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Beh. Neuro Exam 3 Review

by: Donielle Rhone

Beh. Neuro Exam 3 Review 50690

Donielle Rhone
GPA 2.8

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About this Document

These notes cover what's going to be on Exam 3 (minus the textbook).
Behavioral Neuroscience
Cyrille L. Magne
Study Guide
50 ?




Popular in Behavioral Neuroscience

Popular in Psychology (PSYC)

This 22 page Study Guide was uploaded by Donielle Rhone on Thursday July 21, 2016. The Study Guide belongs to 50690 at Middle Tennessee State University taught by Cyrille L. Magne in Summer 2016. Since its upload, it has received 11 views. For similar materials see Behavioral Neuroscience in Psychology (PSYC) at Middle Tennessee State University.


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Date Created: 07/21/16
Exam 3 Wednesday, July 20, 2016 2:49 PM Behavioral Neuroscience Exam 3 Review - 07/22/16 *Ch. 5 - Neurotransmitters **Neurons use neurotransmitters to communicate. **Neurotransmitters are released when action potentials reach the axon terminal. **Characteristics of neurotransmitters are important to know, not only because of their vital function in neural communication, but also because their absence or excess may play a major role in brain diseases and behavioral disorders. **properties of neurotransmitters -Criteria for a molecule to be classified as a neurotransmitter: *Substance exists in presynaptic axon terminals, *Substance is synthesized in presynaptic cells, *Substance is released when action potentials reach axon terminals, *Receptors for the substance exist on the postsynaptic membrane, *When applied, substance produces changes in postsynaptic potentials, *Blocking substance release prevents changes in postsynaptic cell. **modes of action -Neurotransmitters affect target cells by acting on receptors. *Two types of receptors: -postsynaptic *Ionotropic -ligands, fast, conformational change, LGIC (ligand gated ion channel) -Directly coupled to an ion channel. *Metabotropic -Activates G proteins that either open ion channels or cause modification in the target cell -GPCR (G-protein coupled receptor), slow, extended life -presynaptic *autoreceptors -without neurotoxins stops production type of GPCR *Both types of receptors may either excite or inhibit the target cell, depending on which type of ion channel they open. -Receptors add to the complexity of neural signaling because each neurotransmitter may bind onto a wide variety of receptor subtypes. *They may elicit very different effects in the target cell *They may be distributed differently in the nervous system. -The development of drugs relies considerably on the existence of those receptor subtypes. *Drugs can be designed so that they affect only one subtype of receptor. -They will produce only the effect associated with that subtype of receptor. -Any substance that can bind to a receptor is called a ligand: *If the ligand binds to the receptor and initiates the normal effect of that receptor, it is considered as an agonist. *If a ligand binds to a receptor and does not activate it, it is called an antagonist. *If a ligand bind to a receptor and initiates the reverse effect, it is an inverse agonist. -Ligands produced by the brain are considered as endogenous while substances introduced from outside the body are considered as exogenous. -For a long time, scientists believed that each neuron only had one type of neurotransmitter. -With the help of techniques such as immunocytochemistry, we know now that some neurons possess more than one type of neurotransmitter. *It is called co-localization. **types of neurotransmitters -Many types of neurotransmitters have been identified: *Amine neurotransmitters -ex: Acetylcholine, Dopamine, Serotonin *Amino acid neurotransmitters -ex: GABA, Glutamate *Peptide neurotransmitters -ex: Opioids *Gas neurotransmitters -ex: NO **amines -relatively independent building blocks -Acetylcholine (ACh) *a neurotransmitter that stimulates muscle contraction, and it is also found throughout the brain. *It was the first chemical substance identified as a neurotransmitter. -Initially identified in 1914, and later confirmed as neurotransmitter in Otto Loewi’s experiment. *Quaternary amine *receptors: nicotinic & muscarinic *controls muscles in its periphery -There are two types of ACh receptors: *Nicotinic are ionotropic and excitatory. -Muscles use nicotinic ACh receptors. -Named after his agonist, nicotine. -Paralysis can be induced with an antagonist, such as curare. -There are two types of ACh receptors: *Muscarinic are metabotropic and can be excitatory or inhibitory. -They