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FAU / Psychobiology / PSB 3002 / Why would someone want to escape into substances and be at risk of an

Why would someone want to escape into substances and be at risk of an

Why would someone want to escape into substances and be at risk of an

Description

School: Florida Atlantic University
Department: Psychobiology
Course: Biological Bases of Behavior
Professor: Lauren mavica
Term: Spring 2017
Tags: Psychology, Biology, and behavior
Cost: 50
Name: FINAL EXAM Study Guide (Bio Bases of Behavior)
Description: Study guide on Chapters 14 and 7 for Dr. Mavica's Biological Bases of Behavior final exam
Uploaded: 04/27/2017
17 Pages 96 Views 5 Unlocks
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Final Exam – Study Guide


Why would someone want to escape into substances and be at risk of an addiction?



Biological Bases of Behavior

Chapter 14: PSYCHOLOGICAL DISORDERS

Substance Abuse and Addiction 

. ADDICTION = condition marked by repetitive craving and potential to dominate/harm one’s life - Examples: alcohol, drugs, gambling, overeating, videogames

- As an addiction progresses, the pleasures become weaker while the costs and risks increase

Drug mechanisms 

. Most commonly abused drugs are derived from plants (nicotine, caffeine, cocaine, opiates) . ANTAGONIST = drug that blocks a neurotransmitter

. AGONIST = drug that mimics/increases effect

. AFFINITY = tendency of drug to bind to receptor (ranges from strong to weak) . EFFICACY = tendency to activate receptor


What drug blocks neurotransmitters?



If you want to learn more check out What is the second leading cause of cancer deaths in the united states?

- Drug’s effectiveness/side effects vary from person to person (abundance of each type  type of receptor varies between individuals)

- A drug that binds to a receptor but fails to stimulate it has a high affinity but low  efficacy.

. Nearly all abused drugs increase activities at DOPAMINE and NOREPINEPHRINE SYSTEM - NUCLEUS ACCUMBENS = central to reinforcing experiences of all types and location where  addictive drugs release dopamine and norepinephrine

- Sexual excitement, music, sugar, imagining something pleasant also release dopamine in   nucleus accumbens

. Other commonalities between addictions:

- Many people with addiction have more than one addiction

- Abuse of cocaine/amphetamine leads to greater impulsiveness than abuse of opiates - Opiates impair learning more than stimulants


What is the effect of a drug that is an agonist?



If you want to learn more check out What is the process of understanding?

- Higher doses of stimulants drugs impair attention/ learning

Cravings 

. Insistent search for activity (distinctive feature of addictions)

. Even after a long period of abstinence, VISUAL CUES can trigger craving

. Rat study: exposure to addictive substance alters receptors to become more responsive to the   addictive substance and less responsive to other reinforcers

Tolerance and Withdrawal 

. TOLERANCE = decrease in effect as addiction develops

- Drug tolerance is learned to an extent (can be weakened through extinction procedures) . WITHDRAWAL = body’s reaction to absence of drug  

- Person with addiction may use substance to cope with stress

- Studies in rats have shown:  If you want to learn more check out What is the meaning of a low mass star?

 a. Receiving addictive drug during withdrawal is a powerful experience

 b. Associated relief can cause craving of drug under other stressful experiences

Predispositions 

. Certain aspects of brain function and behavior are present from the start in people with familial  disposition to addiction (but not necessarily all of them develop it)

. Genetic influences:

- Twin studies: strong influence of genetics on vulnerability to alcohol and drug abuse - Many addiction-linked genes have been identified, each with a small effect . Environmental influences:

- Prenatal environment contributes to risk for alcoholism  

- Careful parenting supervision decreases likelihood of developing impulsive behavior . TYPE 1 (A) ALCOHOLICS = develop alcohol problem gradually, after age 25  - Depends more on a stressful life and less on genetics

- Generally less severe and more likely to respond well to treatment

. TYPE 2 (B) ALCOHOLICS = associated with early onset, before 25

Behavioral predispositions of abuse 

. Research findings:

- Sons of alcoholics show less than average intoxication after drinking moderate amount a. Low level of intoxication may influence person to keep drinking

b. 60% or more probability of developing alcoholism We also discuss several other topics like Given the amino acids d – k what is the pi?

