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BioKnowledgy presentation on A.5 Neuropharmacology

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BioKnowledgy presentation on A.5 Neuropharmacology

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BioKnowledgy presentation on A.5 Neuropharmacology

  1. 1. Essential idea: Communication between neurons can be altered through the manipulation of the release and reception of chemical messengers. A.5 Neuropharmacology he synaptic cleft between neurons (shown in the mage) are the points at which a neural pathways an be influenced by neurotransmitters and other olecules, both natural and artificial. By Chris Paine http://www.bioknowledgy.info/ https://i.ytimg.com/vi/mItV4rC57kM/maxresdefault.jpg
  2. 2. Understandings, Applications and Skills Statement Guidance A.5.U1 Some neurotransmitters excite nerve impulses in postsynaptic neurons and others inhibit them. A.5.U2 Nerve impulses are initiated or inhibited in post-synaptic neurons as a result of summation of all excitatory and inhibitory neurotransmitters received from presynaptic neurons. A.5.U3 Many different slow-acting neurotransmitters modulate fast synaptic transmission in the brain. A.5.U4 Memory and learning involve changes in neurones caused by slow-acting neurotransmitters. A.5.U5 Psychoactive drugs affect the brain by either increasing or decreasing postsynaptic transmission. A.5.U6 Anesthetics act by interfering with neural transmission between areas of sensory perception and the CNS. A.5.U7 Stimulant drugs mimic the stimulation provided by the sympathetic nervous system. A.5.U8 Addiction can be affected by genetic predisposition, social environment and dopamine secretion. A.5.A1 Effects on the nervous system of two stimulants and two sedatives. Examples of stimulants are nicotine, cocaine or amphetamines. Examples of sedatives are benzodiazepines, alcohol or tetrahydrocannabinol (THC). A.5.A2 The effect of anesthetics on awareness. A.5.A3 Endorphins can act as painkillers. A.5.S1 Evaluation of data showing the impact of MDMA (ecstasy) on serotonin and dopamine metabolism in the brain.
  3. 3. http://outreach.mcb.harvard.edu/animations/synaptic.swf Review: 6.5.U7 Synapses are junctions between neurons and between neurons and receptor or effector cells.
  4. 4. Review: 6.5.U8 When presynaptic neurons are depolarized they release a neurotransmitter into the synapse. AND 6.5.U9 A nerve impulse is only initiated if the threshold potential is reached.
  5. 5. Action potential is the reversal (depolarization) and restoration (repolarization) of the membrane potential as an impulse travels along it. Review: 6.5.U4 An action potential consists of depolarization and repolarization of the neuron. The depolarisation of the membrane potential causes the voltage gated Na+ channels to close and the voltage gated K+ channels open. K+ diffuses out of the neuron rapidly and the membrane potential becomes negative again (repolarisation) 3 http://www.ib.bioninja.com.au/_Media/action_potential_med.jpeg 4 Before the neuron is ready to propagate another impulse the distribution of Na+ (out) and K+ (in) needs to be reset by the Na+/K+ pump, returning the neuron to resting potential. This enforced rest (refractory period) ensures impulses can only travel in a single direction. The sodium-potassium pump (Na+/K+ pump) maintains the electrochemical gradient of the resting potential. Some K+ leaks out of the neuron (making the membrane potential negative, - 70mv). 1 In response to a stimulus (e.g. change in membrane potential) in an adjacent section of the neuron some voltage gated Na+ channels open and sodium enters the neuron by diffusion. If a sufficient change in membrane potential is achieved (threshold potential) all the voltage gated Na+ channels open. The entry of Na+ causes the membrane potential to become positive (depolarisation) 2
  6. 6. Review: 6.5.A1 Secretion and reabsorption of acetylcholine by neurons at synapses. http://faculty.pasadena.edu/dkwon/chap%208_files/images/image61.png Acetylcholine is a neurotransmitter used in many synapses through the nervous system One use is at the neuromuscular junction, i.e. it is the molecule that motor neurons release to activate muscles. Interfering with the action of acetylcholine can cause a range of effect from paralysis to convulsions.