can be found in the heart. -An agonist is muscarine, a substance found in certain mushrooms. -Muscarinic ACh receptors can be blocked by atropine. -In the brain, clusters of cholinergic neurons are present in: *The basal forebrain -They send their axon terminal to the limbic system and various locations in the cerebral cortex. -Loss of cholinergic neurons is found in Alzheimer’s disease. *The Midbrain -They project to different areas of the hindbrain. -There are two main classes of monoamine neurotransmitters. *Catecholamines -dopamine -epinephrine -Norepinephrine *Indoleamines -Serotonin -Dopamine (DA) *is found in two different brain pathways: -Mesostriatal pathway *Originates in the midbrain, specifically the substantia nigra, and innervates the striatum. *Involved in motor control. *Neuronal loss is a cause of Parkinson’s disease. -Mesolimbocortical pathway *Originates in the midbrain and projects to the limbic system and cortex. *Involved in reward, reinforcement and learning. *Abnormalities are associated with schizophrenia. -Norepinephrine (NE) *Also known as noradrenaline. *catecholamine *The central nervous system contains four subtypes of NE receptors. -All metabotropic *Neurons are found in parts of the midbrain, pons and medulla, and they project to various areas of the cerebral cortex, cerebellum, limbic system and thalamus. *NE affects mood, arousal, and sexual behavior. -Serotonin (5HT) *At least 15 subtypes of 5HT receptors have been identified. *Cell bodies of neurons releasing 5HT are mainly found in the raphe nuclei: -various areas of the midbrain, pons and medulla. *Serotonin is involved in the regulation of sleep, mood, sexual behavior, anxiety, and other functions *Antidepressants such as Prozac increase 5HT activity. **amino acid -work together -Glutamate *the main excitatory neurotrasmitter in the brain. *Several subtypes: -AMPA, kainate, and NMDA, -metabotropic receptors (mGluRs). *Glutamate is associated with excitotoxicity. -neural injury such as stroke may cause excess release of glutamate, which is toxic to neurons. *Astrocytes are involved in cleaning-up glutamate from the synaptic gap after transmission. -Gamma-aminobutyric acid (GABA) *the main inhibitory neurotransmitter in the brain. *GABA receptors classes: -GABAᴀ - ionotropic, fast inhibitory effects, -GABAᴃ - metabotropic, slow inhibitory effects, -GABAᴄ - ionotropic with a chloride channel. *Each class contains further subtypes. *GABA agonists, like Valium, are potent tranquilizers. **peptide -Peptides *act as neurotransmitters at some synapses, or as hormones in other systems: *Opioid peptides that mimic opiate drugs such as morphine: -met-enkephalin, -leu-enkephalin, -β-endorphin. *They are involved in different aspects of pain regulation. manmade opium plant base *Peptides that are present in the gut, the spinal cord or the brain. -substance P (Pain perception), -cholecystokinin (regulation of appetite), -neuropeptide Y (regulation of appetite). *Hormones such as: -Oxytocin has a facilitating role in birth and breastfeeding. -Vasopressin is released when the body is dehydrated, and causes the kidneys to conserve water. *Peptides are often co-localized with other neurotransmitters. **gas -Though Nitric oxide (NO) is used as a neurotransmitter, its mode of action differs from other neurotransmitters. *It is produced in locations other than axon terminals, mainly in dendrites, and diffuses as soon as it is produced rather than being released from synaptic vesicles. *It does not act on receptors but enters in the target cell and stimulates the production of second messengers. It serves as a retrograde transmitter by diffusing back from the postsynaptic neuron to the presynaptic neuron where it exerts its effect. *Chapter 6 - Psychoactive Drugs **Drugs -chemical substances that, taken in small amounts, can alter physiological or psychological functions. -Most of the drugs of interest to behavioral neuroscience are exogenous ligands interacting with specific receptor molecules. **principles of Pharmacokinetics -To exert their effect, drugs need to reach their site of action. *1. They enter the body and the bloodstream, *2. They are carried to the target organ through the bloodstream, *3. They exit the blood stream, *4. They act on the target organ by interacting with specific molecules. -The sites of action of psychoactive drugs are located in the nervous system. -To reach the nervous system, drugs need to pass the blood-brain barrier. *Cells that form the capillaries in the body don’t have perfect junctions. -There are gaps in between allowing the movement of substances in and out *But in the brain, cells in