- Alcohol decreases stress for most people but MORE for sons of alcoholics

Treatments 

. Some are able to decrease addiction on their own

. Alcoholics Anonymous (or similar groups)

. Cognitive-behavioral therapy = contingency management includes rewards for remaining drug free . Medications:

- ANTABUSE (disulfiram): sickness after drinking

- NAUSEA-INDUCING DRUG: associate the two (not popular)

- NALOXONE/NALTREXONE: block opiate receptors

- METHADONE: to combat opiate abuse

a. Safer alternative (similar to heroine/morphine)

b. Activates same brain receptors and has same effects

c. Can be taken orally, absorbs/leaves brain slowly (‘rush’ and withdrawal reduced) - Drug effectiveness varies with user’s motivation to qui

Mood Disorders 

Major Depressive Disorder

. Changes in the synapses to the nucleus accumbens make it less responsive to reward . Absence of happiness is a more reliable symptom than increased sadness

- After 14: more common in women

- In children: likely to persist a long time

- Affects 5% of a adults in a given year (10% lifetime prevalence

. Symptoms:

- Feel sad/helpless most of the day every day for long period of time

- Person doesn’t enjoy anything and can’t imagine enjoying anything

a. Experiment: people report average number of unpleasant things as normal people  but far LESS pleasant ones If you want to learn more check out What is the definition of theory?

- Fatigue, feelings of worthlessness, contemplation of suicide

- Trouble sleeping/concentrating

- NUCLEUS ACCUMBENS: less sensitive ???? less reward ???? less motivation  

Genetics 

. Moderate degree of heritability

. No one gene has been identified as clearly linked to depression If you want to learn more check out What is the standards gap?

. EARLY ONSET (before 30)

- More likely to have relatives with depression

- Relatives have other psychological disorders (i.e bipolar)  

. LATE ONSET (after 45)  

- Linked to relatives with circulatory problems

. Hypothesis: effect of genes varies with environment

- Evidence: people with two double short form of serotonin transporters who experienced  stressful experiences had major increase in probability of developing depression   (may be linked to early childhood maltreatment)  

Abnormalities of hemisphere dominance 

. Brain activity associated with depression:

- Decreased activity in left prefrontal cortex

- Increased activity in right prefrontal cortex

- Imbalance stable over the years, despite symptom changes

. People with depression tend to gaze to the left in verbal task (indicating activity in right hemisphere)

Antidepressant drugs 

. Many psychiatric drugs discovered by accident

. Categories:

1) TRICYCLICS  

- Block transporter proteins (ion channels) that reabsorb serotonin, dopamine, norepinephrine   into presynaptic neuron after release (prolong their presence in the synaptic cleft, where they   continue stimulating the postsynaptic cell)

- Also block histamine/acetylcholine receptors and some sodium channels

- Side effects: drowsiness, dry mouth, difficulty urinating, heart irregularities

- Example: imipramine (Tofranil)

2) SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIs)

- Block reuptake of serotonin (work like tricyclics but ONLY for serotonin)

- Example: fluoxetine (Prozac), sertraline (Zoloft), fluvoxamine (Luvox), citalopram (Celexa),  paroxetine (Paxil)

3) SEROTONIN NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIs)

- Block reuptake of serotonin/norepinephrine

- Example: duloxetine (Cymbalta), venlafaxine (Effexor)

4) MONOAMINE OXIDASE INHIBITORS (MAOIs)

- Block monoamine oxidase that metabolizes catecholamines/serotonin into inactive forms - Result: more transmitters in presynaptic terminal available for release

- Usually only prescribed if SSRIs/Tricyclics are not effective

- Side effects: high blood pressure results with some foods

5) ATYPICAL ANTIDEPRESSANTS

- Miscellaneous group of drugs with antidepressant effects and milder side effects - Example: bupropin (Wellbutrin) inhibits reuptake of dopamine and some norepinephrine but  NOT serotonin

Why are antidepressants effective? 

