202 study guide 7 - Professor: Jeff Henriques PDF

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Professor: Jeff Henriques...

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Neurotransmitters -chemical substances that carry signals across the synaptic cleft from one neuron to another -when an action potential travels to the terminal button, it causes the vesicles to attach to the presynaptic membrane and release neurotransmitters into the synaptic cleft -neurotransmitters then spread across the cleft and bind to SPECIFIC receptors on the postsynaptic neuron -the same neurotransmitter can send excitatory or inhibitory postsynaptic signals depending on the particular receptor's properties and its location in the brain -effects of neurotransmitter are a function of the receptor to which it binds, not the neurotransmitter itself Receptors -specialized protein molecules in neurons on the postsynaptic membrane (each receptor can only be influenced by one type of neurotransmitter) -neurotransmitters bind to these after passing through the synaptic cleft -receptor always has a specific response (either excitatory or inhibitory) -once neurotransmitter is released into cleft, it fills the receptor and blocks new signals until its influence is terminated -3 things terminate the neurotransmitters influence (reuptake, enzyme deactivation, and auto reception) Reuptake -process whereby a neurotransmitter is taken back into the presynaptic terminal buttons, thereby stopping its activity -action potential prompts terminal buttons to release neurotransmitter into the synaptic cleft and then take it back for recycling -cycle of reuptake and release repeats continuously Enzyme Deactivation -enzyme destroys the neurotransmitter in synaptic cleft -diff enzymes break down diff neurotransmitters -metabolic breakdown process (catabolism) -NT's broken down into parts, metabolize, and then are eliminated through blood and urine -a type of enzyme is monoamine oxidase Drugs/Toxins Effects on Neurotransmitters 1. can alter how a NT is synthesized 2. can raise or lower the amount of an NT released from terminal buttons 3. can block reuptake (change way NT is deactivated in synaptic cleft) and affect the concentration of the neurotransmitter -can also mimic neurotransmitters and bind with their receptor as if they are the real thing (receptor cannot tell a real NT from a forgery) Agonists

-increase/facilitate/enhance the actions of neurotransmitters -can increase how much NT is made, so there is more inside each vesicle -can block reuptake of NTs -can mimic a particular NT and bind to its receptors L-Dopa -AGONIST (increase/facilitate NT effects) -molecule that is necessary in synthesizing dopamine (in cell body) -first line of defense in onset of Parkinson's disease (help neurons produce more Dopamine) -more L-Dopa in system=potentially more Dopamine product made Amphetamines, Cocaine -AGONIST (increase/facilitate NT effects) -especially powerful effects on dopamine (stimulates pleasure center) Antidepressants (3 types) AGONIST (increase/facilitate NT effects) 1. Tricycling inhibits NT reuptake, old school method that was used before SSRIs-still used if SSRIs don't work 2. Selective Serotonin Reuptake Inhibitor: inhibit 5-HT reuptake, prevent serotonin from being reuptook, resulting in more in the synapse (safer and have less side effects than Tricyclic drugs) 3. Mono-Amine Oxidase Inhibitors: (MAO-Is) slow enzymatic deactivation which prevents catabolism and results in more monoamine neurotransmitters (serotonin, norepinephrine, epinephrine, dopamine) Monoamine Oxidase Inhibitors vs. SSRIs -both agonists of Serotonin and both reduce symptoms of depression, but they have different mechanisms of action -SSRIs block the reuptake of Serotonin and Monoamine Oxidase Inhibitors prevent the breakdown of Serotonin (increasing the amount available in synapse) Ecstasy -AGONIST (increase/facilitate NT effects) -release massive amounts of Serotonin-makes people extremely happy (for time being) -terminal buttons destroyed if ecstasy is taken often which can result in depression later in life Antagonists -drugs that inhibit the actions of neurotransmitters -decrease release of NTs, fewer inside each vesicle -can help destroy NTs in synapse -can mimic an NT to block real NT from binding to that receptor Curare -ANTAGONIST (decreases/interferes with NT effects)

-operates in peripheral nervous system by competing with Acetycholine at junction motor nerve and muscle--temporarily paralyzes -essentially blocks Acetylcholine from fitting in with its receptor Antipsychotic Medications -ANTAGONIST (decreases/interferes with NT effects) -block post-synaptic Dopamine receptors (which results in impaired motor effects) -side effects: produce symptoms that mimic Parkinson's disease (Parkinsonian-like side effects) -main goal of medications: reduce dopamine levels that are interfering with thinking and judgments and that are causing hallucinations and delusions Acetylcholine (ACh) -NT -motor control at junctions between nerves and muscles (binds with receptors on muscles making them contract or relax) -links motor neurons and muscles (synapse at muscle) -usually allows muscle fibers to operate -excites skeletal muscle and inhibits heart muscle -Botulism (Botox) inhibits release of ACh (because of its ability to paralyze muscles) -ACh antagonists can cause temporary amnesia (Curare is ACh antagonist) -ACh agonists may enhance memory -Alzhemirs patients have low levels of ACh -also involved in learning, memory, sleeping, and dreaming (affects memory and attention) IN CNS!!! Alzheimers Disease -associated with diminished Acetylcholine functioning (low levels of ACh) Joseph Martinez Experiment -explores causal relationships between CNS Acetylcholine Processes and Learning and Memory Processes ("consolidation" of learning) -took drug and manipulated them in experiments with mice (Scopolomine and saline injections) -used simple learning situation (maze with 2 arms and food in one arm) -mouse learns quickly to run down the arm with food -because it takes a long time for a memory to become permanent, it allowed for interference of the process by injecting the mice with said drugs (mice were initially trained in a drug-free situation) -Operational IV: Scopolomine (ACh antagonist) vs. Saline injection -Operation DV (what they measured): "time" it took to find food -Theoretical DV (what was inferred): "memory" Scopolomine vs. Saline Injections (Joseph Martinez Experiment) Scopolomine: -injected after mice learned the maze

-as a result, animals don't remember the maze (experimental amnesia) -Scopolomine blocks receptor for neurotransmitter and essentially deactivates the synapse (ACh antagonist=IMPAIRED MEMORY) -lack of consolidation (didn't become a part of long-term memory) Saline: - necessary control group of mice -given to traumatize the mice equally with an injection to make sure they have similar experience/levels of stress Physostygmine Injection (Joseph Martinez Experiment) -ACh agonist (ENHANCEMENT of memory) -stimulates synapse by blocking the enzyme that usually breaks down ACh -prevents enzymatic deactivation of ACh...