion of monosynaptic component in the e.p.s.c. the concentration-effect plots for both 1S3S-ACPD (EC50 1.95 +/- 0.4 microM, n = 8) and L-AP4 (EC50 0.55 +/- 0.20 microM, n = 7) were shifted to the left, suggesting that monosynaptic e.p.cs of primary afferents to ventral horn neurones are more susceptible to L-AP4 and 1S3S-ACPD than are other synapses in polysynaptic pathways. 4. lS3S-ACPD (20 and 50 microM) also caused mean sustained inward currents of 95 +/- 31 pA (n = 6) and248 +/- 49 pA (n = 10) respectively. In the combined presence of AP5 (50 microM) and Mg2+ (2.75 mM) themean response to 50 microM lS3S-ACPD was reduced to 106+/- 18 pA (n = 4). In the presence of tetrodotoxin(1 microM) the corresponding value was 48 +/- 6 pA (n = 4). Similar sustained inward currents produced by N-methyl-D-aspartate (NMDA) were almost abolished to < 10 pA in the presence of AP5 and 2.75 mMMg2+. In the presence of tetrodotoxin the maximum inward current produced by NMDA was undiminished. Thus a large component of the excitatory action of lS3S-ACPD was mediated at non-NMDA receptors both directly at the patch-clamped neurones and indirectly by synaptic relay.

Aminobutyrates↗
PubMed1994

Physiological and pharmacological characterization of the spinal tachykinin NK2 receptor.

The goal of these investigations was to study the role of tachykinin NK2 receptors in neonatal spinal cords using the selective NK2 receptor agonist [beta-Ala8]neurokinin A-(4-10) and the new NK2 receptor antagonist GR 94800. Experiments were performed with superfused hemisected rat and gerbil spinal cords. Dorsal roots were electrically stimulated and the synaptically elicited responses and the DC-potentials were recorded extracellularly from the corresponding ventral roots. [beta-Ala8]neurokinin A-(4-10) depolarized ventral roots (0.01-10 microM) and increased their spontaneous activity in a concentration-dependent manner. These effects of [beta-Ala8]neurokinin A-(4-10) were reduced by GR 94800. The action of GR 94800 was selective because the depolarizing effects of similar magnitude evoked by the NK1 receptor agonist [Sar9,Met(O2)11]substance P were not affected by GR 94800. The pA2 values of GR 94800 amounted to 6.0 +/- 0.4 in the rat and 5.4 +/- 0.3 in the gerbil. The NK2 receptor agonist was more potent in the rat than in the gerbil. The estimated EC50 (mean +/- S.E.M.) was found to be 3.9 + 6.0/-1.3 microM in the rat and 2.4 + 2.9/-1.3 microM in the gerbil spinal cord. The NK2 receptor agonist [beta-Ala8]neurokinin A-(4-10) potentiated the monosynaptic reflex evoked by dorsal root stimulation. The potentiation manifested itself as an increase in the amplitude of the early component of the response. The receptor type mediating this effect could not be elucidated. The potentiation ranged between 30 +/- 27 and 110 +/- 36% (0.3 and 10 microM), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The effects of central myorelaxants on synaptically-evoked primary afferent depolarization in the immature rat spinal cord in vitro.

1. In the immature rat in vitro hemisected spinal cord preparation the dorsal root-evoked depolarizing potential recorded from an adjacent dorsal root DR-DRP had a mean peak amplitude (+/- s.e.mean, n = 27) of 2.9 +/- 0.2 mV and a mean latency to peak amplitude of 106 +/- 3 ms. The DR-DRP amplitude was maximal with a stimulus intensity of four times the threshold intensity required to activate the lowest threshold fibres. The peak amplitude and/or integral over a time-source of 0.5 s were used to assess the effects of applied drugs. 2. The DR-DRP was abolished by baclofen (mean IC50 190 +/- 46 nM, n = 7). The depressant effect of baclofen was reversed by CGP35348 (1 mM). The mean apparent Kd value calculated from dose-ratios was 16.7 +/- 6.4 microM (n = 3). 3. At a maximally effective concentration, tizanidine (1 microM) produced at the most only a 14% depression of the DR-DRP (n = 4). Clonidine (0.3 microM) had an effect similar to that of tizanidine. These depressant effects were reversed by idazoxan (1 microM). 4. The DR-DRP was potentiated by diazepam in a flumazenil (1 microM)-reversible manner. A maximal potentiation of 23.2 +/- 2.7% (n = 5) was produced by 1 microM diazepam. 5. Diazepam (1 microM) induced a mean bicuculline- (10 microM, n = 2) and flumazenil- (1 microM, n = 8) sensitive depolarization in the dorsal root of 0.25 +/- 0.03 mV (n = 8). However, diazepam failed to depolarize dorsal roots (n = 3) which had been excised from the spinal cord. 6. Comparison of the above effects with previously reported depressant effects of these drugs on the synaptic output from ventral roots suggests that actions on presynaptic inhibition, as reflected in the DR-DRP, are of subsidiary importance in explaining the muscle relaxant actions of tizanidine or diazepam.