the walls of the capillaries have tight junctions that prevent many substances to leave the blood. -Drugs can be administered in the body by different ways: *Intravenous: directly in the blood stream *Intramuscular: in the muscle *Skin: using patches *Subcutaneous: under the skin *Intracerebrally: directly in the brain, *Sublingually: under the tongue *Rectally: into the rectum *Inhalation: introduced in the lungs -Each of these various routes of administration has its pros and cons, and a different time courses of action. *A drug may be taken sublingually, while a rectal administration will be used if the drug might upset a person’s stomach. *An intravenous injection will have a faster effect than an oral administration, but it may be more dangerous as the entire dose reaches the bloodstream at once. -Drug effectiveness *Varies across the different drugs. -A small dose of a very effective drug can have a wider effect than a large dose of an ineffective drug. *Measured by plotting the dose-response curve. -Show the amplitude of the drug response in function of the dose injected. -It has a “S” shape because: *At low dose, no response can be measured, *At high dose, most of the receptors are occupied so that increasing the dose does not increase the response further. *the dose-response curve -ED50 Dosage for which the desired effect is seen in 50% of the animal -effect dose 50% - ED50 = ½ of the max effect of a drug -lethal dose 50% - LD50 = dose at which 50% die -can compare potency of 2 drugs -can compare max effect of 2 drugs -can determine therapeutic window *Two factors influence the drug effectiveness: -Site of action *Some drugs have the same behavioral effect, but different sites of action. -Affinity *It corresponds to the degree of attraction between a ligand and a receptor. *While a drug can bind to more than one type of receptor, it will generally binds more strongly to one type than the others. *Effect of repeated treatment -Tolerance *With repeated administration of a drug, the individual becomes less responsive to it. *Tolerance is believed to be responsible for the withdrawal effect. -Unpleasant sensation that arises when someone stops taking a drug. -Sensitization *In some cases, the drug response can become stronger with repeated administration. *May be involved in the drug craving that addicts experience. **sites of drug action -Drugs can affect each stage of the synaptic transmission. *Presynaptic mechanisms. *postsynaptic mechanisms **major classes of drugs -Drugs can be classified according to their specific effect on the behavior or their therapeutic application. *1. Antipsychotic drugs (neuroleptic) -greatly reduce the symptoms of schizophrenia -Typical neuroleptics act as antagonists of dopamine D₂ receptors. *They reduce symptoms such as delusion and frank hallucination. -Atypical neuroleptics block serotonin receptors. *They reduce additional symptoms such as social withdrawal and blunted emotional responses. *2. Antidepressants -relieve chronic mood problems; treat depression -Monoamine oxidase inhibitors (MAOIs) prevent the breakdown of monoamines at the synapses, thus accumulating and prolonging their activity. -Tricyclics increase norepinephrine and serotonin at the synapses by blocking their reuptake. -Selective serotonin reuptake inhibitors (SSRIs) like Prozac allow serotonin to accumulate in the synapses, with fewer side effects than tricyclics. *3. Anxiolytics (tranquilizers) -depressants -These drugs reduce the nervous system activity. -increase GABA -biphasic effect *initial stimulation; prolonged depression -Benzodiazepine agonists like valium act on GABAᴀ receptors and enhance the inhibitory effects of GABA. -barbituates 4. Alcohol -Produced by the fermentation of fruits or grain. -has several effects; its effects are biphasic: *an initial stimulant phase followed by *a depressant phase. -Activates GABAᴀ receptors and increases the inhibitory effects of GABA. *This contributes to social disinhibition and loss of motor coordination. -Alcohol also stimulates dopamine pathways. *This effect causes euphoric effects. 5. Opiates -help relieve pain -Opium contains morphine, an effective analgesic (painkiller). *Morphine and heroin are related and are both highly addictive. *These opiates bind to opioid receptors in the brain. -especially in the locus coeruleus (in the hindbrain) and the periaqueductal gray (in the midbrain). 