{"id":4499,"date":"2018-10-07T01:22:11","date_gmt":"2018-10-07T05:22:11","guid":{"rendered":"https:\/\/www.amyork.ca\/academic\/zz\/?p=4499"},"modified":"2018-10-07T01:44:50","modified_gmt":"2018-10-07T05:44:50","slug":"the-concept-of-synapses","status":"publish","type":"post","link":"https:\/\/www.amyork.ca\/academic\/zz\/biological-basis-of-behaviour\/the-concept-of-synapses\/","title":{"rendered":"The concept of synapses"},"content":{"rendered":"<ul>\n<li>Cajal: anatomically demonstrated narrow gap separating neurons<\/li>\n<li>Sherrington: physiologically demonstrated communication between neuron and next differs from communication along single axon<\/li>\n<li><strong>Synapse <\/strong>&#8211;&gt; specialized gap between neurons<\/li>\n<li><strong><u>The Properties of Synapses <\/u><\/strong><\/li>\n<li><strong>Reflexes<\/strong>: autonomic muscular responses to stimuli. In leg flexion reflex, sensory neuron excites 2<sup>nd<\/sup> neuron \uf0e0 excites motor neuron \uf0e0 excites muscle<\/li>\n<li><strong>Reflex arc<\/strong>: circuit from sensory neuron to muscle response<\/li>\n<li>Reflex must require communication between neurons<\/li>\n<li>Properties of reflexes suggest special process at junction between neuron\n<ol>\n<li>Reflexes slower than conduction along axon<\/li>\n<li>Several weak stimuli presented at slightly different times\/locations produce stronger reflex than single stimulus<\/li>\n<li>When one set of muscles becomes excited \uf0e0 different set relaxes <strong>Speed of a Reflex and Delayed Transmission at the Synapse<\/strong><\/li>\n<\/ol>\n<\/li>\n<li>Impulses have to travel up an axon from skin receptor to spinal cord, then impulse travels from spinal cord back down leg to the muscle<\/li>\n<li>Speed of conduction through reflex arc ~15 m\/s; conduction down an axon is 40 m\/s (AP velocities along sensory\/motor nerves) \uf0e0 delay must occur where one neuron communicates with another <strong>Temporal Summation<\/strong><\/li>\n<li>Repeated stimuli within brief time has cumulative affect (summation over time)<\/li>\n<li><strong>Presynaptic neuron<\/strong>: delivers transmission<\/li>\n<li><strong>Postsynaptic neuron<\/strong>: neuron receiving transmission<\/li>\n<li>Sub-threshold excitation in postsynaptic neuron decays over time, can combine with 2<sup>nd<\/sup> excitation that follows quickly<\/li>\n<li>With rapid successions of pinches, each adds effect, until combo exceeds threshold of the postsynaptic neuron \uf0e0 AP<\/li>\n<\/ul>\n<p>After brief stimulation of axons of presynaptic neurons \uf0e0 slight depolarization of the membrane of postsynaptic cell<\/p>\n<ul>\n<li>Slight depolarization is graded potential; can be excitatory depolarization, excitatory post-synaptic potential (EPSP), or inhibitory hyperpolarization<\/li>\n<li>Results from flow of Na ions into neuron <strong>Spatial Summation<\/strong><\/li>\n<li>Synaptic inputs from separate locations combine effects on a neuron (summation over space)<\/li>\n<li>Pinching 2 points activated separate sensory neurons \uf0e0 axons converged onto neuron in spinal cord (not enough to reach threshold) \uf0e0 combo of excitations exceeded threshold, produced AP.<\/li>\n<li>EPSPs from several axons summate their effects on a postsynaptic cell<\/li>\n<li>Sensory input to brain arrives at synapses \uf0e0 individually produce weak effects; each neuron receives many incoming axons that produce synchronized responses \uf0e0 ensures sensory stimulus stimulates neurons enough to activate them<\/li>\n<li>Temporal and spatial summation usually occur together; neuron might receive input from several axons at approx. same time; different order \uf0e0 different results<\/li>\n<\/ul>\n<h3>Inhibitory Synapses<\/h3>\n<ul>\n<li>Interneuron: (intermediate neuron) in spinal cord \uf0e0 excite motor neurons connected to flexor muscles of leg<\/li>\n<li>At these synapses, input from axon hyperpolarizes postsynaptic cell; increases<\/li>\n<\/ul>\n<p>-ve charge within