2-Amino-5-phosphonovalerate↗
PubMed1993

Antagonism of baclofen-induced depression of whole-cell synaptic currents in spinal dorsal horn neurones by the potent GABAB antagonist CGP55845.

The potencies of two GABAB receptor antagonists P-[3-aminopropyl]- P-diethoxymethyl-phosphinic acid (CGP35348) and the novel compound 3-N[1-(S)-(3,4-dichlorophenyl)ethyl]amino-2-(S)-hydroxypropyl-P- benzyl-phosphinic acid (CGP55845) have been compared in an in vitro spinal cord preparation. They have been tested as antagonists of baclofen-induced depression of EPSCs of patch-clamped dorsal horn neurons following electrical stimulation of dorsal roots. Mean EC50 values for the depressant action of baclofen were increased by 50- and 140-fold respectively in the presence of CGP35348 (200 microM) (n = 5) and CGP55845 (100 nM) (n = 4). This potency of CGP55845 is > 1000-fold higher than that reported previously for other GABAB receptor antagonists.

Action Potentials↗
PubMed1993

The modulation of the monosynaptic reflex by substance P in the hemisected spinal cord preparation of the rat and gerbil.

The effects of substance P and the selective neurokinin-1 receptor antagonist (+/-)-CP-96,345 have been compared on in vitro spinal cord preparations from the rat and the gerbil. Substance P produced a concentration-dependent depolarization of motoneurons recorded from ventral roots of both species. The EC50 values (microM mean +/- S.E.M.) obtained in rat (0.95 + 1.0/-0.49) and gerbil (0.47 + 0.26/-0.17) preparations were comparable. The mean maximal depolarization (mV mean +/- S.E.M.) evoked in rat (2.07 + 0.26/-0.25) was approximately two-fold greater than that evoked in gerbil (1.21 + 0.15/-0.14) preparations. In the rat substance P had a biphasic effect (depression followed by potentiation) on the short latency probably monosynaptic reflex evoked by electrical stimulation of a dorsal root. In gerbil preparations substance P produced only potentiation of the monosynaptic reflex. The EC50 values (microM) mean +/- S.E.M.) for this potentiating action in rat (0.97 + 0.75/-0.43) and gerbil (0.46 + 3.6/-0.4) preparations were similar. This potentiation demonstrates a positive modulation of an endogenous excitatory probably glutamatergic transmission by substance P in the ventral horn of the spinal cord. The depressant phase observed in rat preparations may be related to the relative immaturity of myelination in rat ventral root fibres compared to the gerbil. The selective neurokinin-1 antagonist (+/-)-CP-96,345 was one hundred-fold less potent as an antagonist of substance P-induced depolarizations in the rat (pA2 4.69 +/- 0.18, n = 7) than in the gerbil (pA2 6.79 +/- 0.16, n = 5) spinal cord. This finding suggests that (+/-)-CP-96,345 may not act solely at the neurokinin-1 recognition site. In conclusion this study demonstrates that substance P modulates the monosynaptic reflex in the spinal cord presumably via activation of neurokinin-1 receptors.

Action Potentials↗
PubMed1993

Multiple hepatic cavernous lymphangioma in an aged male cat.

A 10-year-old male Domestic Longhair cat with weight loss, enlarged left testicle, icterus and mild liver enlargement showed, at necropsy, two white, raised, firm, circumscribed masses in the liver and striking enlargement of the left testicle. The histological features of the liver masses were consistent with lymphangioma. Severe, diffuse, coalescing to multifocal, subacute, necrotizing orchitis of the left testicle also was diagnosed. A literature review and examination of the epidemiology of lymphangioma in small domestic animals demonstrated the rarity of this tumour in cats.

Age Factors↗
PubMed1993

A comparison of the actions of agonists and antagonists at non-NMDA receptors of C fibres and motoneurones of the immature rat spinal cord in vitro.