  7. 7. A.5.U1 Some neurotransmitters excite nerve impulses in postsynaptic neurons and others inhibit them. Excitatory and inhibitory neurotransmitters Acetylcholine (ACh) is an example of an excitatory neurotransmitter. It causes an influx of positive sodium ions (Na+) into the post-synaptic neuron making the membrane potential more positive until the threshold is reached (- 50mv) at which point the post-synaptic neuron starts to depolarise. -70mv time threshold resting potential depolarisation hyperpolarisation -50mv Gamma aminobutyric acid (GABA) is the main inhibitory neurotransmitter in mammals. It hyperpolarizes post-synaptic neuron by causing an influx of negative chlorine ions (Cl-) making the neuron’s membrane potential more negative. A release of GABA means that it is harder for ACh to inact depolarisation in the post-synaptic neuron. It either takes longer for the threshold to be reached or the action potential is inhibited and does not occur.
  8. 8. A.5.U2 Nerve impulses are initiated or inhibited in post-synaptic neurons as a result of summation of all excitatory and inhibitory neurotransmitters received from presynaptic neurons. Summation of post-synaptic potential (PSP) When a post-synaptic neuron receives excitatory and/or inhibitory potentials it 'adds' the potentials together. If the summation makes the membrane potential sufficiently positive to reach the threshold then depolarisation is occurs and an action potential is generated in the post-synaptic neuron. http://www.old-ib.bioninja.com.au/_Media/summation_med.jpeg Spatial summation is where the addition of PSPs occurs across a number of synapses Temporal summation is when two or more PSPs arrive from the same synapse in rapid succession Summation involves the addition of both Excitatory (EPSP) and inhibitory (IPSP) potentials
  9. 9. A.5.U3 Many different slow-acting neurotransmitters modulate fast synaptic transmission in the brain. Slow-acting neurotransmitters ACh and GABA are examples of fast acting neurotransmitters. Slow-acting neurotransmitters (such as Epinephrine, Norepinephrine, Dopamine and Serotonin) have a different, slower mode of action, which can modulate the effect of fast-acting neurotransmitters. Fast-acting neurotransmitters Slow-acting neurotransmitters Milliseconds Hundreds of milliseconds Specific - Act across a single synapse Localised to an area – can diffuse to affect a number of neurons Bind to post-synaptic receptors Cause an influx of ions Cause the release of secondary messengers within the neuron Short-lived effect - the neurotransmitter is usually broken down rapidly Longer-lived effect – secondary messengers can still be working several days later Examples: ACh, GABA Examples: Epinephrine, Norepinephrine, Dopamine and Serotonin
  10. 10. A.5.U4 Memory and learning involve changes in neurons caused by slow-acting neurotransmitters. Improving our understanding of slow-acting neurotransmitters therefore can lead to therapeutic applications in related conditions, including depression, Parkinson's disease, epilepsy and neuropathic pain. Slow-acting neurotransmitters – memory and learning Long-term potentiation (LTP) is the persistent strengthening of synapses based on recent patterns of neural activity. LTP associated with slow-acting neurotransmitters increasing synaptic transmission in the affected neurons LTP is widely considered one of the major cellular mechanisms that underlies learning and memory. The strengthening of synapses caused by LTP is an example of neural plasticity. n.b. It is dangerous to assume that without LTP and neural plasticity that no learning or memory can occur; these are highly complex processes influenced by a range of factors. https://commons.wikimedia.org/wiki/File:Epinephrine.svg Epinephrine Dopamine https://commons.wikimedia.org/wiki/File:Dopamin_-_Dopamine.svg
  11. 11. A.5.A3 Endorphins can act as painkillers. Endorphins – natural painkillers https://commons.wikimedia.org/wiki/File:Alpha-endorphin.svg Pain receptors are specialised cells that transmit impulses along neural pathways to the CNS when damage is done to the body, e.g. a cut in the skin. Endorphins (type of oligopeptide) are secreted by the pituitary gland. They act upon the synapses of the neural pathways involved in the perception of pain. Endorphins bind to opioid receptors in the synapse inhibiting synaptic transmission and hence lessening or preventing the perception of pain.