cell, move it further from threshold, decrease probability of AP<\/p>\n<ul>\n<li><strong>Inhibitory Postsynaptic Potential (IPSP)<\/strong>: temporary hyperpolarization of a membrane; resemebles EPSP; occurs when synaptic input selectively opens gates for K+ ions to leave cell or Cl- ions to enter cell<\/li>\n<\/ul>\n<h2>\u00a0Relationship Among EPSP, IPSP and Action Potentials<\/h2>\n<ul>\n<li>NS full of complex patterns of connections, produce variety of responses<\/li>\n<li>Synapses vary in duration of effects<\/li>\n<li>Effect of two synapses at same time can be more than double effect of either one, or less than double<\/li>\n<li><strong>Spontaneous firing rate<\/strong>: periodic production of APs without synaptic input.<\/li>\n<\/ul>\n<p>EPSPs increase frequency of APs above spontaneous rate, IPSPs decrease it<\/p>\n<h2>CHEMICAL EVEiTS AT THE SYiAPSE\u00a0 The Discovery of Chemical Transmission at Synapses<\/h2>\n<p><em>\u00a0<\/em><\/p>\n<p>Sympathetic NS (set of nerves) accelerates heart beat, relax stomach muscles, dilate pupils, regulate organs; sympathetic nerves stimulate muscles by releasing adrenaline (or a similar chemical)<\/p>\n<ul>\n<li>Nerves send messages by releasing chemicals<\/li>\n<li>Chemical transmission predominates over electrical synapses in the nervous system<\/li>\n<\/ul>\n<p><strong><u>\u00a0The Sequence of Chemical Events at a Synapse <\/u><\/strong>\uf0b7 Major Events:<\/p>\n<ol>\n<li>Neuron synthesizes chemicals that serve as neurotransmitters (synthesizes smaller neurotransmitters in axon terminal and neuropeptides in cell body)<\/li>\n<li>AP travel down axon. At presynaptic terminal, AP allows Ca to enter cell; Ca releases neurotransmitters from terminals into synaptic cleft (space between pre and postsynaptic neuron)<\/li>\n<li>Released molecules diffuse across cleft \uf0e0 attach to receptors \uf0e0 alter activity of postsynaptic neuron<\/li>\n<li>Neurotransmitter molecules separate from receptors<\/li>\n<li>Neurotransmitter molecules taken back into presynaptic neuron for recycling or may diffuse away<\/li>\n<li>Some postsynaptic cells send reverse messages to control further release of neurotransmitter by presynaptic cells <strong>Types of ieurotransmitters<\/strong><\/li>\n<\/ol>\n<ul>\n<li>Neurotransmitters: neuron releases chemicals that affect another neuron<\/li>\n<li><strong>Amino acids<\/strong>: contain amine group (NH<sub>2<\/sub>)<\/li>\n<li><strong>Monoamines<\/strong>: chemicals formed by change in amino acids<\/li>\n<li><strong>Acetylcholine<\/strong>: chemical similar to amino acid, but contains a N(CH<sub>3<\/sub>)<sub>3<\/sub><\/li>\n<li><strong>ieuropeptides<\/strong>: chains of amino acids<\/li>\n<li><strong>Purines<\/strong>: category includes: adenosine and several of its derivatives<\/li>\n<li><strong>Gases<\/strong>: nitric oxide and others<\/li>\n<li><strong>iitric oxide<\/strong>: (NO) gas released by small local neurons; many neurons have enzyme that allows them to make if efficiently. When brain area active, blood flow to area increases; neurons release nitric oxide when stimulated, acts as signal, dilates nearby blood vessels, increasing blood flow to that area <strong>Synthesis of Transmitters<\/strong><\/li>\n<li>Neurons synthesize all neurotransmitters from amino acids, from proteins <strong>Catecholamine<\/strong>: contain a catechol and amine group (epinephrine, norepinephrine, and dopamine)<\/li>\n<li>Tryptophan (precursor to serotonin) cross blood-brain barrier by special transport system (compete with larger\/abundant amino acids) \uf0e0 amount of tryptophan in diet controls amount of serotonin in brain <strong>Storage of Transmitters<\/strong><\/li>\n<li>Most neurotransmitters synthesized in presynaptic terminal (near point of release); stores high concentrations of neurotransmitters in vesicles and many outside vesicles<\/li>\n<li>Neuron can have excess neurotransmitters (ex: neurons that release serotonin, dopamine or norepinephrine contain MAO (monoamine