6. Cannabinoids -have a wide array of effects -Marijuana is derived from Cannabis sativa. *Active ingredient is Δ9-tetrahydrocannabinol known as THC. *Effects include relaxation, mood alteration, stimulation, hallucination and paranoia. *Sustained use can cause addiction. -The brain contains cannabinoid receptors to mediate the effects of THC and other compounds. *Receptors highly present in substantia nigra, hippocampus, cerebral cortex and cerebellum. -The brain produces Endocannabinoids that are homolog of marijuana. *They act as retrograde messengers, and influence the release of neurotransmitters from the presynaptic neuron. 7. Stimulants -Stimulants increase nervous system activity. -nicotine *is extracted from tobacco *Activates nicotinic ACh receptors in the ventral tegmental area (in the midbrain). *increases heart rate, blood pressure, hydrochloric acid secretion, and bowel activity. -cocaine, the purified extract: *Can be used as an anesthetic *Is highly addictive. *Cocaine blocks monoamine transporters involved in the reuptake. -Amphetamine *synthetic stimulants that resemble catecholamines in structure. *They cause the release of neurotransmitters even in the absence of action potentials. *Short-term effects of amphetamine include alertness, euphoria and stamina. *Long-term use leads to sleeplessness, weight loss, and schizophrenic symptoms. -caffeine 8. Hallucinogens -alter sensory perception and produce peculiar experiences. -They have diverse neural actions, including on the noradrenergic, serotonergic, and ACh systems. -LSD *resembles serotonin in structure and acts as an agonist on serotonin receptors, including those in the visual cortex. -Alters visual perception. -MDMA (or Ecstasy) *a hallucinogenic amphetamine derivative. *its major actions are: -increase in serotonin levels -change in dopamine and prolactin (an hormone) levels *Chronic ecstasy use produces: -persistent effects -damage to serotonin-producing neurons -PCP **substance abuse and addiction -Substance abuse and addiction have become a social problem that afflicts millions of individuals. *Alcohol: automobile accident, increased rate of heart disease, increased risk of intracerebral hemorrhage. *Smoking: increased risk of lung cancer, heart attack, stroke. *Cocaine: Psychotic behavior, brain damage, as well as competition for illegal market. -What makes those drugs so attractive to many people? -Several models of drug abuse has been proposed varying in their emphasis on physiological, behavioral and environmental factors. *The Moral Model -The earliest approach was to blame the abuser for a lack of moral character or a lack of self-control. *The Disease Model -The abuser requires medical treatment. -However, researchers have not been able to identify an abnormal condition in abusers. *The Physical Dependence Model -Abusers use drugs to avoid unpleasant withdrawal symptoms. -But people can become dependent on drugs even in absence of any clear physical withdrawal symptoms. *The Positive Reward Model -Drug use is a behavior controlled by positive rewards, with no disease. -Model arose from animal research started in the 1950s and the development of drug self-administration apparatus. -Many addictive drugs cause dopamine release in the nucleus accumbens (NA). *As do also food and sex. -Some axons that terminate in the NA originate from neurons in the ventral tegmental area (VTA). *Part of the mesolimbicocortical dopaminergic pathway. -The NA, VTA, and the nerve connection in between, constitute a reward circuit that provides a pleasurable sensation when stimulated. -The addictive power of drugs may come from stimulating this pathway. -Not everyone who uses an addictive drug becomes addicted. *Patients treated with opiates for pain relief rarely will abuse opiates after leaving the hospital. *Individual and environmental factors account for this differential susceptibility to drug abuse. -Factors in susceptibility to addiction: *Biological -Sex, genetic predisposition, *Personal characteristics -aggressiveness, poor emotional control *Family situation -family breakup, poor relationships, sibling drug users *Environmental factors -peer pressure, social factors -Medications to treat drug abuse *Drugs for detoxification -benzodiazepines and drugs to help ease withdrawal symptoms *Agonists or analogs of the addictive drug -Partially activate the same pathways, such as methadone or nicotine patches *Antagonists to the addictive drug -Block effects of the abused drug but may produce withdrawal symptoms *Medications that alter drug metabolism -like Antabuse, which makes drinking produce unpleasant side effects. *Reward-blocking medications -block positive reward effects of the abused drug but may produce a lack of all pleasurable feelings. *Anticraving medications -reduce the appetite for the abused substance


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