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Biomedical subjects

D M Jackson

Publications and source records attributed to D M Jackson.

At least 145 records · Page 8Linked to original sources
PubMed1982

The action of barbiturates on contractile responses of canine and feline bronchial smooth muscle.

Pentobarbitone, thiopentone and phenobarbitone in concentrations ranging from 10(-4) M to 10(-3) M reduced the contractile responses of isolated canine and feline trachealis muscle to electrical field stimulation without affecting contractile responses to acetylcholine. The order of potency was thiopentone, pentobarbitone and phenobarbitone. Experiments using carbachol and neostigmine or physostigmine suggested that the barbiturates act by preventing the release of acetylcholine from nerve endings. In vivo, pentobarbitone (2.5-20 mg/kg i.v.) produced dose-related reductions in the increase in total lung resistance induced by vagal stimulation in chloralose-anaesthetised cats.

Acetylcholine↗
PubMed1982

alpha-methyl-p-tyrosine inhibition of a conditioned avoidance response: reversal by dopamine applied to the nucleus accumbens.

These experiments sought to determine whether dopamine (DA) could reverse the depressive effects of alpha-methyl-p-tyrosine (AMPT) on a conditioned avoidance response (CAR). Rats were randomly allocated to shocked groups (CAR-trained) and non-shocked (CAR-naive) groups. The CAR-trained rats, conditioned to avoid an electric shock, were administered AMPT (150 mg/kg at -24 h and 50 mg/kg at -1 h, both IP), nialamide (80 mg/kg IP at -1 h) and saline (1 microliter) or DA (5 or 10 micrograms/microliters, dissolved in 1 microliter saline, at time 0) directly into the nucleus accumbens. The rats were then tested for CAR at 0.5, 1, 2, 3, 4, 8, 12, 24 an 48 h. The CAR-naive rats, conditioned to the behavioural environment without electric shock being presented, were administered AMPT, nialamide and DA or saline as above. Both doses of DA antagonised the AMPT-induced suppression of the CAR in the CAR-trained rats, reaching a maximum 2-4 h after its local application. In the CAR-naive rats, DA produced a "pseudo-CAR' that lasted about 4 h, but which completely disappeared at 8 h when the DA effect had worn off. These CAR-naive rats did not learn a CAR under the influence of DA. In a third group of rats, DA produced locomotor activation which, in its time course, resembled the effect of DA on CAR. It is concluded that the ability of DA to antagonise AMPT-induced depression of CAR is, in all likelihood, dependent upon DA-induced locomotor excitation, rather than upon an effect of DA on associative learning.

Animals↗
PubMed1982

Intra-ocular pressure and premedication with oral diazepam.

Thirty patients scheduled for routine eye surgery were randomly allocated to receive either diazepam 0.2 mg/kg or ascorbic acid 100 mg orally 90 minutes pre-operatively in a double-blind fashion. Diazepam caused no significant change in intra-ocular pressure.

Administration, Oral↗
PubMed1981

Long-term d-amphetamine in rats: lack of change in post-synaptic dopamine receptor sensitivity.

Treatment of rats with d-amphetamine (5 mg/kg) once daily for 25 days did not change locomotor responses, on day 7 of withdrawal, to dopamine (DA) or d-amphetamine into the nucleus accumbens. Nor was there a change in 3H-spiperone binding of caudate nucleus membranes. There was no effect of treatment on the locomotor response of rats to 1.0, 1.5 or 2.0 mg/kg d-amphetamine IP. However, d-amphetamine-treated rats were significantly less sensitive to 0.5 mg d-amphetamine. Although 1, 2 or 3 mg/kg apomorphine produced in same degree of stereotypy in both treatment groups, there was a significant difference in the response of the two groups to 0.5 mg apomorphine, d-amphetamine-treated animals being less sensitive than vehicle-treated animals. No change was found in brain DA levels with or without synthesis inhibition. The present data do not support the hypothesis that chronic treatment of rats with d-amphetamine can produce supersensitive post-synaptic DA receptors.

