Presentation on theme: "Drugs and Performance. Axon Terminal Post-synaptic receptors Neurotransmitter crossing synaptic cleft Direction of impulse Cell body of receiving neuron."— Presentation transcript:
Axon Terminal Post-synaptic receptors Neurotransmitter crossing synaptic cleft Direction of impulse Cell body of receiving neuron Vesicles containing neurotransmitter Drugs can alter: Pre-synaptic events – Processes in the axon Synthesis of neurotransmitter Storage of neurotransmitter Release of neurotransmitter Synaptic cleft and post-synaptic events – Inactivation/ re-uptake mechanisms Activation of receptor molecules
Caffeine A D N A A A A A A AAD D D D D D D D D N N N N N N N N N A A A Agonist Competes with inhibitory neuromodulator adenosine A Adrenalin D Dopamine N Noradrenalin Tea Coffee Chocolate Cold/flu remedies 70mgs
Caffeine: max blood plasma concentration approx 30 mins after ingestion. > heart rate and blood pressure constricts blood vessels in brain half life of 4/5 hours Withdrawal symptoms: fatigue, headache, nausea, anxiety, weakness and depression Streufart et al (1995) studied caffeine withdrawal in a group of Managers. After 36 hours, performance on a managerial simulation Task had declined significantly.
Caffeine & cognition Kerr, Sherwood and Hindmarch (1991) – choice reaction time faster. motor component improved. Reaction time tasks Lieberman et al (1987) – low and moderate doses improved vigilance and choice reaction time. Usually decreased reaction time rather than improved accuracy Van der Stelt and Snel(1998) – 50% of studies find no effect
Memory No consensus Arnold et al (1987) – improved recall Warburton (1995) – low dose: effects found for problem-solving and delayed recall. No effects on immediate recall. Smith et al (1999) – low (40mg dose) faster responding on delayed recognition, but no effect on free recall. Hameleers et al (2000) – huge sample of 1875 adults. Positive linear relationship between caffeine intake and delayed recall. Likewise, linear relationship with RTs (Hi Caff = fast RTs). inverted-U relationship between caffeine consumption and reading speed. No relationship between consumption and STM, planning or attention.
Attention Inconsistent effects on Stroop and other divided attention Tasks. Smith (1999) – improvements only in RT. Arousal Beneficial effects are well documented (Lieberman, 1992; Smith (1998). James (1994) suggested only alleviation of withdrawal. However, short wash-out periods + effects suggest ‘true’ increase in arousal
Low arousal Smith et al (1990) – post-lunch dip in sustained attention task restored with caffeine. Smith (1998) – reaction time impaired by cold, restored by caffeine. Bonnet & Arnaud (1994) – investigated nap and performance. Caffeine Placebo Baseline tests Baseline tests 4 hr nap 27 hrs testing Performance maintained Performance deteriorated
Methodological issues Caffeine deprivation Dosage of caffeine (30 – 600mgs) Same dose v dose/weight ratio (mgs/kg) Wash-out periods Menstrual cycle, contraception, time of day & nicotine Personality Range of dependent measures.
Alcohol & Performance Wine mentioned on Egyptian papyrus dating from 3,500BC. In UK 92% of men and 86% of women drink alcohol at least occasionally. Alcohol Concern estimated in 2002, cost of alcohol misuse = #3billion to UK. Implicated in 30% of all road accidents; 5,000 deaths directly; 33,000 indirectly. Safety levels: 14 units for women; 21 units for men. 1 unit = glass of wine; half pint of standard strength beer (3.5 - 4.0%) Dept of Health – 2-3 units per day for women; 3-4 units per day for men. No binge drinking and a number of alcohol-free days per week. Absorbed within two hours CNS depressant Stimulates release of dopamine from the nucleus accumbens Low & moderate doses it is an anxiolytic
Reaction Time Alcohol impairs reaction time. Mediated through central cognitive processes rather than peripheral Motor processes (Kerr et al 1991) Negative effect on visual pattern recognition and visual attention Biphasic effect (Kerr & Hindmarsh 1998; Streufert & Pogash, 1998) Low dose improves performance and a high dose impairs it.
