Week 4- Behavioral nueroscience
Week 4- Behavioral nueroscience PSYC 4183-001
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This 6 page Class Notes was uploaded by Celine Notetaker on Saturday February 13, 2016. The Class Notes belongs to PSYC 4183-001 at University of Arkansas taught by Nathan Parks in Spring 2015. Since its upload, it has received 28 views. For similar materials see Behavioral Neuroscience in Psychlogy at University of Arkansas.
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Date Created: 02/13/16
Behavioral Neuroscience - Week 4 Neurotransmitter Systems Glutamate+GABA= foundation of every neural circuit in the brain (COVERED IN WEEK 3 NOTES) EXAMPLE QUESTION 1: What are 2 ways to increase the glutamate levels in the synaptic cleft? Answer: 1. Provide more of the precursor of glutamate (i.e. Stimulate more Ca+ + channels to cause the neurotransmitter to increase) 2. Blocking Reuptake of glutamate Agonist Vs. Antagonist Directbinding Agonist Indirectacting Agonist The first acts just like a Indirectbinding agonists neurotransmitter, binding directly to the enhance the neurotransmitter receptor site – this direct bind allows the actions by stimulating recipient to experience the effects of the neurotransmitters’ release, drug as if they were released directly increasing the emissions. An into the brain. Examples of direct example of an indirectbinding binding agonist drugs include dopamine, agonist is cocaine. apomorphine, and nicotine. Directacting Antagonist Indirectacting Antagonist This set of antagonists work by taking Drugs that work by inhibiting the up the space present on receptors release or production of otherwise occupied by neurotransmitters are known as neurotransmitters. The end result is that indirectacting antagonists. An neurotransmitters themselves are example of this type of drug is blocked from binding to the receptors. Reserpine. The most common example of a drug belonging to this category is Atropine. Acetylcholine (ACh) PNS: Drives all the contractions of the skeletal muscle CNS: consciousness, attention, learning/memory can modulate the release of glutamate for a period of time (inhibit or enhance) Post synaptic receptors: Nicotinic: ionotropic, Na+ Excitatory Muscarinic: metabotropic, K+ inhibitory Reuptake/deactivation: Post-synaptic cell has to break down ACh otherwise the muscle will keep contracting Acetylcholine esterase (AChE): the enzyme that breaks down ACh (found in large amounts) After ACh is broken down, choline will result choline is taken back up to the pre-synaptic cell by a choline transporter (CHT) DRUGS Agonist: Nicotine Muscarine Cholinesterase inhibitors inhibits AChE so that acetylcholine wont break down and it remains in synaptic cleft Alpha-latroxin (black widow venom) keeps voltage-gated Ca++ channels open which increases ACh release endlessly. Could result in rigid paralysis Antagonist Atropinewhen used on the eye it causes relaxation of ciliary muscles so that the pupils will dilate (can be extracted from Nightshade) Curare causes flaccid paralysis (some ___ tribes use it to poison the tip of their weapons, it is extracted from a plant). -It can paralyze the eye if injected into it. Make the eye completely still. Botulinum toxin can result in flaccid paralysis by degrading the synaptic vesicles and preventing the merge of the vesicles and the release of ACh Dopamine (DA) -Classified as a Monoamine (plays modulatory roles in the CNS) **Plays a wide range of roles but it can be specifically tied to: motor planning, learning & memory, reward, and attention Post synaptic receptors D1, D2, D3, D4, D5 = All metabotropic Drugs that inhibit/antagonize the dopamine system are used to treat schizophrenia Drugs that agonize dopamine is used to treat those with Parkinsons disease there is a risk that they could develop the positive symptoms of schizophrenia such as hallucinations. Reuptake/deactivation Dopamine transporter (DAT) takes dopamine back into the pre-synaptic cell Monoamine oxidase (MOA) = breaks down the dopamine in the pre-synaptic cell that is not contained in vesicles Drugs Agonists L-DOPA MAOIs—inhibits MOA so that it can break down dopamine you end up with more dopamine This can also be done through diet, by decreasing intake of MAOI precursors which is used to decrease depression MDMA Methamphetamine