. Most people with depression have normal levels of neurotransmitters

- Decreasing serotonin in control groups does not provoke depression

. Drugs affect proliferation of neurons

- Not about increasing number of neurotransmitters in synapse (since that is done quickly but  improving effects take weeks)

- Proliferation of neurons ???? synaptic plasticity (ability to learn new ways to cope) . People with depression have lower than average brain-derived neurotrophic factor (BDNF): important  for synaptic plasticity

- Result = people with depression show:

a. Smaller than average hippocampus

b. Impaired learning

c. Reduced production of hippocampal neurons

. Prolonged use of antidepressants increase BDNF

. Proliferation of new neurons in the hippocampus is important for antidepressant effects . Studies show that antidepressants may not be helpful at all (especially for mild depression)

Alternatives to antidepressant drugs 

1) COGNITIVE-BEHAVIORAL THERAPY

- Shown to be equally effective for all levels of depression

- Cause increased metabolism in the same brain areas as antidepressants do

- More likely to reduce relapse months/years later

- Exercise: modest benefits

2) ELECTROCONVULSIVE THERAPY (ECT)

- Electrically induced seizure used for treatment of severe depression

- For patients who have not responded to antidepressant medication

- Side effects: memory impairment (minimized when shock is only to right hemisphere) - High risk of relapse without continued treatment

- How ECT relieves depression is unknown (proliferates neurons in hippocampus)

3) TRANSCRANIAL MAGNETIC STIMULATION

- Magnetic field stimulates axons close to the brain’s surface

4) DEEP BRAIN STIMULATION

- Physician implants battery powered device into brain to deliver periodic stimulation - Targets brain areas that increase activity as a result of antidepressants

- Still in experimental stage but has encouraging results

Altered sleep patterns 

. Disruption of sleep is patterns is common in depression:

- Typically fall asleep but awaken and early and can’t go back to sleep

- Enter REM within 45 min

- Sleep pattern disruption in young people increases likelihood of depression - Circadian rhythm: depressed people going to sleep at normal time have same pattern as   normal people going to sleep late

. Combining periodic sleep deprivation with antidepressants sometimes helps

Unipolar/Bipolar Disorder

. UNIPOLAR = characterized by alternating states of normality and depression . BIPOLAR (formally maniac-depressive disorder)

- Characterized by alternating states of depression and mania  

- Mania: restless activity, excitement, laughter self-confidence, rambling speech, no inhibition

Bipolar Disorder 

. BIPOLAR I = characterized by full blown mania episodes

. BIPOLAR II = much milder manic phases (hypomania)

. Onset: teenage years/early 20s

. Brain’s use of glucose increases during periods of mania and decreases during periods of depression . Treatments:

- LITHIUM = salt that stabilizes mood and prevents relapse in mania or depression - Drugs work by =  

a. Decreasing glutamate activity

b. Blocking synthesis of brain chemical arachidonic acid (produced during brain   inflammation)

Seasonal Affective Disorder (SAD) 

. Form of depression that regularly occurs during a particular season  

- Most prominent towards the poles where winter nights are long

. Patients with SAD have phase-delayed sleep and temperature rhythms

- Most depressed people have phase-advanced patterns

. Treatment: often uses bright lights

- Used one hour or more daily

- Benefits are unexplained but substantial

. Many people with SAD have a mutation on a gene responsible for regulating circadian rhythms

Schizophrenia

. Deteriorating ability to function in everyday life for at least 6 months, paired with at least 2 of the  following symptoms, including at least one of the first three:

- Hallucinations (like hearing voices)

- Delusions (unjustifiable beliefs)

- Disorganized speech

- Grossly disorganized behavior

- Weak/absent signs of emotion, speech, socialization

. Diagnosis:

- POSITIVE SYMPTOMS: behaviors that are present that should be absent (hallucinations, delusions, disorganized speech/behavior)

- NEGATIVE SYMPTOMS: absent behaviors that should be present (weak emotion, speech, and  socialization). Usually stable over time and difficult to treat

- Cognitive symptoms

a. Limitations of thought and reasoning common in schizophrenia

b. Example: difficulty using and understanding abstract concepts

c. Hypothesis: due to impairments in attention and working memory

. Differential diagnosis = rules out other conditions with the same symptoms

- Conditions that resemble schizophrenia

a. Substance abuse

b. Brain damage

c. Undetected hearing deficits

d. Huntington’s disease

e. Nutritional abnormalities

Demographic data 

. Half of one percent affected worldwide

. More common for men than women

. Occurs in all ethnic groups and all parts of the world

. Reported prevalence has been declining in many countries since mid-1990s

. Many mysteries remain: links to diabetes and colon cancer, characteristic body odor, and deficits in   pursuit eye movements

