Tutorial work - Mouse lab practical, week 8 PDF

Title Tutorial work - Mouse lab practical, week 8
Course Introductory Pharmacology and Toxicology
Institution University of New South Wales
Pages 4
File Size 92.3 KB
File Type PDF
Total Downloads 27
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Summary

Mouse Lab Practical ...


Description

Drugs that alter the Brain’s reward pathway 1. Drugs of abuse 2. Mouse party 3. Meth mouse and drug use changes the brain over time i. The route(s) of administration ii. The effects on the CNS iii. Physioloigcla changes induced by the drug

Drug Name

Route of Administration Drinking

Effect on CNS

Anabolic steroids

Mouth or injecting

Androgen receptor  Similar to male sex hormones

Cocaine

Snorting, injecting, smoking

Stimulant  speeds up activity

Dissociative drugs

Mouth, snorting, smoking

PCP: Disconnection from reality – unpredictable or violent behaviour Ketamine: (less potent) “terrifying feeling” Dexotromethorphan: Recommended dose – safe (cold and cough) Higher: same as PCP and Ketamin

GHB & Rohypnol

Mouth

GHB: depressant –

Alcohol

Binds to GABA  Depressant – calming or drowsy affect

Physiological changes induced by the drug Loss of motor coordination, impairs reasoning, balance, speech reaction time and judgement Increased risk of heart attacks, strokes and liver problems. Undesirable physical changes such as hair loss and acne Increased energy, and mental alertness and decreased appetite Disturbances in heat rhythm, nausea, respiratory failure, strokes, seizures. Sever withdrawal symptoms Convulsions, coma, high fever, death

Seizures, loss of

relaxing effect, promote muscle growth Rophypnol: Benzodiazepine – treatment for anxiety Hallucinate, rapid mood swings

Hallucinogens

Mouth, snorting and smoking

Heroin

Injecting, snorting or smoking

Inhalants

Sniffing fumes, spraying aerosols, huffing rags Euphoria, Smoked – depressant or cigarette, pipe sleepiness or blunt Mouth Stimulant and hallucinogen – energizing effects and distortions

Marijuana

MDMA (ecstasy)

Methamphetamine Mouth, snorting, injecting and smoking Nicotine Smoking, chewing, dipping

LSD:

Opiate – no medical use Rush of pleasure then drowsiness Immediate high

consciousness, coma, death “date rape drug” – memory loss and unable to resist assault

Dilated pupils, higher body temperature, increased heart rate and blood pressure, sweating, loss of appetite, sleeplessness, dry mouth and tremors Nausea, vomiting, severe itching Severe withdrawal symptoms Permanent brain damage or sudden death

Lower memory, attention, slower reaction time

Physical effects – muscle clenching, reductions in mental abilities, panic attacks, loss of consciousness Stimulant – high Elevate body energy – toxic effects temperature, convulsions, on the brain violent behaviour, anxiety, insomnia, paranoia Stimulant and Withdrawal – intense sedative cravings irritability and sleep disturbances 30% cancer deaths

  

Chemically resembles serotonin and elicits its effect by binding to serotonin receptors LSD interacts with receptors in different ways – inhibit and/or excite  complex sensory effects Excite the Locus Coeruleus (LC)  feelings of wakefulness and evoking a startle response to unexpected stimulus

Cocaine  Dopamine transporters  remove Dopamine molecules from synaptic cleft  Cocaine blocks dopamine transporters  prolong dopamine in the synaptic cleft  dopamine binds again and again to the receptors  overstimulation of the cell  Reward pathway and brain component that controls voluntary movements  fidgety Alcohol  Inhibitory neurotransmitters GABA  inhibits/reduces neural activity  GABA + Alcohol  GABA receptors become more inhibitory  Excitatory neurotransmitter Glutamate  Binds to Glutamate receptors  preventing glutamate from exciting the cell  Affects memory formation, decision making and impulse control Marijuana  Natural cannabinoid (anandamide)  turns off release of inhibitory neurotransmitters  realising dopamine  THC mimics anandamide  binds to cannabinoid receptors  inhibition is turned off  increase dopamine Methamphetamine  Meth mimics dopamine  dopamine enters the cell  Meth enters dopamine vesicles forcing dopamine molecules outside  excess is released into the synapse  Excess becomes trapped in the cleft  over stimulation  Reward pathway  intense pleasure and exhilaration Ecstasy  Serotonin transporters are responsible for removing serotonin molecules from the synaptic cleft after they have done their job  Ecstasy mimics serotonin  Alters and reverses serotonin transporters  transporting serotonin out of the cell  Excess serotonin is trapped in the synaptic cleft  over stimulation  Serotonin pathways  mood, sleep, perception and appetite  Reward pathway  mild dopamine release

Heroin:  Inhibitory neurotransmitters – inhibit dopamine release  Natural opiate + opiate receptors  blocks release of inhibitory neurotransmitters  dopamine release  Heroin mimics natural opiates  dopamine release  immediate feelings of sedation and well-being  Opiate receptors  transmission of pain signals, stress response and emotional attachment...


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