Search PubMed⌕ Search

Biomedical subjects

A Reid

Publications and source records attributed to A Reid.

At least 127 records · Page 7Linked to original sources
PubMed1989

Lesions to ascending noradrenergic and serotonergic pathways modify antinociception produced by intracerebroventricular administration of morphine.

Ascending noradrenergic and serotonergic pathways were lesioned by injection of 6-hydroxydopamine into the dorsal bundle or 5,7-dihydroxytryptamine into the ventromedial tegmentum respectively, and the antinociceptive effect of morphine, administered by intracerebroventricular injection assessed using the tail-flick test 3-14 days later. Lesions of the dorsal bundle selectively depleted levels of noradrenaline (NA) in the forebrain and increased the antinociceptive effect of morphine early, but not later, in the time course of action. Lesions to the locus coeruleus depleted NA in the forebrain and spinal cord but had no effect on the antinociceptive action of morphine. Lesions of the ventromedial tegmentum selectively depleted 5-hydroxytryptamine (5-HT) in the forebrain and transiently reduced the action of morphine. 5,7-Dihydroxytryptamine given intraventricularly depleted 5-HT in the forebrain and spinal cord and also transiently reduced the antinociceptive effect of morphine. These results indicate that aminergic pathways, projecting to the forebrain, are involved in the suppression of the tail-flick reflex produced by injection of morphine into the lateral ventricle.

5,7-Dihydroxytryptamine↗
PubMed1989

Objective tinnitus and tympanic membrane displacement.

A young girl with objective tinnitus is presented. Using tympanic membrane displacement, the probable origin of the tinnitus has been demonstrated. The patient has responded well to treatment with a tinnitus masker.

Child↗
PubMed1989

Comparison of intracranial pressure between spina bifida patients and normal subjects using a non-invasive pressure assessment technique.

A comparison of mean intracranial pressure (ICP) between 36 spina bifida patients and 24 patients with clinically normal ICP was undertaken. A new non-invasive method of assessing ICP was used throughout this study. The technique relates tympanic membrane displacement to ICP and has been shown to be a reliable measure of mean ICP by comparison with direct measures via ventricular catheters and reservoirs, subdural catheters and lumbar punctures. Using this non-invasive method the results of this study indicated that the patients with spina bifida and without a ventricular shunt have a higher than average mean ICP. The results demonstrated a significant difference (99.9%) in the measures of ICP between the spina bifida and normal populations. A significant difference (99.9%) in the ICP was also found between patients with spina bifida and with and without ventricular shunts, and thus presumably those with and without diagnosed hydrocephalus. It is suggested that patients with spina bifida and without ventricular shunts probably have higher than average mean ICP when compared with the normal population.

Adolescent↗
PubMed1989

Mean intracranial pressure monitoring by a non-invasive audiological technique: a pilot study.

Intracranial pressure is normally transmitted to the perilymph of the cochlea via the cochlear aqueduct. The relationship between perilymphatic pressure, indirectly measured by tympanic membrane displacement, and mean intracranial pressure defined either clinically or by direct measurement has been examined in 58 patients (aged 5-77 years), with hydrocephalus, benign intracranial hypertension, intracranial tumours, subarachnoid haemorrhage and head injuries. The most consistent results were obtained in young patients with hydrocephalus and benign intracranial hypertension. However, the technique was not suitable when the stapedial reflex was absent as a result of middle ear/brainstem dysfunction and did not reflect intracranial pressure when the cochlear aqueduct was not patent. This pilot study suggests that the tympanic membrane displacement technique may provide a useful non-invasive method for serial monitoring of intracranial pressure in young patients with hydrocephalus or benign intracranial hypertension.

Acoustic Impedance Tests↗
PubMed1989

Human cysticercosis and taeniasis: molecular approaches for specific diagnosis and parasite identification.