Genetics 

. Research suggests a genetic component, but does not depend on a single gene . Monozygotic twins have a much higher concordance rate (agreement) than dizygotic twins - BUT monozygotic twins only have a 50 percent concordance rate

. Greater similarity between dizygotic twins than siblings: prenatal/postnatal environmental effect . Adopted children studies suggest a genetic role

- Prenatal environment of the biological mother cannot be discounted

- Environmental influence shown to have a role (greater risk if dysfunctional adopting family)

Prenatal and Neonatal Environment 

. Intermediate risk factors:

- A father over 55 years old

- Living in a crowded city

- Toxoplasma gondii: parasite reproduced in cats that infects brain of child and affects   development (presence of antibodies to it suggests the child had the  

 parasite and now has more risk to develop schizophrenia)

. Low risk factors:

- Poor maternal nutrition

- Premature birth or low birth weight

- Complications during delivery

- Head injuries in early childhood

- Extreme stress of mother during pregnancy

. Mother/child blood type differences increase the likelihood of schizophrenia

- If the mother has a Rh-negative blood type and baby is Rh-positive: child twice as probable of   developing schizophrenia

- Response weak in first child but stronger in later pregnancies, and especially for boys\

. Season-of-birth effect

- Tendency for people born in winter to have slightly (5-8%) greater probability of developing   schizophrenia

- More pronounced in latitudes far from the equator

- Possible explanation: increased likelihood of viral infection in mother (get more colds) - Result of viral infections in the mother:

a. Increased cytokines in the mother that impairs brain development of fetus b. Fever that slows divisions of fetal neurons

- Conclusion: wide variety of genetic and environmental influences can cause schizophrenia

Mild Brain Abnormalities 

. Most people with schizophrenia have:

- Less gray matter and white matter an larger than average ventricles

- Minor abnormalities in subcortical areas

- Smaller hippocampus: areas of increased metabolism, followed by atrophy

- Deficits of memory and attention consistent with damage to the prefrontal cortex . Lateralization difference:

- Right planum temporale slightly larger

- Lower than normal activity in left hemisphere

- More likely to be left-handed

Treatments 

1) Chlorpromazine (Thorazine)

- Drug used to treat schizophrenia

- Relieves the positive symptoms of most patients

2) Antipsychotic/neuroleptic drugs

- Category of drugs tend to relieve schizophrenia and similar conditions

- Two chemical families:

a. Phenothiazines: includes chlorpromazine b. Butyrophenones: includes halperidol (Haldol) - Dopamine hypothesis of schizophrenia

Both block dopamine synapses

a. Schizophrenia results from excess activity at dopamine synapses in areas of the brain b. Research: shows increased activity specifically at the D2 receptor (twice as many  receptors occupied than normal)

- Substance-induced psychotic disorder

a. Hallucinations and delusions resulting from repeated large doses of amphetamines,  methamphetamines, or cocaine

• Each prolongs activity at dopamine synapses

The Role of Glutamate 

. Hypothesis: problem relates partially to deficient activity at glutamate synapses, especially in the   prefrontal cortex

- In many brain areas, dopamine inhibits glutamate release

- Alternately, glutamate stimulates neurons that inhibit dopamine release

- Increased dopamine thus produces the same effects as decreased glutamate . Two Dopamine Pathways:

 1) The mesolimbocortical system

- Set of neurons that project from midbrain tegmentum to limbic system and prefrontal cortex - Site where drugs that block dopamine synapses produce their benefits

 2) The mesostriatal system

- Drugs also block dopamine in the mesostriatal system that projects to the basal ganglia - Result: tardive dyskinesia, characterized by tremors and involuntary movements

Second-Generation Antipsychotics 

. Atypical antipsychotics: clozapine, amisulpride, risperidone, olanzapine, aripiprazole - Seldom produce movement problems

- Less effect on dopamine D2 receptors than haloperidol

- More strongly antagonize serotonin type 5-HT2 receptors

Autism Spectrum Disorder

. Includes autism and what was called Asperger’s syndrome in the past

. Includes people with varying degrees of difficulty (from relatively mild to severe) . Once rarely diagnosed (more commonly diagnosed today)

