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120 Cards in this Set

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Glial Cells
*
-Repairs, supports, and protects neurons
-Doesn't transport info
-90% in brain-majority in CNS
-Can regenerate as needed
Types of Glial Cells
*
1)Oligodendrocytes-CNS-brain & spinal cord
2)Schwann Cells-PNS - build up myelin sheaths
3)Microglia-smallest-clean debris, remove waste-trigger inflammatory response
4)Astrocytes-largest-part of blood brain barrier
5)Ependymal-line central canal of spinal cord
6)Satellite-help regrowth of muscle fibers
Neurons-Types
*
1)Sensory Neurons(Afferent)- specialized at 1 end to be sensitive to stimulation (touch)
2)Motor Neurons(Efferent)- Receives excitation signals & conducts impulses to muscles
Afferent vs. Efferent Neurons
*
1)Afferent - brings info into a structure-towards CNS - unipolar - 1 process

2)Efferent - Carries info away from CNS to muscles-Multipolar Neuron-
Interneurons
*
-Integrate activity within a brain structure
-Cells dendrites are entirely contained within a single structure and axon
-Intrinsic Neuron
-only communicates with other cells
-Only found in CNS
Neuron Anatomy
*
1.Dendrites-branching fibers carry nerve impulses to cell body-important for long term changes, learning, memory
2.Cell Body-
-Nuclues-contains DNA
3.Axon-long narrow fiber that carry impulses away from cell body
4.Terminal Bouton(presynaptic terminal)-releases chemicals to cross to next neuron-small nodules containing chemicals
5.Myelin Sheath-fatty tissue around axon-adds speed to impulse conduction-helps prevent electrical current from leaving axon
Dualism
Belief that mind and body are different kinds of substance-mental and physical substance-that exist independently
Genes
-Units of heredity that maintain structural identify from 1 generation to another-Come in pairs=Alleles
-Dominant Gene-Strong effect in either homozygous or heterozygous-prominent in women
-Recessive Gene-Effect only in homozygous-prominent in men
Sex-Limited Genes
-Present in both sexes but have effects mainly or exclusively in 1 sex
-Activated by sex hormones & makes effect evident in 1 sex or the other
Mutation
-Change in single gene
-Rare and random
-Source of gene variation
-
Depolarization
*
-Reduction of polarization
-Decrease negative charge - move toward 0
-EPSP
-when sodium enters
Hyperpolarization
*
-Increased polarization
-Increase negative
-IPSP
-potassium leaves
EPSP
Excitatory Postsynaptic Potential
-Graded polarization
-occurs when sodium enters
-depolarization
IPSP
Inhibitory Postsynaptic Potential
-Temporary hyperpolarization
-Occurs when synaptic input selectively opens gates for potassium to leave
Concentration Gradient
*
-Difference in distribution of ions across the membrane
-Sodium is more concentrated outside the cell so more likely to enter the cell
Electrical Gradient
*
-Difference in electrical charge between inside & outside of cell
-Pulls potassium in because it has a negative charge
-Potassium is more concentrated inside cell so concentration gradient pushes it out
Sodium-Potassium Pump
*
3Sodium:2Potassium
-uses 40% of cells energy
-Transports 3 sodium out while drawing 2 potassium in
Resting Potential
-Electrical potential across a membrane when a neuron is not being stimulated
-When at rest--steady negative inside axon
Threshold of Excitation
*
-Level of depolarization at which a brief stimulation triggers rapid, massive electrical change by the membrane
-Stimulus beyond certain level produces massive depolarization
-When threshold is met-->Action Potential
Nucleus Accumbens
*
-Structure involved in addiction
-Lots of dopamine receptors
-Major part of reinforcement system
Types of Receptors
1)Ionotropic-Open & close quick - Direct opening
2)Metabotropic-Initiates sequence of internal molecular events which in turn open specific ion channels
-can open & close channels
-Autoreceptors-bind to own neuron
Dopamine
-Only in CNS
-Excitatory or inhibitory
-Involved In: coordinated movement, reward/reinforcement
-Schizophrenia:
-Parkinson's-loss of dopamine in substantia nigra
Norepinephrine
-PNS-Fight/Flight

-CNS-Arousal, sustained & selective attention

-Can function as hormone when released into blood
Serotonin
-PNS-Cardiovascular regulation, smooth muscle, GI functions

-CNS-sleep/wake
Directions in CNS
*
-Dorsal-top & toward back
-Ventral-bottom & toward stomach
-Coronal- (|)

-Horizontal- (--)
-Medial(Mid-Sagittal)- Front square plane
PNS
*
Located outside brain & spine
1)Somatic
-voluntary
-Always excitatory
-skeletal muscle
2)Autonomic
-involuntary
-smooth muscle
-excitatory or inhibitory
3 Divisions: (1)Sympathetic, (2)Parasympathetic, (3)Enteric
Autonomic NS
*
1)Sympathetic-Fight/Flight, Exercise, excitement, emergency

2)Parasympathetic-Vegetative responses-Rest, relaxation, digestion...

