Drugs Flashcards
Communication in the brain
Electricity - action potentials - high enough - release Chemistry - neurotransmitters - carry info - define quality of content
Neurotransmitters
- l-glutamine and GABA
- perform vital functions in the CNS, excitatory and inhibitory
- dopamine - increase HR and BP, memory and attention
- serotonin - depression, suicide and impulsiveness
Modes of Action
- usually react with receptors (“lock and key”)
- agonist or antagonist of NT and NM
- naturally secreted substance that acts like NT
- not restricted to synaptic cleft, diffuses through extracellular fluid
- agonist - drug that facilitated effect of NT on postsynaptic cell
- antagonist - inhibits or opposed effects of NT on postsynaptic cell
How do drugs work?
Alter presynaptic events
Affect processes in the axon (conduction of action potentials)
Affect synthesis and storage of NT and NM
Neural mechanisms
All natural reinforcers cause release of dopamine in nucleus accumbens
Addictive drugs also trigger the release of dopamine
Drug effects
Drugs can:
- stop chemical reactions creating NT
- empty NT from vesicles where stored to protect from breakdown
- block NT entering/leaving vesicles
- bind to receptor in place of NT
- prevent NT returning to sending neuron (reputable)
- interfere with second messenger
Messengers
- Neurotransmitters
- Chemical produced when G protein activate another enzyme
- carries signal to open ion channel or cause other events in the cell
G protein - conveys messages to other molecules
Reuptake - reentry of NT liberated by terminal button back though membrane and terminating post
Synaptic Events
Interfere reuptake mechanisms
Affect activation of receptor molecules (e.g. antipsychotics may block dopamine receptors, dopamine antagonist)
Alter number of receptor molecules (alcohol increases GABA receptors)
Alter second messenger activity
May affect the release of synaptic transmitters
Neural mechanisms
Cocaine
Inhibits the active uptake of dopamine and norepinephrine into neuron terminal allowing accumulation of transmitters in synapses
Accumulation of dopamine and it’s action an receptors is responsible for the stimulant, euphoric activity of the drug, and consequent abuse
Tolerance
- must take larger and larger amounts to be effective
- will suffer withdrawal symptoms if they stop taking the drug
Caffeine
- stimulates CNS: increase alertness, wakefulness, ability to work and concentrate
- enhance cognition and stimulate encoding
- competes with NT adenosine (inhibits release of cataholamines)
- class of amines, include dopamine and epinephrines
- acts as cateholaminergic agonist
Warburton (1995)
- regular coffee drinkers prescribed caffeine
- computer cognitive tasks
- improve cognitions (attention, problem solving, delayed recall)
- not immediate recall or working memory
Caffeine research
- focus on effects of cognitive performance
- evidence mixed (Van der Stelt and Snel, 1998)
- mood results also mixed
- positive often attributed to arousal from caffeine
Caffeine Research Critique
Methodology issues
- inconsistent (Lieberman, 1987)
Design issues
- dietary doses, weight related doses, dose dependency
- within vs between subjects
Participant variables
- use of other drugs
- interactions (caffeine and nicotine, alcohol, other drugs)
- sex (menstrual cycle), age, personality
Controls - washout period, dosage, time of day
Alcohol
- wide range of CNS effects
- increase GABA receptors
- dopamine release
- opiate antagonists suppress consumption in rats (Froelich et al, 1990)
- genetic vulnerability and stressful environment cause alcoholism (McGue, 1999)
Effects of Alcohol
- neg affect of basic perceptual, simple performance measures and complex tasks
- biphasic: stimulation through depression
- driving: even at low dose impair psychomotor coordination and sustained attention
- acute alcohol cons impairs WM
- chronic alcohol cons impairs LTM
- protective effect of low/moderate cons and dementia (Panza et al, 2012)
Nicotine
- acts mostly on ANS
- stimulation of reward centre
- cholinergic agonist: interacts with cholinergic receptors (crucial in cog)
- biphasic: stimulant and depression
Nicotine Research
- twin studies show genetic component (65%) (Lerman et al,1999)
- only 20% attempts to quit successful (Schelling, 1992)
- enhance performance of cog tasks in humans and animals (Pritchard and Robinson, 1998)
- reaction time and errors in smokers (Pritchard and Robinson, 1998)
- short term but not long term memory (Heishman et al, 2010)
Lack of Nicotine
Withdrawal Heart and BP changes Sleeping problems Anxiety, irritability, impatience, hostility, depression Difficulty concentrating Restlessness Increased appetite and weight gain
Alcohol and Nicotine
Often taken in combination but few studies
Alcohol associated with increase cigarette consumption (Istavan and Matarazzo, 1984)
Alcohol and Caffeine
Caffeine used as cure but no clear evidence
May reduce alcohol absorption
Nicotine and Caffeine
Nicotine reduces half life of caffeine
Both show to improve performance
Caffeine intake doesn’t increase smoking -link may have non pharmacological basis
Summary
- major drugs mimic structure of NT
- NT underlie every though, emotion, memory, learning
- carry signals between all nerve cells or neurons in the brain
- neurochemistry supporting addiction: places, people and objects associated with drugs imprinted on the brain