. Much more common in boys than in girls

Characteristics 

. Deficits in social and emotional exchange

. Deficits in nonverbal communications: gestures, facial expressions

. Repetitive movements

. Resistant to change in routine

. Unusually weak or strong responses to stimuli

Causes 

. Infants with autism make a normal amount of eye contact at two months

- Eye contact declines over time

. Genetics and other causes

 - Many genes linked to autism, but no one gene is found in a high percentage   - Many cases may result from mutations and microdeletions in one or more genes . Some mothers of children with autism have antibodies that attack certain brain proteins . Prenatal nutrition: adequate amounts of folic acid during pregnancy halves risk of autism in child

Treatments 

. No medical treatment for central problems of decreased social behavior and communication . Risperidone: sometimes reduces stereotyped behaviors but has serious side effects . Behavioral treatments focus on attention and reinforcing favorable behaviors

Chapter 7: MOVEMENT

Control of Movement 

. Brain linked to concept of doing something: MOVEMENT

. Internal processing would be useless without movement

Muscles 

. All normal movement depends on muscle contractions

- SMOOTH = control digestive system and other organs

- SKELETAL/STRIATED = control of movement of body in relation to environment  - CARDIAC = properties of skeletal/smooth (has to be different)

Muscle Fibers 

. Muscles are composed of many individual fibers

- Each fiber receives info from ONLY one axon but a single axon may innervate many fibers - The LESS fibers an axon innervates, the MORE precision (eg: the eye)

- Example: the eye muscles have a ratio of about one axon per three muscle fibers, and the   biceps muscles of the arm have a ratio of one axon to more than a hundred fibers . NEUROMUSCULAR JUNCTION = synapse between motor neuron axon and fiber . Release of acetylcholine cause muscle to contract (absence of it = muscle relaxes)

* Video details:

. Action potential ???? motor neuron ???? skeletal muscle fiber

- Excites at neuromuscular junction (chemical synapse): point of contact between axon terminals  and the motor end plate of the skeletal muscle fiber

- Steps:

1) Action potential travels length of axon of motor neuron to an axon terminal 2) Voltage-gated calcium channels open and calcium ions diffuse into the terminal 3) Calcium entry causes synaptic vesicles to release acetylcholine via exocytosis 4) Acetylcholine diffuses across synaptic cleft and binds to receptors which contain ligand gated cation channels

5) Ligand-gated cation channels open

6) Sodium enters the muscle fiber, potassium exits it: less negative membrane 7) Action potential

. Neural transmission to muscle fiber ceases when acetylcholine is removed from synaptic cleft - Can be removed in two ways:

1) Acetylcholine diffuses away from the synapse

2) Broken down by acetylcholinesterase (enzyme) to acetic acid and choline (choline then  transported into axon terminal for the resynthesis of acetylcholine)

Antagonistic muscles 

. Movement requires alternating contraction of opposing set of muscles

. Acetylcholine always EXCITES skeletal muscles to CONTRACT

- FLEXOR = flexes/raises and appendage (bicep)

- EXTENSOR = extends/straightens appendage (triceps)

- Both can’t contract at same time  

- Example: At your elbow, your flexor muscle brings your hand toward your shoulder and   your extensor muscle straightens the arm

Fast and Slow Muscles 

. Skeletal muscles range from:

- FAST-TWITCH = fibers produce fast contractions but fatigue rapidly  

a. Anaerobic and use reactions that don’t require oxygen (depend on fatty acids) b. Behaviors requiring quick movements use these

- SLOW-TWITCH = fibers produce less vigorous contraction without fatigue

a. Aerobic and require oxygen during movement

b. Nonstrenuous activities utilize these and intermediate fibers

. People have varying percentages of fast-twitch/slow-twitch muscles based on genetics/training . Temperature:

- Cold: muscles work slower (chemical process) ???? rely more on white muscles

- Fish need to compensate speed in cold water by recruiting more muscles (not making a set   work harder)

- A fish has 3 kinds of muscles:

a. RED = produce slowest movements but don’t fatigue (duck meat: travel big distances) b. PINK = intermediate in speed/rate of fatigue

c. WHITE = produce fastest movements but fatigue rapidly (chicken meat)

Muscle control by proprioceptors 

. PROPRIOCEPTORS = receptors that detect position/movement of body part

1) Muscle spindles

- Proprioceptors parallel to muscle that respond to a stretch (negative feedback: causes   contraction of muscle)

- A stretch reflex occurs when proprioceptors detect stretch and send messages to spinal   cord to contract it (CAUSED by stretch, doesn’t produce one)