Animals↗
PubMed1981

Chronic L-DOPA treatment of mice: a behavioural and biochemical study.

Mice were pretreated once daily with L-DOPA (200 mg/kg) plus benserazide (B) (50 mg/kg) for ten days and challenged with various doses of L-DOPA + B on the first, fourth or sixteenth days of withdrawal. L-DOPA + B-pretreated mice were more sensitive the locomotor stimulant effect of L-DOPA + B challenge one and four days, but not sixteen days after withdrawal. The enhanced response was most marked on the first day of withdrawal. Other mice, pretreated once daily with B (50 mg/kg), responded one day after the tenth dose with a slightly enhanced response to L-DOPA + B challenge compared to the response to vehicle-pretreated animals. Moreover, vehicle-pretreated mice challenged with B alone, were significantly less active than those challenged with vehicle. On the first day of withdrawal, the L-DOPA + B-pretreated animals were supersensitive to locomotor stimulant effects of apomorphine but subsensitive to dexamphetamine (Bailey et al., 1979). On the fourth day of withdrawal, there were no differences in the responses of the L-DOPA + B-pretreated mice compared to the vehicle-pretreated mice, to apomorphine or apomorphine plus clonidine, but L-DOPA + B-pretreated mice were still subsensitive to the locomotor stimulant effects of dexamphetamine. Clonidine produced a dose-dependent, but similar, degree of hypothermia in both pretreatment groups. On the first and fourth days of withdrawal L-DOPA + B-pretreated mice exhibited higher brain levels of dopamine (DA) and DOPA than vehicle-pretreated mice in response to an acute dose of L-DOPA + B. The biochemical results suggest that the enhanced locomotor response to L-DOPA + B in L-DOPA + B-pretreated mice is probably dependent on changes in the amount of L-DOPA (and DA) available in the brain. Moreover, it is not ruled out that some of the effects of L-DOPA + B pretreatment were due to the B alone. Some of the enhanced response to L-DOPA + B on the first day of withdrawal may have been dependent on the same mechanism as that underlying the apparent supersensitivity to apomorphine. The subsensitive response to dexamphetamine would appear to be independent of changes in post-synaptic DA and alpha-adrenergic receptor sensitivity.

Animals↗
PubMed1981

Swim-induced grooming in mice is mediated by a dopaminergic substrate.

Grooming induced in mice after a period of swimming was potently and dose-dependently blocked by neuroleptics. The order of potency of the neuroleptics was spiroperidol greater than haloperidol greater than cis-flupenthixol greater than pimozide greater than chlorpromazine greater than thioridazine. The trans isomer of flupenthixol was inactive at 40 microM/kg. The alpha-adrenergic receptor antagonists, phentolamine and phenoxybenzamine, and the catecholamine synthesis inhibitor, alpha-methyl-p-tyrosine were essentially without effect on the grooming behaviour. Amitriptyline inhibited grooming behaviour only in doses which severely affected the animals motor function. Fluoxetine was without effect. Cis-flupenthixol was less active in inhibiting grooming in animals chronically treated with haloperidol than in control animals, indicating the presence of supersensitive dopamine receptors. The data indicate that swim-induced grooming in mice is mediated via dopaminergic systems.

Adrenergic alpha-Antagonists↗
PubMed1980

Subacute L-DOPA in mice: biochemical and behavioural effects.