3)Enteric-Regulates digestion, 2nd brain=gut feeling, own neurons
Lobes of Brain
*
1)Frontal Lobe
2)Parietal Lobe
3)Temporal Lobe
4)Occipital Lobe
Frontal Lobe
*
-Higher cognitive functions, executive functioning, problem solving, judgment...
Structures:
1.Broca's Area-Language production
2.Prefrontal Cortex-executive functions
3.Motor Cortex-Precentral Gyrus=fine motor movements
Parietal Lobe
*
-Sensations, spatial awareness, numerical info, hand-eye coordination
Strctures:
1.Somatosensory Cortex-touch sensations, info from muscles
2.Sensory Homunculus (Postcentral Gyrus)
Temporal Lobe
*
-Emotions, memory, understanding music, aggressiveness, sexual behavior
Structures:
1.Primary Auditory Cortex
2.Wernicke's Area-Language comprehension
Occipital Lobe
*
-Vision & recognition
Structures:
1.Primary visual cortex
Thalamus
*
-Sensory relay center
-Movement
-Aphasia-language impairment
Amygdala
Emotions, Aggressions
-Kluver-Bucy syndrome
Hypothalamus
*
-Controls Endocrine system (stress response cycle)
-Regulates body temp, food intake, thirst, sleep/wake cycle
-Emotional responses & behaviors
-Sexual activity
Basal Ganglia
*
-Motor Control
-Parkinson's, Huntington's (when basal ganglia deteriorates)
-3 Major Structures
1.Caudate Nucleus
2.Putamen
3.Globus Palidus
Corpus Callosum
*
-Large set or bundles of axons that connect 2 hemispheres of the cerebral cortex
-messages relayed from 1 hemisphere to the other
-Disconnection syndrome
Synaptogenesis
*
-Rapid formation of new synapses
1.Axons sprout to innervate many targets
2.Axon target interactions cause target to choose which axon
-Synapse Survival-Neurotrophic
-Promotes neuron survival
-Triggers apoptosis
Enriched Environment
*
-Thicker cortex
-increased neuron connections
-increased dendritic branching
1.Mind Activity
2.Physical Activity
3.Social Networking
Cerebrum
-largest portion of brain-2 hemispheres
1.Corpus Callosum
Spinal Cord
-White Matter=myelinated axons
-Gray Matter=Cell bodies, dendrites, 'H' Shape
Bell-Magendie Law
-Dorsal fibers carry sensory info
-Ventral fibers carry motor info
Proliferation
-New cell production -
-cells lining ventricles
Migration
-Whole neurons move toward destination
-neocortex is last layer to develop
Axons in CNS & PNS
CNS-Axons don't grow back, don't regenerate
--why:oligodendrocytes don't provide guidance, scar tissue build up

PNS-Axons Grow Back
-Schwann cells provide guidance
Cellular Recovery
-Axon regeneration
-Denervation supersensitivity
-Rerouting
-Sprouting
Structural Recovery
-Amputation
-Brain can reorganize to account for loss
-Requires somatosensory cortex
(Sleep)
Protein Production
*
-Per & Tim proteins build up
-Period & Timeless
-Increase throughout the day
-Highest at night
-Interact with clock protein
-Increase activity of neurons in SCN
Locus of Clock
*
SCN-Suprachiasmatic Nucleus
-In hypothalamus
-Damage abolishes sleep/wake cycle
How the SCN Keeps Time--Proof
-Still keeps time in culture dish
Tracts in Hypothalamus
*
1.Tract Releases Histamine

2.Tract Releases Orexin (Hypocretin)--Stimulates Acetylcholine
Basal Forebrain
*
-Acetylcholine Neurons
-GABA Neurons--required for sleep
Adenosine
*
-Anti-inflammatory agents
-Inhibits neurons in Basal Forebrain that release Acetylcholine--Decreases arousal
-Sleep Debt=Build up of Adenosine
Heat Production
*
1.Metabolism (main method)
2.Exercise(voluntary)
3.Shivering
4.Radiation
Heat Loss
*
1.Radiation-no contact

2.Conduction-contact

3.Convection-transfer to air/water

4.Evaporation-sweat

-Temp regulation is interaction between internal regulation and behavior
Temp Regulation-Feedback Circuit
*
Homeostasis-Maintenance of constant internal environment

Negative Feedback-Reduces discrepancies

Positive Feedback-Stops negative feedback
BioBasis of Temp Regulation
(thermostat)
*
Hypothalamus
-Anterior Hypothalamus & Preoptic Area (AH/POA)
-Thermostat of the Body
4 Stages of Sleep
1)Floating stage-brief stage before sleep-Alpha & Theta waves

2)Daydreaming-3 characteristic
1.Theta Waves, 2.Sleep Spindles, 3.K Complex

3)Some delta wave, spindles decrease

4)Delta Waves - Synchronized

NREM=2-4
REM Sleep
-occurs 80-100 min after sleep
-sleep lightens
-Some Beta Wave
-lasts about 10min
Behavioral Characteristics
-muscles relax(loss of tone)
-rapid eye movement
-dreams
Reticular Activating System
Pontomesencephalon(Pon-Midbrain)
-maintains arousal-cortical arousal
-Releases Acetylcholine & Glutamate
-Stimulations results in awake