  12. 12. A.5.U5 Psychoactive drugs affect the brain by either increasing or decreasing postsynaptic transmission. Learn more using the animation: http://www.jellinek.eu/brain/index.html?KeepThis=true&TB_iframe=true&height=588&width=672 How do psychoactive drugs affect the brain? Before thinking about how drugs affect the synapses, be sure you understand how they work and are reset. • Some NTs have a normal excitatory function • Other NTs have a normal inhibitory function In general, psychoactive drugs can: 1. Increase or decrease the release of NTs (e.g. THC – cannabis) 2. Breakdown re-uptake proteins which are responsible for returned used components of NTs to the pre-synaptic neuron (ready to use again) 3. Block re-uptake proteins (e.g.cocaine) so the NTs remain in the synapse 4. Mimic or block NTs, binding to the receptors on post-synaptic membranes 5. Inhibit production of new NTs
  13. 13. A.5.U5 Psychoactive drugs affect the brain by either increasing or decreasing postsynaptic transmission. e.g. alcohol enhances GABA’s effects
  14. 14. A.5.U7 Stimulant drugs mimic the stimulation provided by the sympathetic nervous system.
  15. 15. A.5.A1 Effects on the nervous system of two stimulants and two sedatives. Stimulant drugs increase post-synaptic transmission Examples: • Nicotine, amphetamines, cocaine What is the effect of cocaine? Without cocaine: • Dopamine is re-uptaken by pumps on the pre-synaptic membrane. With Cocaine: • Cocaine blocks re-uptake pumps • Dopamine remains in synaptic cleft • More dopamine continues to be released • Summative increase in post-synaptic transmission Effects on mood: • Dopamine is involved in reward pathways and causes enhanced feelings of pleasure, which last longer than normal. Effects on behaviour: • feelings of euphoria • increased energy and alertness • highly addictive • association with depression as body reduces production of own dopamine over timehttp://is.gd/Jellinek
  16. 16. A.5.A1 Effects on the nervous system of two stimulants and two sedatives. Stimulant drugs increase post-synaptic transmission Examples: • Nicotine, amphetamines, cocaine What is the effect of nicotine? Without cocaine: • Dopamine is re-uptaken by pumps on the pre-synaptic membrane. With nicotine: • Nicotine mimics the action of ACh; it binds to Ach receptors triggering action potential in the post-synpatic neuron • Unlike ACh Nicotine is not easily broken down and remains in synaptic cleft and continues to stimulate the post-synpatic neuron Effects on mood: • Ach causes the release of dopamine, which in turn causes enhanced feelings of pleasure Effects on behaviour: • feelings of euphoria • increased calmness and alertness • Addictive - as the brain develops a tolerance for nicotine is becomes needed for normal functioninghttp://is.gd/Jellinek
  17. 17. A.5.A1 Effects on the nervous system of two stimulants and two sedatives. http://is.gd/Jellinek Sedative drugs decrease post-synaptic transmission Examples: • Alcohol, benzodiazapines, THC What is the effect of tetrahydrocannibol (THC)? Without THC: • Dopamine release is moderated (inhibited) by GABA With THC: • THC mimics anandamide cannabinoids and inhibits GABA release by binding to cannabinoid receptors • GABA cannot inhibit dopamine release therefore more dopamine is released Effects on mood: • Dopamine is involved in reward pathways and causes enhanced feelings of pleasure Effects on behaviour: • intoxication • hunger • memory impairment • potential dependency
  18. 18. A.5.A1 Effects on the nervous system of two stimulants and two sedatives. http://is.gd/Jellinek Sedative drugs decrease post-synaptic transmission Examples: • Alcohol, benzodiazapines, THC What is the effect of Alcohol? Without Alcohol: • GABA inhibits the post-synaptic transmission • Glutamate is an excitatory NT that binds to receptors increasing post-synaptic transmission With Alcohol: • Alcohol increases the inhibitory effect of GABA by causing GABA to remain bound to it’s receptor for longer • Alcohol binds to glutamate receptors preventing glutamate from stimulating the the post-synaptic neuron. Effects on mood: • Alcohol indirectly causes a dopamine release that in turn causes enhanced feelings of pleasure Effects on behaviour: • Calm relaxed feeling • memory impairment • Increases (worsens) reaction speeds • Affects breathing, body temperature regulation and appetite • potential dependency