The construction and antibody screening of Taenia solium cDNA libraries, generated in the Escherichia coli bacteriophage lambda gt11, with the identification of clones putatively expressing antigen B, T. solium-specific and other antigens is described. Lysogens were produced from a number of selected clones and beta-galactosidase fusion peptides ranging in Mr of approximately 135,000-150,000 were demonstrated. These proteins were shown by immunoblotting to be reactive with a pool of sera from cysticercotic patients originally used in the cDNA library screening. We report a method whereby Taenia (T. saginata and T. pisiformis) eggs can be detected with high sensitivity in a specific DNA dot-blot hybridisation assay using total parasite DNA as probe. We show also that intra-specific DNA variability occurs in T. solium isolates obtained from different geographical areas and discuss the potential significance of this heterogeneity.

Animals↗
PubMed1988

Role of G-proteins and adenylate cyclase in antinociception produced by intrathecal purines.

The effects of pertussis toxin, forskolin and phosphodiesterase inhibitors on the antinociceptive action of intrathecal purines were examined to investigate the possible involvement of adenylate cyclase in spinal antinociception. Pretreatment with pertussis toxin (0.25 and 0.5 microgram) inhibited the antinociceptive action of L-phenyl-isopropyladenosine (L-PIA), N6-cyclohexyladenosine (CHA) and 5'-N-ethylcarboxamide adenosine (NECA) in the tail flick and hot plate tests. Forskolin (10-30 micrograms) reduced the effect of CHA and NECA in the hot plate test. Ro 201724 (30 micrograms) and Rolipram (20 micrograms) inhibited CHA in the tail flick and hot plate tests, but did not affect NECA in either test. These results suggest (1) spinal antinociception by purines is mediated by interactions with G-proteins (Gi linked to adenylate cyclase and/or Go linked to ion channels) (2) spinal antinociception by CHA is due to inhibition of adenylate cyclase (3) a separate mechanism, which does not involve stimulation of adenylate cyclase, may be involved in the spinal action of NECA.

Adenylate Cyclase Toxin↗
PubMed1988

Pertussis toxin inhibits antinociception produced by intrathecal injection of morphine, noradrenaline and baclofen.

The effect of intrathecal pretreatment with pertussis toxin on the spinal antinociceptive effect of morphine, noradrenaline and L-baclofen was examined in rats implanted with chronic indwelling cannulas. Pretreatment with 0.25-0.75 micrograms pertussis toxin for 2-7 days inhibited antinociception produced by intrathecal injection of all three agents in the tail flick test. Inhibition also occurred in the hot plate test, but was less pronounced than in the tail flick test. When doses of the three agents giving similar levels of antinociception were compared in a single group, the degree of inhibition of antinociception was comparable. Inhibition of the effect of noradrenaline was observed up to 14 days following pretreatment. The sensitivity of spinal antinociception to pertussis toxin suggests involvement of a guanine nucleotide regulatory protein in spinal actions of morphine, noradrenaline and L-baclofen. There is support in the literature for the additional involvement of adenylate cyclase in the action of morphine and noradrenaline but not of baclofen.

Adenylate Cyclase Toxin↗
PubMed1988

Role of ascending and descending serotonergic pathways in the antinociceptive effect of baclofen.

The role of ascending and descending serotonergic pathways in the antinociceptive effect of baclofen was examined by lesioning specific pathways with the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). Antinociception in rats was assessed using the tail flick and hot plate tests 3/4 and 10/11 days after lesioning and the placement of lesions verified by analysis of serotonin (5-HT) in brain and spinal cord. Lesions to the ventromedial tegmentum depleted 5-HT selectively in brain and inhibited the antinociceptive effect of baclofen in the tail flick test 3/4 but not 10/11 days after lesioning. Lesions to the nucleus raphe medianus produced a marked depletion of 5-HT in the hippocampus and produced the same effect on baclofen. Lesions to the nucleus raphe dorsalis were less selective, depleting 5-HT in a number of brain regions and in the spinal cord, and inhibited the antinociceptive effect of baclofen at the later but not the earlier time interval. Lesions to descending pathways by microinjection of 5,7-DHT into the ventral raphe or nucleus raphe magnus did not affect the action of baclofen significantly. Lesions to both ascending and descending pathways by intracerebroventricular 5,7-DHT increased the effect of baclofen. The hot plate test generally was less sensitive to these manipulations, although changes parallel to the tail flick test were observed in a number of instances. Both the destruction of 5-HT pathways and development of supersensitivity at 5-HT receptors may contribute to the interactions observed.