oxidase): breaks down transmitters into inactive form<\/li>\n<\/ul>\n<h3>Release and Diffusion of Transmitters<\/h3>\n<ul>\n<li>At end of axon, AP doesn\u2019t release neurotransmitter; depolarization opens voltage-dependent Ca gates in presynaptic terminal \uf0e0 causes exocytosis (release of neurotransmitter in bursts from presynaptic neuron into synaptic cleft; separates one neuron from another). AP often fails to release any neurotransmitter \uf0e0 amount can vary<\/li>\n<li>Neurotransmitter diffuses across synaptic cleft to postsynaptic membrane; attaches to receptor<\/li>\n<li>Most neurons release a combo of 2 or more transmitters<\/li>\n<li>Motor neurons in spinal cord have one branch to muscles \uf0e0 release acetylcholine and another branch to other spinal cord neurons \uf0e0 release Ach and glutamate<\/li>\n<li>Combo makes neuron\u2019s message complex (brief excitation \uf0e0 prolong inhibition)<\/li>\n<li>A neuron can receive and respond to many neurotransmitters at different synapses<\/li>\n<\/ul>\n<h3>Activating Receptors of the Postsynaptic Cell<\/h3>\n<ul>\n<li>Sherrington\u2019s concept: input produced excitation\/inhibition (on\/off)<\/li>\n<li>Effect of neurotransmitter depends on receptor on postsynaptic cell Ionotropic Effects<\/li>\n<li>Brief on\/off effects. When neurotransmitter binds to ionotropic receptor, twists receptor enough to open central channel; shape lets certain ion pass through<\/li>\n<li><strong>Transmitter\/ligand-gated channels<\/strong>: controlled by neurotransmitter; when it attaches, the gate opens (ligand binds to other chemicals)<\/li>\n<\/ul>\n<p>Used to convey visual\/auditory info and anything that needs to be updated quickly<\/p>\n<ul>\n<li><strong>Glutamate<\/strong>: most abundant (excitation)<\/li>\n<li><strong>GABA<\/strong>: (inhibitory) opens chloride gates so Cl- ions enter membrane fast<\/li>\n<li><strong>Glycine<\/strong>: (inhibitory) found mostly in spinal cord<\/li>\n<li><strong>Acetylcholine<\/strong>: (excitatory) outer portion embedded in neuron\u2019s membrane, inner portion surrounds Na+ channel. When receptor at rest, inner portion coils together to block Na passage. When Ach attached, receptor folds outwards, opening the Na+ channel<\/li>\n<\/ul>\n<p>Metabolic Effects and 2<sup>nd<\/sup> Messenger Systems<\/p>\n<ul>\n<li>Initiate sequence of metabolic reactions; slower\/longer lasting than ionotropic effects<\/li>\n<li>Many neurotransmitters (dopamine, norepinephrine, serotonin, glutamate, GABA)<\/li>\n<li>When neurotransmitter attaches to metabotropic receptor, bends receptor protein that goes through membrane of cell. Other side of receptor attached to <strong>G protein<\/strong> (protein coupled to GTP, energy-storing molecule)<\/li>\n<li>Bending detaches G protein (take energy elsewhere) \uf0e0 increased conc. of <strong>2<\/strong><strong><sup>nd<\/sup><\/strong><strong> messenger<\/strong> (communicates to many cell areas; 1<sup>st<\/sup> messenger: carry info to postsynaptic cell) \uf0e0 open\/close ion channels in membrane or activate part of chromosome.<\/li>\n<li>Influences activity in much\/all of the cell over a long time<\/li>\n<li>Better suited for enduring effects (ex: taste, smell, pain, arousal, attention, pleasure, emotion)<\/li>\n<li>Receptors differ in chemical properties, responses to drugs, and roles in behaviour<\/li>\n<\/ul>\n<p>Neuropeptides<\/p>\n<ul>\n<li><strong>ieuromodulators<\/strong> \uf0e0 synthesizes neuropeptides in cell body, slowly transports to other parts of cell; released by dendrites, cell body and sides of axon<\/li>\n<\/ul>\n<p>(neurotransmitter synthesized in the presynaptic terminal)<\/p>\n<ul>\n<li>Neuropeptide release requires repeated stimulation; after a few dendrites release, primes other dendrites to release same neuropeptides<\/li>\n<li>Don\u2019t release often, but when released \uf0e0 in large amounts<\/li>\n<li>Diffuse widely, affect many neurons in brain area<\/li>\n<li>Involved in hunger, thirst, pain, LT changes