drugs and addiction lect 2 Flashcards
(38 cards)
what is the biological basis of drugs
-introducing drug to the brain upsets the natural balance the brain is striving for
-brain seeks to minimise the effect of drug and restore homeostasis
what is homeostasis in the brain called
neuroadaptation
what are the 2 types of neurotransmission
agonists and antagonists
what are agonists
-increase neural activity
-activate receptors either by mimicking the neurotransmitter or by increasing the existing neurotransmitter
-can also block reuptake
what are antagonists
-decrease neural activity by blocking the activation of receptors
what is tolerance
-when we use a drug repeatedly the effects diminish
-we need more and more to get the effects we had when we first used it
-applies to all drugs of abuse
-happens at diff rates and to varying extents for diff drugs
-neg effects like nausea of often have fastest tolerance
what is the biology behind tolerance
-metabolic tolerance: the body becomes more efficient at breaking the drug down (pharmacokinetic tolerance) (small effect)
-cellular tolerance: (pharmacodynamic tolerance), change in no of receptors e.g downregulation in receptor function/ or post synaptic function (large effect)
what are the primary effects of drugs
1.more alert and improve conc (caffeine)
2.decrease social inhibitions, relaxation and hedonism/pleasure (alcohol)
3.euphoria, confidence, increased energy, alertness (cocaine)
4.hallucinations, altered sensory perception, laughing (psychodelics)
5.altered sensory perception, energy, connection with others (MDMA, ecstasy)
caffeine
-works on adenosine as antagonist
-block adenosine receptors
-adenosine = tiredness so high at night
-blocks GABA receptors but only in v high doses
-psychoactive substance
-mostly in tea and coffee but added into many soft drinks particularly in USA
what are the pos effects of caffeine
+increases alertness when needed (smith et al)
+consumption of caffeine in simulated driving break reduced driver impairments and sleepiness when driving
tolerance for caffeine
Evans and Griffiths
-daily caffeine or placebo
-caffeine cond = less sig subjective effects of caffeine than placebo cond
Shi et al
-chronic administration of caffeine in mice
-found upregulation of A adenosine receptors, serotonin receptors, GABA receptors and others
-down regulation of other receptors
nicotine
-agonist effect on acetylcholine transmitters
-stimulates nicotine receptors of acetylcholine neurons
-most neg effects of smoking come from inhalation of tobacco rather than the nicotine
nicotine pos effects
-performance enhancement e.g attention, protective attributes against health e.g ADHD, parkinsons etc
-BUT regular smoking is neg reinforced and governed by withdrawal
alcohol
-acts on multiple neurotransmitters
-crosses BBB very quickly, detected in brain in minutes
-specific and non specific actions on brain
non specific actions of alcohol on brain
acts as a depressant on all brain neurons and disturbs neuronal membrane lipids (membrane fluidisation)
primary specific mechanisms of action of alcohol
-inhibits glutamate by reducing effectiveness at NMDA glutamate receptor
-stimulates GABA release
-increases GABA receptor sensitivity, depressing neural system (leads to sedation)
-enhances endorphin activity in dopaminergic reward pathways leading to disinhibition of dopamine release in nucleus accumbens
-effects serotenergic neurotransmitters impacting general state of wellbeing
alcohol and sugar
-sugar dependent rats increased intake of alcohol when deprived of access to sugar (Avena 2004)
-access to alcohol increased sugar intake in rats
-bingeing on either sugar or alcohol fostered the intake of the other (implications for human diet and alcohol intake)
cannabis
-active ingredient is delta 9-THC and CBD
-only THC is psychoactive
- cannabinoid receptors identified in brain only responsive to cannabis, specifically the THC
-found anandamide which is an endogenous cannabinoid (decreases GABA and increases synaptic dopamine levels)
what does repeated use of cannabis cause
-linked with interaction between THC and presynaptic CB1 receptors on inhibitory GABAergic interneurons in reward pathway
(reduction in release of GABA: disinhibition of dopaminergic neurons and elevation in synaptic dopamine levels
changing the landscape of cannabis use
-legal for recreational use in many places e.g canada, africa, thailand etc
-decriminalised in netherlands and portugal
-legal for medical use in 49 countries including UK
-hardly prescribed at all in uK
reasons for legalisation of cannabis
1.adverse health effects from cannabis are quite modest in relation to other drugs
2.criminal penalties for cannabis are harmful to users and the community and outweigh the neg consequences of using the drug (what is the benefit of criminalising people who use cannabis for personal use? waste of money and resources?)
3.if legal, cannabis can be better monitored and taxed
Chiu et al research
-systematic review of trends in US attitudes towards cannabis legalisation
-attitudes were liberal across most demographic groups
-key findings contributing to more liberal views in general public:
–increase in no of people who use cannabis
–decrease in religious views
–increase in political liberalism
–decrease in perceived harmfulness of cannabis
strength of cannabis for medical use
+good evidence for cannabis for medical uses, relief of chronic pain, neuropathic pain, spasticity can be eased (hill 2015)
risks of cannabis for medical use
-clear but small risk for psychosis (Murray), worse for synthetic cannabinoids e.g spice
-mixed evidence about whether cannabis is carcinogenic (cancer causing)
-addiction and gateway risk (Volkow 2014), once you use one drug you are likely to try another, and you know people who may encourage use of other drugs