Mice, pretreated orally with L-DOPA (200 mg/kg) plus benserazide (50 mg/kg) (L-DOPA-B) responded when challenged 24 h later with the same drug combination, with significantly greater locomotor stimulation than animals pretreated with the vehicle. The enhanced response was not due to an intrinsic effect of benserazide. Nor was it dependent on a change in central dopamine (DA) receptor sensitivity, because the two pretreatment groups (L-DOPA-A and vehicle) did not differ in their locomotor response to a range of apomorphine doses (300--3,000 micrograms/kg, IP). The enhanced response was, however, due to DA receptor stimulation because it was antagonised by premedication of the mice with haloperidol or pimozide. Moreover, the enhanced response to L-DOPA-B chf L-DOPA alone (without benserazide) (1,200 mg/kg, orally). Animals which had been pretreated with L-DOPA-B had significantly higher brain levels of L-DOPA and DA after a subsequent challenge dose of L-DOPA-B administered 24 h later. Thus the enhanced response to L-DOPA-B observed in the present experiment appears to be dependent on some mechanism which produces higher concentrations of L-DOPA (and consequently DA) in the brain.

Animals↗
PubMed1980

Post-swim grooming in mice inhibited by dopamine receptor antagonists and by cannabinoids.

After a period of swimming, mice engaged in vigorous grooming activity. This behaviour was inhibited in a dose dependent manner by dopamine receptor antagonists and by the cannabinoids, delta 9-tetrahydrocannabinol and cannabinol. Cannabidiol was inactive. It is suggested that the post-swin grooming behaviour involves a dopaminergic mechanism. The mechanism of action of the cannabinoids on this behaviour is unknown.

Animals↗
PubMed1980

The action of sodium cromoglycate on 'C' fibre endings in the dog lung.

The effect has been studied of sodium cromoglycate (SCG) on the activity of 'C' fibre sensory nerve endings in the canine lung. Pretreatment with SCG (100 microgram/kg i.v.) reduced the excitation of these endings by capsaicin (10 microgram/kg i.v.) for approximately 45 min. This property of SCG may explain its ability to suppress certain types of bronchoconstrictor responses in man.

Airway Resistance↗
PubMed1980

The effects of 5-hydroxytryptamine, histamine and acetylcholine on the reactivity of the lung of the anaesthetized dog.

1. Anaesthetized dogs were given aerosols of 5-hydroxytryptamine (5-HT), histamine and acetylcholine; the effects on the changes in total lung resistance (RL) and dynamic lung compliance (Cdyn) produced by electrical stimulation of the peripheral cervical vagi, and I.V. histamine and acetylcholine were studied. 2. Pretreatment with 5-HT significantly potentiated the increases in RL caused by vagal stimulation, histamine or acetylcholine. Pretreatment with histamine significantly potentiated the increases in RL caused by vagal stimulation but the potentiation of the increases in RL produced by histamine and acetylcholine were not significant. Pretreatment with acetylcholine did not potentiate the increases in RL due to vagal stimulation, histamine or acetylcholine. The falls in Cdyn produced by vagal stimulation, histamine or acetylcholine were not potentiated by pretreatment with aerosols of 5-HT, histamine or acetylcholine. 3. The effects of I.V. histamine, 5-HT and acetylcholine on RL and Cdyn were studied when given alone and when combined with vagal stimulation. 4. Vagal stimulation significantly potentiated the increases in RL due to 5-HT and histamine, but did not affect the increases in RL caused by acetylcholine or the falls in Cdyn produced by any of the three agonists. 5. By comparing these results with those from a previous study, it is concluded that, for the three agents studied, in order for increased irritant receptor discharge to reflexly increase RL, the agent has to increase the reactivity of the airway to vagal stimulation. It is also concluded that the degree of vagally mediated broncho-constriction can be varied by changing either the afferent limb through a change in irritant receptor discharge, or the efferent limb, by a change in airway reactivity.

Acetylcholine↗
PubMed1980

A study of the afferent and efferent nerve distribution to the lungs of dogs.

The distribution of afferent and efferent nerves to the lung has been studied using dogs anaesthetised with chloralose in which the lungs had been separated, enabling independent inflation and measurement of lung mechanics. Reflex bronchoconstriction produced by giving an aerosol of 5-hydroxytryptamine (5HT) or histamine to either the right or left lung failed to elicit a change in resistance (RL) of the contralateral lung. In vagotomised dogs, electrical stimulation of the peripheral end of the left or right cervical vagus produced frequency-dependent increases in RL of the ipsilateral lung. Stimulation of the left vagus also produced significant changes in RL of the right lung.