  19. 19. A.5.U6 Anesthetics act by interfering with neural transmission between areas of sensory perception and the CNS. AND A.5.A2 The effect of anesthetics on awareness. Anaesthetics Anaesthetics cause a temporary loss of sensation, there are two main types of anaesthetic: • Local - cause numbness (a loss of sensation) in an area of the body, e.g. no feeling of the gums during a dental procedure • General - cause unconsciousness and therefore a lack of sensation throughout the body https://commons.wikimedia.org/wiki/File:Preoxygenation_before_anesthetic_induction.jpg Many anaesthetics have multiple roles and hence affect the body in different ways, due to this and the incomplete understanding we have of them they are usually administered by specialised medical practitioners called Anaesthetists. Anaesthetics are very varied group of molecules that affect neural pathways in different ways. How different anaesthetics work is not fully understood, but it is known that many do affect the receptors found in synapses. General anaesthetics block ‘long- distance communication’ hence affecting (often inhibiting) the transmission of impulses from receptors (areas of sensory perception) and the CNS.
  20. 20. A scale of harm for drugs Draw markers on the graph for each drug to indicate how much physical harm and dependence (addiction) you think it causes: • Nicotine • Cocaine • Amphetamines (speed) • Alcohol • Canabis (THC) • Ecstasy (MDMA) Discuss: • How can drugs cause physical harm? • How can drug use lead to addiction (dependency)? • What factors contribute to development of addiction? https://commons.wikimedia.org/wiki/File:Rational_scale_to_assess_the_harm_of_drugs_(mean_physical_harm_and_mean_dependence).svg
  21. 21. A scale of harm for drugs https://commons.wikimedia.org/wiki/File:Rational_scale_to_assess_the_harm_of_drugs_(mean_physical_harm_and_mean_dependence).svg Draw dots on the graph for each drugs to indicate how much physical harm and dependence (addiction) you think they cause: • Nicotine • Cocaine • Amphetamines (speed) • Alcohol • Canabis (THC) • Ecstasy (MDMA) Discuss: • How can drugs cause physical harm? • How can drug use lead to addiction (dependency)? • What factors contribute to development of addiction?
  22. 22. A.5.U8 Addiction can be affected by genetic predisposition, social environment and dopamine secretion. Addiction Breaking an addiction is very difficult and can cause severe physical and mental reactions (withdrawal symptoms). Genetic predisposition • Many genes with roles in addiction have been identified (with the help of animal models, especially mice) • For example the A1 allele of the dopamine receptor gene DRD2 is more common in people addicted to alcohol or cocaine. dependence on a substance or activity resulting in its repeated and compulsive use Causes of Drug Addiction Dopamine secretion • Dopamine activates pleasure pathways of the brain, it is normally released to reward positive behaviours. • Many drugs affect, often enhacing, dopamine activity (e.g. cocaine, heroin) • Abuse of some drugs to lead to down-regulation of dopamine receptors, requiring higher doses to achieve same effect (habituation) Social environment factors • The social environment plays a significant role; individuals raised in environments with prevalent substance abuse are at a higher risk • Peer pressure (from those that use drugs), poverty and social deprivation, traumatic life experiences and mental health all make drug addiction more likely • Culture, religion and traditions can both positively and negatively affect addiction and this in part explains the variation in addiction patterns found between different countries