1. The shift in d.c. potential in dorsal roots (EC50 8.0 microM +/- 0.9 s.e. mean, n = 5) or depression of the C elevation of the compound action potential (EC50 3.0 microM +/- 0.3, n = 7) have been used to measure the depolarizing action of kainate on dorsal root C fibres of immature (3 to 5 day old) rats. Depolarization of motoneurones was measured from the shift in d.c. potential in ventral roots. 2. 6-Cyano-7-nitroquinoxaline,2-3,dione (CNQX) (pA2 5.78 +/- 0.06, n = 8) and 6-nitro-7-suplhamobenzo(f)quinoxaline-2,3-dione (NBQX) (pA2 5.75 +/- 0.04, n = 7) had similar potencies as antagonists of kainate at dorsal root fibres. The potency of NBQX as a kainate antagonist was similar also at motoneurones (pA2 5.72 +/- 0.07, n = 3). At motoneurones, NBQX was less potent as an antagonist of domoate (pA2 5.29 +/- 0.05) and more potent as an antagonist of S-alpha-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) (pA2 6.80 +/- 0.09) than as an antagonist of kainate. 3. Application of L-glutamate, quisqualate and RS-AMPA to dorsal roots produced only short lasting depolarizations but kainate concentration-effect plots were shifted to the right in the presence of these three agonists (pA2 5.08 +/- 0.08, (n = 3), 5.59 +/- 0.04, (n = 4) and 4.46 +/- 0.04 (n = 4) respectively). Slopes of dose-ratio against concentration were significantly less than one for the latter antagonism. 4. The amplitude of depolarizations induced by L-glutamate, AMPA and quisqualate were increased up to ten fold and those induced by kainate up to two fold following treatment of dorsal roots with concanavalin A. The duration of the responses was increased also by the latter treatment. Folowing 85 s applications of glutamate, quisqualate, AMPA and kainate the mean respective times (s +/- s.e.mean (n))taken for responses to decay to half the peak amplitude were increased from 63 +/- 7 (10), 86 +/- 17 (4),95 +/- 19 (4) and 135 +/- 3 (12) to 202 +/- 49 (10), 147 +/- 7 (4), 160 +/- 13 (6) and 163 +/- 10 (10). Under similar conditions the mean decay time of y-aminobutyric acid-induced responses was 145 +/- 7 (10). This was not significantly altered by concanavalin A treatment.5. Application to dorsal roots of L-aspartate at concentrations up to 5 mm (with or without concanavalin A treatment), the selective metabotropic agonist 1S,3R-trans-1-aminocyclopentane-1,3-dicarboxylate (1 mM,) and D-serine (20 pM) in the presence or absence of N-methyl-D-aspartate (NMDA,500 pM) neither depolarized the preparations nor shifted the kainate concentration-effect plot.6. It is concluded that primary afferent C fibres possess only one type of non-NMDA receptor which is activated strongly by domoate or kainate but only weakly by AMPA. This receptor is readily desensitized by glutamate, quisqualate or AMPA and it is less readily desensitized by kainate.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1992

The effect of centrally acting myorelaxants on NMDA receptor-mediated synaptic transmission in the immature rat spinal cord in vitro.