in behaviour and experience <strong>ieurogliaform cell<\/strong>: release GABA, form \u201ccloud\u201d, spreads to neurons in area \uf0e0 widespread inhibition Hormones<\/li>\n<li>Secreted by cells in 1 part of body, conveyed by blood to influence other cells<\/li>\n<\/ul>\n<p>(neuropeptides intermediate, diffuse only within brain)<\/p>\n<ul>\n<li>Endocrine glands (hormone-producing)<\/li>\n<li>Useful to coordinate long-lasting change in many parts of body<\/li>\n<li><strong>Protein hormones\/Peptide hormones<\/strong>: chains of amino acids (proteins longer; peptide shorter) attach to membrane receptors, activate a 2<sup>nd<\/sup> messenger within cell<\/li>\n<li>Hormones secreted by brain control secretion of many other hormones<\/li>\n<li><strong>Pituitary gland<\/strong>: attached to hypothalamus, consists of 2 glands\n<ol>\n<li>Anterior pituitary: made of glandular tissue; synthesizes 6 hormones (hypothalamus controls release); hypothalamus secretes releasing hormones (flow through blood to the anterior pituitary) \uf0e0 stimulate\/inhibit release of many hormones<\/li>\n<li>Posterior pituitary: made of neural tissue, extension of hypothalamus; neurons in hypothalamus synthesize oxytocin and vasopressin<\/li>\n<\/ol>\n<\/li>\n<\/ul>\n<p>(antidiuretic hormone) migrate down axons to posterior pituitary \uf0e0 then released to blood<\/p>\n<ul>\n<li>Hypothalamus maintains constant circulating levels of certain hormones through negative feedback system.<\/li>\n<\/ul>\n<h3>Inactivation and Reuptake of ieurotransmitters<\/h3>\n<ul>\n<li>After Ach activates receptor, broken down by <u>acetyl-cholinesterase<\/u> (acetate and choline); choline diffuses back to presynaptic neuron, takes it up, reconnects it with acetate already in cell to form Ach again (rapid series of APs can deplete neurotransmitter faster than presynaptic cell can replenish it<\/li>\n<li>Serotonin and catecholamine don\u2019t break down into inactive fragments at postsynaptic membrane; just detach from receptor<\/li>\n<li><strong>Reuptake<\/strong>: In some brain areas, presynaptic neuron takes up most of released neurotransmitter intact and reuses them; occurs through membrane proteins, <strong>transporters<\/strong> (differ in function, abundance)<\/li>\n<li>Dopamine: some areas transporters efficient, in others, slower: if dopamine released fast into areas, COMT breaks down excess to inactive chemicals that can\u2019t stimulate dopamine receptors; products wash away in blood\/urine; neurons diminish supply of dopamine, can\u2019t release dopamine rapidly for long Neuropeptides diffuse away; because resynthesized slowly, neuron can temporarily use up supply <strong>iegative Feedback from the Postsynaptic Cell<\/strong><\/li>\n<li>Presynaptic terminals have receptors sensitive to same transmitter released (<strong>auto-receptors<\/strong> \uf0e0 respond to released transmitter by sending chemicals that travel back to presynaptic terminal and inhibit further synthesis\/release) <strong>Electrical Synapses<\/strong><\/li>\n<li>Some synapses operate electrically; faster than chemical transmission in cases where need exact synchrony between 2 cells<\/li>\n<li><strong>Gap junction<\/strong>: At electrical synapse, membrane of 1 neuron comes into direct contact with membrane of another (contact)<\/li>\n<li>Large pores of membrane of 1 neuron line up with pores in membrane of other cell (large enough so ions pass through); always open. When 1 neuron depolarized, Na+ ions from cell pass quickly into other neuron and depolarize it too<\/li>\n<\/ul>\n<h2>SYiAPSES, DRUGS AiD ADDICTIOiS<\/h2>\n<ul>\n<li>Nearly every drug with psychological effects acts at synapses<\/li>\n<li>Most of the commonly abused drugs derive from plants<\/li>\n<li>Nearly all neurotransmitters\/hormones same in humans and other species <strong><u>Drug Mechanisms <\/u><\/strong><\/li>\n<li><strong>Antagonist<\/strong>: blocks neurotransmitter (inhibit transmission)<\/li>\n<li><strong>Agonist<\/strong>: mimics\/increase effects, can be mixed agonist- antagonist<\/li>\n<li>Drug can: increase\/decrease synthesis of neurotransmitter, leak from vesicles, increase release, decrease reuptake, block breakdown into inactive chemicals, act on postsynaptic receptors<\/li>\n<li><strong>Affinity<\/strong>: drug will bind to the receptor (key in lock)<\/li>\n<li><strong>Efficacy<\/strong>: tendency to activate the receptor (drug that binds to receptor but fails to stimulate has high affinity but low efficacy<\/li>\n<li>Effectiveness\/side effects of drugs vary between people, drugs affect many receptors and people vary in # of each kind of receptor<\/li>\n<\/ul>\n<h2>\u00a0A Survey of Abused Drugs<\/h2>\n<h3>What Abused Drugs have in common<\/h3>\n<ul>\n<li><strong>iucleus Accumbens<\/strong>: areas with axons that directly\/indirectly increase release of dopamine\/norepinephrine; central to reinforcing experiences (ex: sexual excitement, sugar, imagine something pleasant)<\/li>\n<li>Reinforcement involves wanting (motivation; more brain) and liking (pleasure) Addictive drugs activate nucleus accumbens by releasing dopamine or norepinephrine; show drive to obtain drug even if it doesn\u2019t provide pleasure<\/li>\n<\/ul>\n<p>(liking-wanting)<\/p>\n<h3>Stimulant Drugs<\/h3>\n<ul>\n<li>Increase excitement, alertness, activity while elevating mood and decreasing fatigue<\/li>\n<li>Amphetamine\/cocaine stimulate dopamine synapses in nucleus accumbens by increasing the presence of dopamine in presynaptic terminal<\/li>\n<li>Presynaptic terminal usually reabsorbs released dopamine through dopamine transporter; drugs inhibit transporter, decreasing reuptake, prolonging effects of dopamine<\/li>\n<li>Amphetamines have similar effects on serotonin\/norepinephrine receptors, methamphetamines have similar effects but stronger<\/li>\n<li>Stimulant drugs increase accumulation of dopamine in synaptic cleft; excess dopamine in synapse washes away faster, presynaptic cell makes more to replace it. After use, deficit of neurotransmitters \uf0e0 withdrawal (reduced energy, motivation and depression)<\/li>\n<li>Varied behavioural affects; low doses: increase attention (treat ADHD); high doses: impair attention and learning, alters blood flow thereby increase risk of stroke and epilepsy<\/li>\n<li><strong>Methylphenidate <\/strong>(Ritalin) \uf0e0 (stimulant) prescribed for ADHD \uf0e0 block reuptake of dopamine; same affect as cocaine, but cocaine produces a rush effect on brain when sniffed, Ritalin has gradual increase in concentration then slow decline.<\/li>\n<li>Those with ADHD more likely to abuse tobacco, alcohol, other drugs <strong>iicotine<\/strong><\/li>\n<li>Compound in tobacco, stimulates Ach receptors (nicotine receptors); many exist on neurons that release dopamine in nucleus accumbens; decreased dopamine release; Nicotine increases dopamine release in same cells cocaine stimulates (Nicotine enhances reward)<\/li>\n<li>Repeated exposure to nicotine \uf0e0 receptors in nucleus accumbens become more sensitive to nicotine; less responsive to other kinds of reinforcement <strong>Opiates<\/strong><\/li>\n<li>Derived from opium poppy (morphine, methadone, heroin) heroin enters brain faster than morphine \uf0e0 bigger rush of effect\/more addictive<\/li>\n<li>Relax people, decrease attention, decrease pain sensitivity<\/li>\n<\/ul>\n<p>Used as painkillers<\/p>\n<ul>\n<li>Opiates attach to specific receptors in brain meant for certain neuropeptides called <strong>endorphins<\/strong> (relieve pain by acting on receptors)<\/li>\n<li>Endorphins indirectly activate dopamine release; synapses inhibit neurons that release GABA (inhibit dopamine) \uf0e0 increase dopamine release<\/li>\n<li>Endorphins have rewarding effects too, and also depend on dopamine <strong>Marijuana<\/strong><\/li>\n<li>Contain THC and cannaboids (used to relieve nausea, combat glaucoma)<\/li>\n<li>Psychological effects: intense sensory experience, illusion time slowed down, impaired memory