Afferent Pathways↗
PubMed1979

The effect of cannabidiol, alone and in combination with ethanol, on human performance.

Fifteen volunteers received cannabidiol (CBD) (320 microgram/kg) or placebo (both orally, T0), and 60 min later they consumed an ethanolic beverage (0.54 g/kg) or placebo. The effects were measured at T1 (100 min after CBD ingestion), T2 (160 min) and T3 (220 min) using cognitive, perceptual and motor function tests. Factorial analysis indicated that test procedures could be adequately expressed by three rotated factors: A reaction speed factor (I), a standing steadiness factor (II) and a psychomotor coordination/cognitive factor (III). Ethanol produced a significant decrement in factor III. There was no demonstrable effect of CBD, either alone or in combination with ethanol. Neither CBD nor ethanol produced any significant effect on pulse rate. Prior administration of CBD did not significantly affect the blood ethanol levels. Whilst the subjects were able to identify correctly when they were given ethanol, they did not report any subjective effects of CBD.

Adolescent↗
PubMed1979

The effect of (-) trans-delta9-tetrahydrocannabinol, alone and in combination with ethanol, on human performance.

Twenty five volunteers received (-) trans-delta9-tetrahydrocannabinol (THC) (320 microgram/kg) or placebo (both orally, T0), and, 60 min later, they consumed an ethanolic beverage (0.54 g/kg) or placebo. The effects of this medication were measured at T1 (100 min after THC ingestion), T2 (160 min), T3 (220 min) and T4 (280 min) using a battery of cognitive, perceptual and motor function tests. Factorial analysis indicated that the test procedures could be adequately expressed by four rotated factors: a reaction speed factor (I'), a cognitive factor (II'), a standing steadiness factor (III') and a psychomotor coordination factor (IV'). The first principal component (I) was used as a measure of general performance across the whole test battery. Both THC and ethanol produced significant decrements in the general performance factor. Ethanol produced significant decrements in standing steadiness and psychomotor coordination, while THC caused a significant deterioration in performance on all the four rotated factors. In all cases the peak effect of ethanol occurred at T1 and by T4 the effect had worn off. The performance decrements induced by THC were slower in onset and lasted longer than those induced by ethanol. In general, the peak effect of THC occurred at T1 and T2. There was no evidence of any interaction between THC and ethanol, and the effects of a combination of THC and ethanol were no more than additive. THC (but not ethanol) produced a significant rise in pulse rate. Prior administration of THC did not significantly affect the blood ethanol levels obtained. The subjects were able to identify correctly which of the treatments they had received.

Adolescent↗
PubMed1979

Interactions among the cannabinoids in the antagonism of the abdominal constriction response in the mouse.

The ability of delta 9-tetrahydrocannabinol (THC), cannabinol (CBN), cannabidiol (CBD), 11-OH THC and 8 alpha, 11-diOH THC to antagonise the abdominal constriction response in the mouse induced by formic acid, phenylquinone, 5-hydroxytryptamine, prostaglandin E1 (PGE1) and bradykinin was tested. THC was an effective antagonist against all nociceptive agents with an ED50 in all cases between 1.0 and 2.6 mg/kg. CBN, while also effective against all nociceptive agents, was less potent than THC, with an ED50 range between 46.2 and 112.5 mg/kg. CBD in doses as high as 200 mg/kg was without effect. Using PGE1 as the nociceptive agent, 11-OH THC was equipotent to THC while 8 alpha, 11-diOH THC was inactive. Naloxone, while able to antagonise the antinociceptive effect of morphine against formic acid-induced writhing, did not reverse the antinociceptive effects of THC. There were no pharmacological interactions between THC, CBD and CBN.

Abdominal Muscles↗