1. The effect of the myorelaxant drugs baclofen, diazepam and tizanidine have been compared on in vitro preparations of baby rat spinal cord and adult rat superior cervical ganglion. 2. Dorsal root-elicited long duration (time to half decay 9.71 +/- 0.29 s.e. mean, n = 31) ipsilateral ventral root reflexes (DR-VRP), measured as integrated area, of immature rat spinal cord preparations were abolished by RS-2-amino-5-phosphonopentanoate (AP5) (EC50 8.13 +/- 0.92 microM, n = 3). The initial short latency component of DR-VRP was resistant to AP5. 3. Baclofen abolished both components of the DR-VRP. Respective EC50 values for the AP5-insensitive and AP5-sensitive components were 237 +/- 68 nM (n +/- 7) and 57 +/- 10 nM (n = 7). These effects of baclofen were reversed by the GABAB antagonist, CGP35348. The apparent Kd values (16.7 +/- 6.4 microM, n = 3 and 14.3 +/- 3.9 microM, n = 6 respectively) for this reversal were not significantly different. 4. Tizanidine, clonidine and diazepam had no effect on the AP5-insensitive component of the DR-VRP. 5. The AP5-sensitive long duration component of the DR-VRP was depressed to respective maximal levels of 23.2 +/- 1.4% (n = 7), 18.8 +/- 3.8% (n = 4) and 47.6 +/- 1.6% (n = 5) of control (100%) levels by tizanidine (EC50 135 +/- 33 nM), clonidine (EC50 26.0 +/- 2.2 nM) and diazepam (EC25 114 +/- 12 nM, n = 4). The depressant effects of tizanidine and clonidine were reversed by idazoxan (1 microM). Flumazenil (I microM) failed to reverse the depressant effect of tizanidine. The depressant effect of diazepam was reversed by flumazenil (1 microM) but not by idazoxan (1 microM). Naloxone 1 M did not reverse the effects of either tizanidine or diazepam.6. In the presence of tetrodotoxin (0.1 SAM) which abolished synaptic activity, clonidine, tizanidine or diazepam (10, 100 and 101JM respectively) produced no significant antagonism of NMDA-induced depolarizations recorded from ventral roots.7. Control (100%) synaptic responses of rat superior cervical ganglion preparations were depressed respectively to near maximal levels of 60.0 +/- 5.2% (n = 4) and 60.7 +/- 5.6% (n = 5) by clonidine (0.5 JAM,EC25 15.3 +/- 3.0 nM) and tizanidine (1 JAM, EC25 227 +/- 83 nM). These depressant effects were reversed by idazoxan (1 AM). Baclofen (EC25 28.7 +/- 10.0, n = 3) depressed the postganglionic response to a maximum level of 71.8 + 2.4% (n = 4) control at a concentration of 100 microM. The latter depressant action was reversed by the GABAB receptor antagonist, CGP35348 (1 mM). Diazepam (1 microM) had no significant effect on ganglionic transmission.8. It is concluded that the activation of benzodiazepine or M2-noradrenaline receptors can modulate NMDA receptor-mediated excitatory synaptic pathways whereas synaptic excitation from primary afferent terminals, mediated by non-NMDA receptors, appears to lack the propensity for this type of modulation. The results show also that the isolated spinal preparation can be used to identify central myorelaxant actions that are mediated through functional benzodiazepine or X2-noradrenaline receptors.

Animals↗
PubMed1991

Potentiation of synaptic reflexes by D-serine in the rat spinal cord in vitro.

6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM) depressed dorsal root-evoked ventral and dorsal root potentials of the in vitro immature rat spinal cord to 26.3 +/- 5.2 S.E.M. and 40.8 +/- 2.7% of control values respectively. These depressant effects of CNQX were partially reversed by D-serine (EC50 values 39.7 microM +/- 8.7 S.E.M. N = 6 and 34.9 +/- 12.5 microM, N = 5 for ventral root potential and dorsal root potential respectively). Under our experimental conditions, which included the presence of Mg2+ (0.75 mM) in the bathing medium, no measurable potentiation of these synaptic reflexes by D-serine was recorded in the absence of CNQX. These data indicate that CNQX, in addition to its depressant effect at non-NMDA receptors, depresses an NMDA receptor-mediated component of segmental transmission through its action at the glycine site of the NMDA receptor complex.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1991

The influence of assay conditions on measurement of excitatory dibasic sulphinic and sulphonic alpha-amino acids in nervous tissue.

Major improvements to the HPLC separation of fluorescent derivatives of excitatory sulphur-containing amino acids have been made. Quisqualate was used as the internal standard since no endogenous derivatives coeluted with it. The artefactual generation of sulphinic and sulphonic amino acids from the oxidation of cysteine (56 microM) and homocysteine (1.2 microM) has been investigated using deionised water, an acidic phosphate/methanol mixture, perchloric acid and trichloroacetic acid (TCA) as extraction media. Of the four extraction media examined, TCA in combination with ether extraction was shown to be the most potent oxidative treatment and resulted in 23% oxidation of original cysteine or homocysteine to sulphinic and sulphonic acids. This oxidation was partially resistant to the presence of physiological concentrations of glutathione (1.5 mM) such that in the case of cysteine, 6% oxidation was observed. A 10% (v/v) mixture of methanol in 75 mM phosphate solution (pH 4.6) was found to be the most artefact-free extraction method and in spinal cord tissue processed with this medium, cysteine sulphinic acid was the only excitatory sulphur-containing amino acid consistently detectable (0.24 +/- 0.01 pmol/mg wet weight, n = 6).

Amino Acids, Sulfur↗
PubMed1991

Comparison of the capsaicin- and amino acid-sensitivity of dorsal root C fibres in the rat and the toad.