  23. 23. A.5.U8 Addiction can be affected by genetic predisposition, social environment and dopamine secretion. Addiction dependence on a substance or activity resulting in its repeated and compulsive use Learn more about addiction from the links below: http://learn.genetics.utah.edu/content/addiction/ http://learn.genetics.utah.edu/content/addiction/mouse/ https://www.drugabuse.gov/publications/drugs-brains-behavior- science-addiction/drug-abuse-addiction “The mentality and behaviour of drug addicts and alcoholics is wholly irrational until you understand that they are completely powerless over their addiction and unless they have structured help they have no hope.” Russell Brand: my life without drugs https://www.theguardian.com/culture/2013/mar/09/russell-brand- life-without-drugs
  24. 24. A.5.S1 Evaluation of data showing the impact of MDMA (ecstasy) on serotonin and dopamine metabolism in the brain. The impact of MDMA (ecstasy) on serotonin and dopamine metabolism https://www.atrainceu.com/images/img_166_designer_drugs/stimulants_in_bath_salts_NIDA.png Mephedrone and Methylone are active components of the recreational designer drug ‘Bath Salts’ Ecstasy is a recreational designer drug that users take to feel energised, happy, to stay awake and to dance for hours. MDMA is the active component of ecstasy. The effects take about half an hour to start and tend to last between 3 to 6 hours, followed by a gradual comedown. Users often develop temporary feelings of love and affection however some users experience anxiety or panic attacks. Saline is the control. Serotonin is neurotransmitter that contributes to a sense of well being and happiness The data shown in the graphs was collected from studies using rats.
  25. 25. A.5.S1 Evaluation of data showing the impact of MDMA (ecstasy) on serotonin and dopamine metabolism in the brain. The impact of MDMA (ecstasy) on serotonin and dopamine metabolism https://www.atrainceu.com/images/img_166_designer_drugs/stimulants_in_bath_salts_NIDA.png 1. Describe the effect 0.3 mg/kg (body mass) and 1.0 mg/kg of MDMA on serotonin levels over time. 2. Compare and contrast the effect of MDMA on serotonin and dopamine. 3. Discuss whether the changes measured are significant or not.
  26. 26. Nature of science: Assessing risks associated with scientific research - patient advocates will often press for the speeding up of drug approval processes, encouraging more tolerance of risk. (4.5) https://natureofscienceib.wordpress.com/category/option-a-neurobiology/ Rigorous testing of drugs is important to determine: • Effectiveness • That it is safe to use • Appropriate dosage • Side effects One ethical concern is that the testing process understandably takes years to complete, but during that time patients are suffering and possibly dying from a condition that a drug under development could treat. In this situation patients and their advocates will pressure health services and governments to speed-up the drug’s approval. This increases the risk of the drug causing harm to the patients. Speeding up drug approval http://images.techtimes.com/data/images/full/138196/ebola-treatment-research.jpg
  27. 27. Nature of science: Assessing risks associated with scientific research - patient advocates will often press for the speeding up of drug approval processes, encouraging more tolerance of risk. (4.5) https://natureofscienceib.wordpress.com/category/option-a-neurobiology/ Rigorous testing of drugs is important to determine: • Effectiveness • That it is safe to use • Appropriate dosage • Side effects One ethical concern is that the testing process understandably takes years to complete, but during that time patients are suffering and possibly dying from a condition that a drug under development could treat. In this situation patients and their advocates will pressure health services and governments to speed-up the drug’s approval. This increases the risk of the drug causing harm to the patients. Speeding up drug approval http://images.techtimes.com/data/images/full/138196/ebola-treatment-research.jpg FDA Gives Fast Track Approval To ZMapp Experimental Ebola Drug http://www.techtimes.com/articles/85927/2015091 8/fda-gives-fast-track-approval-to-zmapp- experimental-ebola-drug.htm Experimental Ebola drug ZMapp gets fast track status from FDA http://edition.cnn.com/2015/09/17/health/zmapp-status-fast-tracked/ The Ebola outbreak in West Africa in 2014-15 prompted the fast tracking of an experimental drug called Zmapp.
  28. 28. https://youtu.be/eZundDVPIYw
  29. 29. Bibliography / Acknowledgments

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