* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download doc Behavioural_Neuroscience_Jan_16
Survey
Document related concepts
Compounding wikipedia , lookup
Polysubstance dependence wikipedia , lookup
Nicotinic agonist wikipedia , lookup
Pharmacogenomics wikipedia , lookup
Theralizumab wikipedia , lookup
Pharmaceutical industry wikipedia , lookup
Drug discovery wikipedia , lookup
Pharmacognosy wikipedia , lookup
Prescription costs wikipedia , lookup
Prescription drug prices in the United States wikipedia , lookup
Pharmacokinetics wikipedia , lookup
Drug design wikipedia , lookup
Drug interaction wikipedia , lookup
Psychopharmacology wikipedia , lookup
Transcript
Behavioural Neuroscience 4/19/2012 5:30:00 PM How do neurons communicate with each other? The Synapse: A synapse is a junction between the terminal button of the sending neuron and a portion of the dendritic membrane of the receiving neuron. Synaptic transmission is the transmission of messages from one neuron to another through a synapse Detail of the Synapse: Synaptic vesicles contain molecules of neurotransmitter o They attach to the presynaptic membrane and release neurotransmitter into the synaptic cleft Synaptic cleft is the space between the pre- and postsynaptic membranes. It is filled with an extracellular fluid. Presynaptic membrane is the membrane of the terminal button (the sending cell). This is where neurotransmitter is released Postsynaptic membrane is the membrane of the receiving cell either on the soma or the dendrite Postsynaptic Potentials (PSP): Excitatory Postsynaptic Potential (EPSP): Sodium-potassium channels keep Na+ outside the cell. When sodium channels are opened, the influx of Na+ causes a depolarisation Inhibitory Postsynaptic Potential (IPSP): If potassium channels open, K+ leave the cell. Potassium is positively charged. It’s efflux causes a hyperpolarisation PSP’s are influenced by other ions depending on the state of the membrane. o E.g. if the membrane is resting, Cl! will have no effect, but if the membrane has been depolarised, Cl! channels will permit Cl! to enter the cell thus neutralising the EPSP. Neural Integration Neural Integration: Neural Integration: The interaction of the excitatory and inhibitory synapses on a particular neuron o If several excitatory synapses are active at the same time, the EPSP will travel toward the axon and the axon will fire o If several inhibtitory synapses are active at the same time as the EPSP, the IPSP will diminish the size of the EPSP and prevent the axon from firing Neural inhibition does not always produce behavioural inhibition: For example, a group of neurons may prevent me from putting my hand in the fire. If, however, those neurons are inhibited (i.e. prevented from producing an IPSP), those neurons will NOT suppress my behaviour and I will put my hand in the fire. o Inhibition of inhibitory neurons makes the behaviour more likely to occur Neural excitation does not always produce behavioural excitation: For example, when we are dreaming, a group of inhibitory neurons are activated to prevent us from acting out our dreams. If this activation fails to occur, people will act out their dreams. o Excitation of neurons that inhibit a behaviour, suppresses that behaviour Psychopharmacology: Drugs and their Effectiveness What is a Drug?: a) A chemical substance used in the treatment, cure, prevention or diagnosis of disease or used to enhance physical or mental well being. b) A chemical substance that has “perceived” beneficial effects on perception, consciousness, personality and behaviour (e.g. narcotics, hallucinogens). Some drugs can cause addiction if abused (e.g. cocaine, heroin) c) An exogenous chemical that significantly alters the function of certain cells when taken in relatively low doses. Psychopharmacology is the study of the effects of drugs on the nervous system and behaviour. Routes of Drug Administration: Drugs have to reach their site of action which is the point where drug molecules interact with molecules located on or in cells of the body. 1. Intravenous (IV) injection - into the vein 2. Intraperitoneal (IP) injection - into the abdominal wall (peritoneal cavity) 3. Intramuscular (IM) injection - into the muscle 4. Subcutaneous (SC) injection - into the space between the skin 5. Oral administration - by mouth 6. Sublingual administration - under the tongue 7. Intrarectal administration - as suppositories 8. Inhalation - by smoking 