1. The C elevation of the compound action potential (CAP) was recorded with suction electrodes from dorsal roots of rats at 25 degrees C and toads (Bufo bufo) at 10 degrees C. The C fibre CAP had a conduction velocity of 0.5 +/- 0.07 SE M per sec (N = 10) and 0.25 +/- 0.04 M per sec (N = 8) in the rat and toad nerves respectively. 2. The depressant effect of applied drugs on the amplitude of the C fibres CAP was measured. Nerves from both species had similar sensitivities to GABA. EC50 5.0 microM +/- 0.5 SEM (N = 3) and 5.5 microM +/- 1.4 (N = 3) for the rat and toad respectively. Maximum depressant effects of GABA produced in rat and toad nerves were 35% +/- 5 SEM and 17% +/- 2.5 respectively. 3. In five out of ten of the rat nerves tested kainate had a clear depressant effect (maximum 36% +/- 4.3 SEM, EC50 6.8 microM +/- 0.9 SEM, N = 3) on the C fibre CAP. Kainate, at concentrations from 100 to 500 microM, had no effect on seven toad nerves. 4. Toad nerves were about 100 times less sensitive, than rat nerves, to capsaicin (ED50 values 430 microM +/- 190 SEM and 0.7 microM +/- 0.2 respectively, N = 4). 5. The similar sensitivity of nerves in both species to GABA and differing sensitivities to kainate and capsaicin suggests that amphibian C fibres specifically lack sensitivity to capsaicin and kainate.

Action Potentials↗
PubMed1991

Histopathologic features, environmental factors, and serum estrogen, progesterone, and prolactin values associated with ovarian phase and inflammatory uterine disease in cats.

Forty-four female American Shorthair cats with inflammatory uterine disease or infertility were evaluated. Data collected included age, month of diagnosis, housing, reproductive history, results of bacteriologic culture of uterine specimens, serum concentrations of estrogen, progesterone, and prolactin and histopathologic features of the ovaries and uterus. Histologically, the ovaries of 19 cats were dominated by active or cystic follicles, whereas 25 cats had luteal-phase ovaries. Of the 25 cats with active corpora lutea, 20 had either recently weaned litters (n = 11) without subsequent exposure to a male cat, or had been housed individually for lengthy periods (n = 9). The finding of active corpora lutea under these circumstances indicates that in queens, ovulation may occur by mechanisms not involving coitus. Prominent, active corpora lutea on the ovaries were associated with adenomatotic proliferative changes in the superficial and glandular epithelium of the uterus and with myometrial hyperplasia, compared with the uterus of cats with follicular ovaries (P less than 0.01). Serum progesterone concentration greater than or equal to 1.87 ng/ml was consistently associated with luteal-phase ovaries. Serum progesterone values less than or equal to 0.15 ng/ml were consistently associated with follicular-phase ovaries. Escherichia coli was the organism most commonly isolated from uterine contents.

Animals↗
PubMed1990

Effects of N-methyl-D-aspartate antagonists and spantide on spinal reflexes and responses to substance P and capsaicin in isolated spinal cord preparations from mouse and rat.

Electrical stimulus intensity, capsaicin, excitatory amino acid antagonists and the substance P antagonist, spantide, have been used to investigate the roles of primary afferent C fibres and excitatory amino acid receptors in the generation of long duration (half time 9.1 s +/- 1.1 S.E.M., N = 24) contralateral reflexes recorded in ventral roots of immature rat spinal cords in vitro. The relationship between C fibre compound action potentials recorded in the dorsal root and duration of the dorsal root-evoked contralateral ventral root potential appeared to be coincidental rather than causal. Dorsal root-evoked contralateral ventral root potentials of greater than 2 s in duration could not be evoked in mature mouse spinal preparations. Application of capsaicin (1 microM for 15-120 min) produced a long lasting increase in spontaneous activity of ventral roots as well as blockade of C fibre conduction in dorsal roots. The dorsal root potential evoked following stimulation of adjacent dorsal roots at intensities insufficient for activation of C fibres was depressed by capsaicin. Dorsal root-evoked contralateral ventral root potentials were abolished by kynurenate (EC50 56 +/- 13 microM, N = 3) and depressed to 38.2 +/- 6.9% S.E.M. (N = 7) of pre-drug levels by the N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonopentanoate (20 microM) or to 51.8 +/- 9.0% (N = 7) by the substance P analogue spantide (33 microM). Spantide consistently antagonised substance P-induced, but not capsaicin-induced, depolarizations recorded in ventral roots (+-)-2-Amino-5-phosphonopentanoic acid (10-50 microM) depressed both substance P- and capsaicin-induced depolarizations. The depressant effect of spantide, unlike that of (+/-)-2-amino-5-phosphonopentanoic acid, was associated with a long lasting excitatory action. In the presence of tetrodotoxin (0.1 microM), spantide (33 microM) failed to antagonize substance P-induced depolarizations. It is suggested that long duration of the dorsal root-evoked contralateral ventral root potential is a consequence of the activation of the N-methyl-D-aspartate receptor operated ion channels by excitatory amino acid transmitters.

Afferent Pathways↗