2) Golgi Tendon Organ

- Proprioceptor that responds to increase in muscle tension

- Located in tendons at opposite ends of muscle (while muscle spindles ON muscle) - Acts as brake against excessively vigorous contraction by sending and impulse to spinal   cord where motor neurons are inhibited (muscle relaxes)

Voluntary/Involuntary movements 

. REFLEXES = involuntary (insensitive to reinforcement/punishment/motivation), consistent, automatic  response to stimuli

. Most movements are a combination of involuntary and voluntary (reflexive/non-reflexive) - Example: walking

. Some movements are ballistic (can’t be changed once initiated)

. Others are guided by feedback

Sequences of Behavior 

. Many behaviors consist of rapid sequences of individual movements

. CENTRAL PATTERN GENERATORS= neural mechanisms in spinal cord/elsewhere that generate rhythmic   patterns of motor output (wing flapping, wet dog shaking)

- Stimuli that activates it does not alter frequency of output (always same rate) - Example: cat will always scratch at same rate regardless of itching stimulus

. MOTOR PROGRAM = fixed sequence of movements that’s is either learned/built into nervous system  (yawning, mouse grooming itself)

- Once begun, sequence is fixed from beginning to end

- Automatic: thinking/talking about it interferes with action

- Affected by evolution: flight loss in ostriches

Brain Mechanisms of Movement 

. PRIMARY MOTOR CORTEX = in precentral gyrus in frontal lobe, in front of somatosensory cortex - Doesn’t send message DIRECLTY to muscles: axons from precentral gyrus connect to brainstem   and spinal cord, which generate impulses that control muscles

. Cerebral cortex is involved in complex movements

- Example: important for talking but no so much for involuntary actions

Planning a movement 

. Specific areas of primary motor cortex control specific areas of opposite side of body (some overlap) . Motor areas of human cortex:

1) PRIMARY MOTOR CORTEX

- Active when people INTEND a movement

- Orders an OUTCOME: spinal cord receives order, figures out muscle combinations a. Cortical activity represents idea of movement, not just muscle contraction  

 (lead to a particular outcome regardless of the contractions needed)

2) SOMATOSENSORY = communication between sensing/moving is essential

- Motor cortex represents body parts aligned with those of somatosensory cortex 3) POSTERIOR PARIETAL = keeps track of position of body relative to the world - Damage to this area causes difficulty in coordinating visual stimuli

- Important for planning movement (in experiment: less active in delay phase when NO   movement was required)

Active during planning of a  movement

4) PREMOTOR = (in frontal lobe) active during preparation for movement

- Most active IMMEDIATELY BEFORE movement

- Receives info about a target and integrates info about position/posture of body to   organize direction of movement

5) SUPPLEMENTARY = organizes rapid sequences of movements in a specific order - Inhibitory if necessary (inhibit turning left where you’re used to if you have to go  somewhere else)

- Active seconds BEFORE the movement

6) PREFRONTAL CORTEX = stores sensory info relevant to a movement

- Active during a DELAY before a movement (inactive in dreams = illogic dreams) - Important for considering probable outcomes of possible movements

- Damage: disorganizes/illogic actions (absent-minded)

Inhibition of Movement 

. ANTISACCADE TASK = inhibits a saccade from one target to another

- Performing this well requires sustained activity in parts of prefrontal cortex and basal ganglia  before seeing moving stimulus

- Ability to do it matures through adolescence

Mirror neurons 

. Active during preparation of movement, while watching someone else perform same/similar  movement, while you are doing action or see cue of it (read about it, visualize it) - May be important for understanding, identifying, imitating others

- Unknown whether they cause/result from social behavior

. Thought to be born with it because babies imitate faces (especially tongue protrusion) - BUT need to practice first in order for mirror neurons to respond

- Conclusion: mirror neuron system NOT essential for learning movement if practice is needed

Connections from brain to spinal cord 

. Messages from brain must reach medulla/spinal cord to control muscles

. CORTICOSPINAL TRACTS = paths from cerebral cortex to spinal cord (both contribute in some way to  nearly all movements but a movement may rely more on one than the other) 1) LATERAL CORTICOSPINAL TRACT

- Set of axons from primary motor cortex/surrounding areas, red nucleus (midbrain area) to   spinal cord (info crosses before at pyramids of medulla)