9. Topical administration - through the skin 10. Intracerebral administration - directly into the brain Dose Response Curve: A dose response curve is the magnitude of an effect of a drug as a function of the amount that is administered. It is obtained by giving subjects various doses of drug (according to weight). o Higher doses cause larger effects until the point of maximum effect o The difference between the two curves is the drugs margin of safety Drug Efficacy: Drugs vary in effectiveness because: o They have different sites of action. o They have different affinities for the molecules to which they attach. The affinity of a drug is the readiness with which two molecules join together. A drug with a high affinity will produce an effect at low doses whereas a drug with a low affinity may have to be administered at a high dose. o The same drug may have a high affinity at one site of action and a low affinity at a different site of action. Effects of Repeated Administration: 1. Tolerance is when the effect of drug diminishes because of repeated administration. o E. g. A regular heroin user must take larger and larger amounts for the drug to be effective. Having developed tolerance to heroin, the user will suffer withdrawal symptoms which are opposite effects of the drug (i.e. euphoria vs dysphoria). o Tolerance is the body’s attempt to compensate for the effects of the drug. 2. Sensitization occurs when a drug becomes more and more effective through repeated use. o E. g. barbiturates have sedative and depressive effects. The sedative effect shows tolerance but the depressive effect does not. o Thus, if larger doses of barbiturates are taken to achieve a sedative effect, you run the risk of taking a dangerously high dose of the drug. 3. A placebo is an inert substance which has no physiological effect. It is given to subjects to control the effects of mere administration of the drug. o Is the observed behavioural effect a specific cause of the drug? How drugs influence synaptic transmission The Neurotransmitters: Amino Acids o Glutamate o Gamma-aminobutyric acid (GABA) o Glycine Aspartate Monoamines o Catecholamines Dopamine (DA) Norepinehprine (NE) Epinephrine o Idolamines Serotonin (5-HT) Cholinergic o Acetylcholine (ACh) Neuropeptides o Endorphins o Other neuropeptides Distribution of Neurotransmitters in Rat Brain: Mechanisms of Drug Action: Competitive Binding: Neurotransmitter release stimulates the postsynaptic receptor. o Drugs can bind to these neurotransmitters. o These drugs can be an: An agonist, a drug that facilitates postsynaptic transmission An antagonist, a drug that blocks or inhibits postsynaptic transmission Competitive binding: o A direct agonist will attach itself to the binding site where the neurotransmitter would normally bind. o The binding causes ion channels to open. o The ions pass through and causing a postsynaptic potential. o A direct antagonist (receptor blocker) can also occupy the binding site therefore preventing the opening of the ion channel. Mechanisms of Drug Action: Noncompetitive Binding: Neurotransmitter release stimulates the postsynaptic receptor. o Drugs can bind to these neurotransmitters. o These drugs can be an: An agonist, a drug that facilitates postsynaptic transmission An antagonist, a drug that blocks or inhibits postsynaptic transmission Noncompetitive binding: o Some receptors have multiple binding sites. o The neurotransmitter binds with one site while the drug binds with another. o An indirect agonist binds with an alternative binding site and facilitates the opening of the ion channel. o An indirect antagonist binds with an alternative binding site and prevents the channel from opening. The Basics of Neurotransmitter Action: Psychoactive Drugs: Cocaine o A potent catecholamine agonist that is highly addictive o Increases activity of DA and NE by blocking their reuptake from the synapse o cause euphoria, insomina, loss of appetite, and addiction Benzodiazepines (e.g. diazepam) o Acts as a GABA agonist but do not mimick GABA's action. o Reduce anxiety (anxiolytic), sleep inducing (sedative) and anticonvulsant. Botox (Botulinium toxin) o A nicotinic antagonist which blocks ACh release. o At minute doses it can reduce tremor and reduce wrinkles Curare o A cholinergic receptor blocker (works specifically on nicotonic receptors) o Blocks transmission at neuromuscular junctions causing paralysis 4/19/2012 5:30:00 PM 4/19/2012 5:30:00 PM