5,7-Dihydroxytryptamine↗
PubMed1988

A brief study of the selectivity of norbinaltorphimine, (-)-cyclofoxy, and (+)-cyclofoxy among opioid receptor subtypes in vitro.

Norbinaltorphimine (nor-BNI) is a bifunctional reagent developed as a selective antagonist of the kappa opioid receptor. In this paper we examined the in vitro selectivity of nor-BNI, 6-desoxy-6 beta-fluoronaltrexone (cycloFOXY), and the enantiomer of cycloFOXY, among opioid receptor subtypes. Nor BNI exhibited the highest affinity for kappa binding sites labeled by 3H-U69593 (Ki = 1.8nM), and was 27- to 29-fold less potent at mu and delta binding sites. In contrast, cycloFOXY had the highest affinity for mu binding sites (Ki = 2.62 nM), and bound to kappa and delta binding sites with Ki's of 9.3 nM and 89 nM, respectively. The enantiomer of cycloFOXY, did not inhibit binding even at concentrations greater than 10 microM, validating in part the use of 18F-labeled (+)-cycloFOXY to estimate "non-specific binding" in positron emission tomography. Additionally, we report that (S,S)-U50 488 and (R.R)-U50 488 bind to kappa binding sites labeled by 3H-U69 593 with Ki's of 0.89 nM and 299 nM, respectively.

Animals↗
PubMed1987

Effect of 6-hydroxydopamine-induced lesions to ascending and descending noradrenergic pathways on morphine analgesia.

A systematic study of the role of descending, ascending and both aspects of noradrenergic pathways in the analgesic action of morphine was undertaken. The neurotoxin 6-hydroxydopamine (6-OHDA) was microinjected into the medullary A1 region, the dorsal bundle (DB), locus coeruleus (LC) or the cerebral ventricles (i.c.v.) to deplete noradrenaline (NA) in these pathways. The analgesic effect of systemically administered morphine 7-15 mg/kg was generally tested 7-12 days postlesion, and at the end of the experiment, brain and spinal cord regions were extracted and NA and dopamine (DA) measured by HPLC to verify the placement of lesions. Medullary A1 lesions profoundly depleted spinal cord NA with only a modest effect on mesencephalic levels. Such lesions inhibited the effect of morphine in a pressure test, but not in thermal tests (tail flick and hot plate) for nociception. DB lesions reduced NA in the cortex, hippocampus, hypothalamus and midbrain, but not in the spinal cord, and potentiated morphine analgesia in thermal tests for nociception. DA levels in the striatum were normal in this group. In another group where different stereotaxic coordinates were used, the pattern of NA depletion was similar, but DA levels in the striatum were reduced. In this group, potentiation of analgesia was no longer observed. LC lesions depleted NA throughout the neuraxis and potentiated morphine analgesia in both pressure and thermal tests for nociception. I.c.v. 6-OHDA depleted NA to a comparable degree to LC lesions, but striatal DA levels also were reduced and potentiation of morphine analgesia was not observed. These results indicate that central NA pathways are critical to the expression of morphine analgesia. The effect of depletion of NA in both ascending and descending aspects is the same as depletion in ascending pathways only, suggesting that this pathway is an important mediator of morphine analgesia. Simultaneous depletion of DA in the striatum can reverse the potentiating action of NA depletion indicating a critical role for DA with respect to NA pathways and mechanisms of analgesia.