- Controls movement in periphery areas on contralateral side (hands/feet)

- Red nucleus: output mainly to arm muscles

2) MEDIALCORTICOSPINAL TRACT

- Axons from many parts of cortex (reticular formation, midbrain tectum, vestibular nucleus) - Axons go to both sides of spinal cord

a. Allows control of muscles of neck, shoulders, trunk (bilateral)

b. Enables coordinated movements (walking, turning, standing, sitting, bending) . TOUCH PATHS = touch comes into left side of body and CROSSES at medulla and activates right side  (ascending) and vice versa (descending)

Disorders of spinal cord 

1) PARALYSIS = lack of voluntary movement in part of the body

- Cause: damage to spinal cord, motor neurons, or their axons

2) PARAPLEGIA = loss of sensation/voluntary muscle control in both legs. Reflexes remain. Genitals  respond reflexively to touch although no mssgs. pass between brain/genitals, and still  experience orgasm w/o genital sensations

- Cause: cut through spinal cord above the segments attached to legs

3) QUADRIPLEGIA = loss of sensation/muscle control in all 4 extremities

- Cause: cut through spinal cord above segments controlling arms

4) HEMIPLEGIA = loss of sensation/muscle control in arm and leg on one side

- Cause: cut halfway through the spinal cord or damage to one hemisphere of cortex 5) TABES DORSALIS = impaired sensation in legs/pelvis region, impaired leg reflexes/walking, loss  of bladder and bowel control

- Cause: late stage of syphilis, dorsal roots of the spinal cord deteriorate

6) POLIOMYELITIS = paralysis

- Cause: virus that damages cell bodies of motor neurons

7) AMYOTROPHIC LATERAL SCLEROSIS = gradual weakness/paralysis, starting with arms and then  legs. Motor neurons and axons from brain to motor neurons are destroyed

- Cause: unknown

Cerebellum 

. Structure in brain associated with balance/coordination

. More neurons in cerebellum than in all other brain areas combined

. Damage: trouble with rapid movements requiring aim/timing

- Example: clapping hands, speaking, writing, etc.

- BUT can do continuous tasks (drawing circles)

- Symptoms resemble those of someone intoxicates

. Functions:  

- Important for establishment of new motor programs that allow the execution of a sequence of   actions as a whole (tasks that need timing)

- Critical for aspects of attention: ability to shift attention and to attend to visual stimuli - Responds to violations of sensory stimuli  

. Cellular organization

- Cerebellum receives input from spinal cord and from each of the sensory systems, and sends it  back to cerebellar cortex (surface of cerebellum)

- Cerebellar cortex neurons arranged in precise geometrical patterns that provides outputs of  well-controlled duration

a. PURKINJE CELLS = flat parallel cells in sequential planes

b. PARALLEL FIBERS = axons parallel to one another, perpendicular to Purkinje cells c. The greater amount of Purkinje cells excited, the greater their collective duration of  response (cerebellum control duration of movement)

d. Parallel fibers excite Purkinje and these transmit inhibitory messages to cells in nuceli of  cerebellum (cluster of cell bodies in its interior) and vestibular nuclei (in brain stem) e. Messages then sent to midbrain/thalamus

Basal Ganglia 

. Group of large subcortical structures in forebrain

. Responsible for initiating action NOT guided by a stimulus (essential for NEW movements, not guiding  old ones)

. Comprises:

- CAUDATE NUCLEUS - PUTAMEN  

STRIATUM/DORSAL STRIATUM

Receive input from cerebral cortex and send output to global pallidus

- GLOBAL PALLIDUS: Connects and INHIBITS thalamus, which relays info to motor areas   and prefrontal cortex

. Basal ganglia selects movement to make by CEASING to inhibit it (activity = lack of inhibition) . Pathways:

1) DIRECT = from striatum, inhibits global pallidus

- Inhibiting and inhibitor ???? NET RESULT = excitation

2) INDIRECT = essential for learning, inhibits inappropriate competing movements to those that the   direct pathway is trying to enhance

. Brain Areas and Motor Learning: learning of new skills requires brain areas that control movement - BASAL GANGLIA = critical for learning motor skills, organizing sequences of movement,  “automatic” behaviors, new habits (driving car)

- Pattern of activity of neurons in motor cortex becomes more consistent as new skill is learned