Alcohol and driving BAC = 80mgs/ 100mls in UK & Ireland 50mgs/ 100mls in EU Impairs driving behaviour: brake reaction time and steering, Even at low and moderate doses. Increases risk behaviour (Burian, Ligouri & Robinson, 2002). Narrows attention to sub-set of components at expense of others. This suggests competency to the driver,,which is at odds with objective reality. Methodological Issues: individual differences in response to Alcohol; gender; age; body size ; genetics; tolerance; food consumed; Time of day; mood; hormones; stress; health etc.,
Nicotine Smoking kills 120,000 people per year in UK. Responsible for 30% of UK cancer deaths. 29% of UK adults are smokers. Nicotine- agonist for acetylcholine Cholinergic systems critical for cognition, and cholinergic agonists (nicotine) tend to improve performance. Antagonists (scopolamine) tend to impair it (Levin, 1992). Alzheimer’s disease associated with decline in cholinergic activity (Perry et al 1986). Cholinergic hypothesis of age –related cognitive decline. Difficulty of calculating a smoker’s intake of nicotine: Puffs and depth of inhalation. Smokers – self-selected population
Nicotine & Performance Levin (1992) – rats in maze learning task. Performance of rats that ingested nicotine better than controls over a three week period. Pritchard & Robinson (1998) – improves reaction time and decreases errors in human subjects. Wesnes & Warburton, (1983) – smoking improved speed and accuracy On a rapid visual information processing task. Wesnes & Warburton, (1984) – tablets: same results Reaction time
Memory STM – increased speed of learning, but not accuracy (Sherwood et al, 1992). Increased STM errors (Williams, 1980). Improves free recall, paired associate learning, serial recall, retention of nonsense syllables and recall of prose (Pritchard & Robinson, 1998). Attention Visual and auditory signal detection improved by nicotine. Reduces the vigilance decrement. Reduced interference on the Stroop (Provost & Woodward).
Cannabis Cannabis Sativa – leaves flower heads and resin. Smoked in a joint or pipe, but can be eaten. Widely used illegal drug 10% of UK adults 16-59 yrs have used it in past year (Aust et al., 2002) Active ingredients – alkaloids know as cannabinoids. Most important is delta-9-tetrahydrocannabinol. CB1 receptors in hippocampus, cerebellum and striatum (Ameri, 1999). CB2 receptors found in immune system cells. Triggers release of dopamine from the nucleus accumbens. Used to treat Glaucoma; prevents vomiting and has been used to Treat side effects of chemotherapy (McKimm, 1997). THC used to treat tremor in experimental model of MS (Baker et al 2000). Cannabinoids can act as neurotoxins and cause cell death (Ameri, 1999)
Cannabis & Performance Slower and less accurate on psychomotor performance tasks (Kurtzhaler et al., 1999; Varma et al., 1988). Cannabis dependent teenagers v controls – impaired short term visual and auditory memory (Schwartz, 1991). Rodgers et al (2001) – examined self-reports of Prospective and Everyday memory. THC use predicted poor STM; use of ecstasy predicted poor LTM. Gruber et al, (2001) examined abstinence. THC users showed Impairments for 7 days, but by 28 days no different to controls.
Ecstasy Name given to the synthetic amphetamine derivative MDMA (3,4-methylenedioxymethamphetamine). 10% of 15-29 year olds in UK have tried it. Often also includes caffeine, codeine, ketamine and ephedrine. Positive emotions & euphoria. Acts as agonist for serotonin, dopamine and noradrenalin. Massive release and blocks re-uptake. Increased heart and respiration rates. Disruption of thermoregulation. Low mood on following day.