and cognition<\/li>\n<li>Cannaboids receptors abundant (not in medulla; controls breathing\/heart)<\/li>\n<li>2 chemicals that bind to cannaboids receptors: anandamide, and 2-AG<\/li>\n<li>Cannaboid receptors located on presynaptic neuron: when certain neurons depolarized, release chemicals as retrograde transmitters that travel back to incoming axons, inhibit further release of glutamate or GABA. Tell presynaptic cell that message received, even though nothing released; chemicals in marijuana decrease excitatory\/inhibitory messages<\/li>\n<li>Cannaboids increase release of dopamine indirectly; inhibit GABA in midbrain (major source of axons that release dopamine in nucleus accumbens); increases activity of neurons that release dopamine<\/li>\n<li>Relieve nausea, stimulate receptors that increases rewarding value of a meal <strong>Hallucinogenic Drugs<\/strong><\/li>\n<li>Distort perception (ex: LSD resemble serotonin and provide stimulation at inappropriate times\/longer duration)<\/li>\n<li>MDMA (ecstasy): stimulant at low doses \uf0e0 increase dopamine release; higher doses &#8211;&gt; releases serotonin, alters perception and cognition; side-effects: lethargy, depression, increased body temperature<\/li>\n<li>Repeated users: long-term loss of serotonin receptors \uf0e0 depression, anxiety, impaired learning\/memory<\/li>\n<\/ul>\n<h2>\u00a0Alcohol and Alcoholism<\/h2>\n<ul>\n<li>Habitual use of alcohol despite medical\/social harm (most common of abused drugs)<\/li>\n<li>Moderate amounts: relaxes people, decrease anxiety; larger amounts: causes health problems, impairs judgement<\/li>\n<\/ul>\n<p>Affect on neurons: response at GABA receptor (inhibitory: risky behaviors), blocks glutamate receptors (excitatory: increase stimulation of dopamine receptors) \uf0e0 decreased brain activity. <strong>Genetics<\/strong><\/p>\n<ul>\n<li><strong>Type I (A)<\/strong>: develop alcohol problems gradually, 25+, may\/may not have relatives with history of alcohol abuse<\/li>\n<li><strong>Type II (B)<\/strong>: rapid onset, before 25, close relatives with alcohol problems<\/li>\n<li>Genes influences chance of alcoholism in many ways (ex: dopamine type 4 receptor has 2 forms, long form less sensitive \uf0e0 craves more alcohol)<\/li>\n<li>Gene controls COMT (enzyme breaks down dopamine after release); active form<\/li>\n<\/ul>\n<p>\uf0e0 breaks down more dopamine \uf0e0 decrease reinforcement \uf0e0 more impulsiveness<\/p>\n<ul>\n<li>Genes influence alcohol: effects on risky behaviour, responses to stress, reactions to anxiety-provoking situations<\/li>\n<li>Prenatal environment contributes to risk of alcoholism: if mother drinks alcohol during pregnancy \uf0e0 increase chance child will be an alcoholic<\/li>\n<li>Biological forces interact with stressful experiences, opportunities for alcohol use and other environmental factors <strong>Risk Factors<\/strong><\/li>\n<li>People at risk: impulsive, risk-taking, easily bored, sensation seeking, outgoing<\/li>\n<li>Sons of alcoholics often alcoholics themselves: less intoxication after drinking, decreases stress more (in sons of alcoholics), smaller amygdala in right hemisphere (predisposition to alcohol abuse) <strong><u>Addiction <\/u><\/strong><\/li>\n<li>Habit does more harm than good, pleasure becomes weaker while risks increases; still difficult to quit<\/li>\n<\/ul>\n<h3>Tolerance and Withdrawal<\/h3>\n<ul>\n<li><strong>Tolerance<\/strong>: As addiction develops, many effects decrease; learned response<\/li>\n<li><strong>Withdrawal<\/strong>: As body expects a drug, reacts strongly when absent<\/li>\n<li>Effect of drug cessation (anxiety, sweating, diarrhea, irritability, fatigue, convulsions, insomnia, headache, distress)<\/li>\n<li>Addiction is seen as an attempt to avoid withdrawal symptoms<\/li>\n<li>Someone with an addiction learns to use substance to cope with stress<\/li>\n<li>Receiving a drug in withdrawal period is powerful; user learns drug relieves distress caused by withdrawal \uf0e0 generalizes to other situations \uf0e0 learn to crave the drug during all types of distress<\/li>\n<\/ul>\n<p><em>\u00a0<\/em><\/p>\n<h3>Cravings in Response to Cues<\/h3>\n<ul>\n<li>User learns to associate cues with a drug; after abstinence, exposure to cues triggers renewed craving; drug-related cue increases activity in nucleus accumbens and several related areas, but after instruction to inhibit craving, people can decrease arousal <strong>Brain Reorganization<\/strong><\/li>\n<li>Addiction hijacks person\u2019s motivation \uf0e0 changes brain so reinforcing experiences become less powerful and less able to compete with the drug<\/li>\n<li>Events change expression of genes<\/li>\n<li>Cocaine increases certain genes that control changes in dendrites within nucleus accumbens \uf0e0 drug stimulates more dendrites, other events stimulate fewer, sexual stimulation less rewarding, induce changes that impair extinction (drug-seeking response of reinforcement ceases, even if drug less enforcing, responding persists)<\/li>\n<\/ul>\n<h2>\u00a0Medications to Combat Substance Abuse<\/h2>\n<p>\uf0b7 Overcome substance abuse: AA, NA, psychotherapy, medication available<\/p>\n<h3>Medications to Combat Alcohol Abuse<\/h3>\n<ul>\n<li>After someone drinks ethyl alcohol, enzymes in liver metabolize it to acetaldehyde (poison); acetaldehyde dehydrogenase, converts acetaldehyde to acetic acid (chemical body uses for energy)<\/li>\n<li>People with weaker gene for acetaldehyde dehydrogenase, metabolize acetaldehyde slower \uf0e0 accumulate enzyme \uf0e0 flushed face, increased heart rate, impaired breathing, tissue damage<\/li>\n<li><strong>Disulfiram<\/strong> <strong>(Antabuse)<\/strong>: antagonize effects on acetaldehyde dehydrogenase, binding it to copper ion \uf0e0 lead to illness\/vomiting; works when supplements alcoholic\u2019s commitment to stop drinking (take daily pill)<\/li>\n<li>Drink alcohol then take a drug that produces nausea \uf0e0 learned aversion to the taste of alcohol. Effective, but not for long-term<\/li>\n<li>Naloxone: blocks opiate receptors, decrease pleasure from alcohol; works with people motivated to quit; more with Type II then I <strong>Medications to Combat Opiate Abuse<\/strong><\/li>\n<li>Switch to <strong>methadone<\/strong>: taken orally, gradually enters blood stream and brain, effects slowly, withdrawal symptoms more gradual, avoid use of injection<\/li>\n<li>LAAM (similar to methadone) used to treat opiate addiction; produce long-term effect \uf0e0 visit clinic 3x\/week (not daily) \uf0e0 live healthier and longer, easier to hold a job<\/li>\n<li>These drugs don\u2019t end addiction, just satisfy craving in a safer way<\/li>\n<\/ul>\n<p>\uf0b7<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Cajal: anatomically demonstrated narrow gap separating neurons Sherrington: physiologically demonstrated communication between neuron and next differs from communication along single axon Synapse &#8211;&gt; specialized gap between neurons The Properties&hellip; <a class=\"continue\" href=\"https:\/\/www.amyork.ca\/academic\/zz\/biological-basis-of-behaviour\/the-concept-of-synapses\/\">Continue Reading<span> The concept of synapses<\/span><\/a><\/p>\n","protected":false},"author":4,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[114],"tags":[],"_links":{"self":[{"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/posts\/4499"}],"collection":[{"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/users\/4"}],"replies":[{"embeddable":true,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/comments?post=4499"}],"version-history":[{"count":0,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/posts\/4499\/revisions"}],"wp:attachment":[{"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/media?parent=4499"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/categories?post=4499"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/tags?post=4499"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}