Conscious decision of movement 

. Conscious decision to move and movement occur at 2 different times

. READINESS POTENTIAL = type of activity in motor cortex that occurs BEFORE any voluntary movement - Begins at least 200 ms before movement

- Implies we become conscious of decision to move AFTER the process has already begun   (Libet’s study)

MOVEMENT DISORDERS 

. Brain disorders (Parkinson’s/Huntington’s) not only affect movement, also mood, memory, cognition

Parkinson’s

. Movement disorder characterized by muscle tremors, rigidity, slow movements, difficulty initiating  physical/mental activity (1 to 2% of people over 65 affected)

- Impairment in initiating spontaneous movement in absence of stimuli to guide action - Other symptoms: depression, memory/reasoning deficits, loss of olfaction, cognitive deficits . A loss of dopamine-releasing axons to the striatum (part of the basal ganglia)

Immediate Causes 

. Gradual and progressive death of neurons (especially in substantia nigra)

- Substantia nigra usually sends dopamine-releasing axons to caudate nucleus and putamen - Decreased excitation from sub. nigra to putamen/all consequent steps ???? NET RESULT: less excitation from thalamus to cortex

. Loss of dopamine leads to less stimulation of motor cortex and slower onset of movements . Genetic influence:

- Genetic link for EARLY ONSET  

- Genetics is small factor in LATE ONSET (after 50)

- 20 genes identified that could increase risk but lots of individual differences

- Twin studies: more recent research suggests disease not as hereditary as once thought to be . Environmental influence

- Exposure to toxins, insecticides, herbicides, fungicides (common in farmers, rural areas) - MPTP: synthetic heroin that accumulates in neurons and impairs mitochondria to move from cell body to synapse

. Traumatic head injury

. Study: cigarretes/coffee are related to decreased chance of Parkinson’s

. Damaged mitochondria of cells: common to most factors that increase probability of Parkinson’s . Parkinson’s probably results from a mixture of causes we don’t fully understand yet

Treatments 

. Drug L-dopa: primary treatment (precursor to dopamine that easily crosses blood-brain barrier) - Often ineffective (especially for those in late stages)

- Doesn’t prevent continued loss of neurons

- Enters other brain cells producing unpleasant side effects

. Drugs that directly stimulate dopamine receptors and drugs that block its metabolic breakdown - Reduce symptoms but don’t halt underlying disease

. Implanting electrodes to stimulate areas deep in brain

. Experimental strategies:

- Transplanting brain tissue of aborted fetuses (4 to 8 needed)  

a. Small benefits (people getting this procedure already too far into disease)

b. Implantation of stem cells (immature cells that can differentiate into any type)   programmed to produce lots of L-dopa

. Brain transplant (in sub. nigra for example)

- Transplanted tissue does not survive but recipients show behavioral recovery - It released neurotrophins that stimulated axons and dendrite growth in brain

Huntington’s  

. Neurological disorder characterized by various motor symptoms (basal ganglia not inhibiting thalamus) - Affects 1 in 10000 in US

- Onset: between 30-50

. Associated with gradual/extensive brain damage (mostly basal ganglia but also cerebral cortex)

Symptoms 

. Initial motor symptoms: arm jerks, facial twitches

- Because the output from the basal ganglia is inhibitory to the thalamus, damage to the basal   ganglia leads to increased activity in motor areas of the thalamus

- Progress to tremors that affect walking, speech, voluntary movements

. Associated with various psychological disorders (often confused with schizophrenia) - Depression, memory impairment, anxiety, hallucinations/delusions, poor judgement,  alcoholism, drug abuse, sexual disorders

Heredity and Presymptomatic Testing 

. Presymptomatic tests: identify who will develop disease

- Controlled by autosomal dominant gene on chromosome #4

- The higher the number of consecutive repeats of combination C-A-G, the more certain/earlier  the person is to develop the disease

a. Up to 35 repeats = safe from disease

b. Above 35 = will likely get it (the more, the earlier)

C-A-G repeats and Huntingtin 

. A variety of neurological diseases related to C-A-G repeats

- The earlier the onset, the greater probability of a strong genetics influence

. Identification of the gene for Huntington’s led to discovery of protein that codes it (huntingtin) - Mutant form impairs neurons in brain

- Future drug therapy may address huntingtin

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