Analgesia↗
PubMed1987

Cyclothymic disorder and bromocriptine: predisposing factors for postpartum mania?

Women are most susceptible to psychotic reactions during the postpartum period, a time of intense psychological and physiological stress. Mania and depression are particularly common at this time, especially in women with past or family histories of major or minor affective disorders, specifically cyclothymia and dysthymia. Close attention after childbirth is warranted to alleviate and prevent these episodes in such women. Sympathomimetic drugs such as bromocriptine and the over-the-counter diet aids, which are linked to the induction of manic episodes, are frequently used in the puerperal period and may act as catalysts. This case report documents a postpartum manic episode in a cyclothymic woman who was prescribed bromocriptine, a dopamine agonist, for prevention of lactation.

Adult↗
PubMed1987

The effect of raised intracranial pressure on intracochlear fluid pressure: three case studies.

The effects of changes in intracranial fluid pressure (ICP) on cochlear fluid pressure have been studied in 3 patients who underwent ventriculo/lumbar-peritoneal shunt operations. The operations were performed in order to alleviate problems caused by an abnormally raised ICP. Indirect measurements of perilymphatic pressure were made before and after surgery using a non-invasive technique which measures tympanic membrane displacement. This technique proved extremely sensitive and revealed changes in cochlear fluid pressure brought about by changes in the ICP. The results emphasise the need to consider audiological measurements in the context of ICP abnormalities. These findings have important implications in that an audiological technique may be used for the simple and non-invasive serial monitoring of changes in ICP and may even assist differential diagnosis in a number of neurological patients.

Adolescent↗
PubMed1986

Role of ascending and descending noradrenergic pathways in the antinociceptive effect of baclofen and clonidine.

Baclofen and clonidine interact with central noradrenaline (NA) pathways by a variety of mechanisms. The specific role of ascending and descending pathways in antinociception produced by these agents was examined by lesioning the dorsal bundle (DB), locus coeruleus (LC) and descending NA pathways by the microinjection of the neurotoxin 6-hydroxydopamine (6-OHDA). Lesions were verified using high-performance liquid chromatography analysis of NA. Both baclofen and clonidine were injected intraperitoneally in all experiments. The antinociceptive effect of baclofen in the tail-flick test was inhibited 7-21 days after DB lesions. This manipulation decreased NA levels in cortex, hippocampus and hypothalamus but did not alter spinal cord levels. Lesions of the LC potentiated the effect of baclofen 12-16 days postlesion. NA levels were reduced in all the regions just mentioned. DB lesions produced a transient decrease in the effect of clonidine, being observed 7 but not 12-16 days postlesion. Neither acute depletion of NA levels with alpha-methyl-p-tyrosine (alpha-MPT), nor LC lesions significantly affected antinociception produced by clonidine. Intraspinal 6-OHDA potentiated the antinociceptive action of clonidine in the tail-flick test. This treatment markedly reduced spinal cord NA levels, but had minimal effects on brain NA. The results of this and previous studies in this laboratory suggest that the antinociceptive effect of baclofen is mediated by interactions with both ascending and descending NA pathways. These pathways appear to interact in a complex manner. Interpretation of data for clonidine is complicated because lesions can both deplete endogenous NA as well as inducing postsynaptic supersensitivity of alpha 2-receptors. Clonidine does not depend on endogenous NA pathways for producing antinociception because acute depletion of NA with alpha-MPT does not alter its action. Spinal sites of action are of importance following systemic clonidine because intraspinal 6-OHDA produces supersensitivity. Altering NA activity in ascending pathways alone produces a transient inhibition of the effect of clonidine, but supersensitivity is not apparent. Simultaneous lesions of both ascending and descending pathways do not produce supersensitivity, again suggesting important interactions between such pathways can occur.

Afferent Pathways↗