Cocaine Methylphenidate Antagonists Thorazine – antagonist for D2 Clozapine –antagonist for D2 Haloperidol –antagonist for D2 Reserpine works by blocking the transporter which means the neurotransmitter can’t be packaged into the vesicle. So at the end of the Action potential, when the vesicle goes to the membrane to release its contents, the vesicle will release nothing. antagonist for dopamine, NE, and serotonin Norepinephrine (NE) Also a Monoamine Involved in: Attention, awareness, vigilance, autonomic functions Post-synaptic receptors = all metabotropic Alpha1 Alpha2 Beta1 Beta2 Beta3 Reuptake/deactivation Reserpin also blocks NE NE is taken back up into the presynaptic cell by a norepinephrine transporter (NET). In the presynaptic cell, NE not contained in vesicles is broken down by the enzyme monoamine oxidase (MAO) Drugs Agonists Norepinephrine Reuptake Inhibitor (NRI) Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) MAO Inhibitors (MAOIs) Antagonists Alpha-blockers People take this when nervous, to reduce the positive feedback that normally makes people more nervous Beta-blockers Reserpine Serotonin (5-HT) -Also a monoamine -Derived from tryptophan MYTH: that thanksgiving turkey eating will make you sleepy. You would have to eat a TON of turkeys to ingest enough tryptophan to make you sleepy Involved in: arousal, attention, sleep, eating =not the only neurotransmitter involved in sleep circuitry GABA agonists can also make you sleepy, Anti-histamines make you sleepy too Post-Synaptic Receptors 5-HT 1 5-HT 2 5-HT 3 5-HT 4 5-HT 5 5-HT 6 5-HT 7 The 5-HT3 serotonin receptor is ionotropic (Na+). All others are metabotropic Reuptake/deactivation Serotonin (5-HT) is taken back up into the presynaptic cell by a serotonin transporter (SERT). In the presynaptic cell, 5-HT not contained in vesicles is broken down by the enzyme monoamine oxidase (MAO). Drugs Agonists: Selective serotonin reuptake inhibitors (SSRIs)Selectively acting agonist on serotonin by preventing reuptake, doesn’t affect other monoamine Serotonin & Norepinephrine reuptake inhibitors (SNRIs) MAO Inhibitors (MAOIs) Lysergic acid diethylamide (LSD) psilocin (mushrooms) natural substance in psychedelic mushrooms mescaline (peyote) traditionally used in folk medicine to treat various disorders Antagonists: Reserpine Risperidone Thursday, February 11, 2016 Building Neural Circuits Multipolar neurons: multiple branches come off the cell body - motor neuron of spinal cord - pyramidal cell of hippocampus - purkinje cell of cerebellum unipolar neurons: only one branch leaves the cell body, the axon. Dendrites come off the axon - invertebrate neuron Bipolar: two branches leave the cell body. A single dendrite branch on one side and axon on the other side - Bipolar cell of retina Pseudo-unipolar neuron: single axon with dendrites on one end and axon terminals on the other. The cell body branches off the AXON. - Ganglion cell of dorsal root **Despite the diverse neural structure, neural communication proceeds in the same functional steps Force= stimulus that acts on the Muscle Spindle which builds a graded potential activating a trigger action by pulling on the trigger zone in the musculature. An Action potential shoots down the myelinated axon Stretch reflex Tapping on the muscle stretches the muscle spindle in the quads creates graded potential in the muscle spindle. An Action potential occurs that is sent to the spinal cord. EXCITATORY The axon terminal in the spinal cord will release glutamate which will activate a motor neuron that links back to the same muscle (quads) which will then contract INHIBITORY Another branch of the axon terminal in the spinal cord simultaneously releases GABA. GABA causes the hamstring to relax, allowing the leg to kick by making sure only the quads contract. Flexion Reflex Pain in one foot send an action potential to the spinal cord. Four interneurons receive information. The leg experiencing the pain will have the extensor muscle relaxed and the flexor muscle contracted in order to bend the leg away from the painful stimulus Simultaneously, the other leg will have the flexor muscle relaxed and the extensor muscle contracted so that it can straighten to take on more weight and to allow the weigt shift as you bend the other foot off the floor.
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