Raphe Nuclei-releases serotonin
Clinico-Anatomical Hypothesis
-dreams are similar to thinking, just under unusual circumstances
Activation-Synthesis Hypothesis
-Dreams are side effects of mental stimulation from pons
-Synthesis of motor & visual neuron firing with stored memories
-Amygdala activation provides emotional context
-Frontal cortices deactivated--allows for illogical dreams
Narcolepsy
Not enough Orexin
PGO Waves
Pons
Geniculate
Occipital
-REM sleep-High amplitude electrical potentials
Volumetric (Hypovolemic) Thirst
*
-Low body fluids-low blood volume
-Need Water & Salt
Detection:
1.Baroreceptors on Venus Return
2.Kidney's
3.Adrenal Glands
Osmotic Thirst
*
-Need Water
-Increased levels of salt produce thirst
-Cellular dehydration
Receptors:
1.Supraoptic Nucleus
2.OVLT & Subfornical Organ
Thirst Regulation
Pituitary Gland:
-Releases Vasopressin-antidiuretic
Role of Hormones
*
Estrogen/Progesterone:Increased sexual behavior
Testosterone:promotes sexual behavior in men
Oxytocin:
-females-social interaction & maternal behavior
-males-cuddle hormone
Prolactin:
-females-milk production
-males:inhibitory effect on sexual behavior-coolidge
Brain Structures-Sex-Females
*
1)Ventromedial Hypothalamus
-center for female sex behavior
-moderates Oxytocin release

2)Periaqueductal Gray
-mediates influence of VMH
Brain Structures-Sex-Males
*
1)Medial Preoptic Area
-sexual dimorphic nucleus-larger in males
-increased dopamine & opioids released during sex & orgasm

2)Lateral Tegmental Area
-some neurons only fire during sex
Congenital Adrenal Hyperplasia
CAH
-Too much testosterone
-Adrenal glands secrete abnormal amounts of androgens
-Males develop normally
-Females develop external genitals
Androgen Insensitivity Syndrome
-Individual with XY but is insensitive to Androgen
-Develops female external appearance
-Develops as women without ovaries or uterus-testes stay internal
-testes release enough estrogen to feminize body
Lipostatic Theory
*
-Long term hunger regulation
-Fat monitoring system
-Body fat cells produce leptin- more fat cells=more leptin
-Obese people are less sensitive to leptin & have genetic inability to produce leptin
Orexin
-Stimulates activity & onset of meals
-cells increase release of orexin only after prolonged food deprivation
-motivates starving animal to search for food but has little influence on most meals
Arcuate Nucleus
2 Inputs
1.Hunger Signals
2.Satiety Signals

Melanocortin=Satiety
Neuropeptide Y=Overating
Ventromedial Hypothalamus
*
-Overeating
-Increase set point for weight
-does not appear to result in death
Lateral Hypothalamus
*
-Decrease eating
-Death if not force fed
Response:
-taste pathway, facilitates ingestion & swallowing, increases senses, food seeking behavior, insulin production, & stomach secretions (digestion)
Vagus Nerve
Cranial Nerve X
-conveys info about stretching of stomach walls-->Satiety
Splanchnic Nerves
conveys info about nutrient content of stomach
Duodenum
Part of small intestine adjoining the stomach
-1st digestive site that absorbs nutrients
-when distended-->Satiety
Cholecystokinin
CCK
-Limits meal size
-released by duodenum
(1)Closes sphincter muscle between stomach & duodenum so stomach fills quickly
(2)Stimulates vagus nerve
Glucostatic Theory & Insulin
-Hungry if glucose is low
Insulin
-enables sugar to enter cells
-stored as fat & carbs
-Increases before, during, & after meals
-High insulin level suppress appetite
Disgust
*
-Provoked by bad taste or bad smell
Neural Mechanisms:
(1)Insular Cortex:Primary taste region
(2)Basal Ganglia
Lesions to Amygdala
*
-effects of emotions on memory
-flashbulb memories
-The more the Amygdala is damages, the less likely you'll remember emotionally charged memories
Aggression & Impulse Control
*
Prefrontal Cortex=Faulty Emotional Regulation
-Areas in Emotional Regulation
-(1)Orbitofrontal Cortex
-(2)Ventromedial Prefrontal Cortex
Effects of Chronic Stress
-long levels of stress damage hippocampus
-Dendrite & axon retraction
-Inhibition of hippocampal neurogenesis
-long-term depression
General Adaptation Syndrome
1)Alarm Stage(initial response)
-SNS arousal
2)Resistance Stage(Adaptation)
-Release of cortisol
-anti inflammatory,immunosupression
3)Exhaustion
-resources depleted
-damage to hippocampus
James-Lange Theory
*
-Physiological Arousal
-Emotions are result of physiological change(not cause)
1)Cognitive Appraisal
2)Physiological response(ANS)
3)Situations elicit behavior
4)Brain receives sensory feedback from muscles & organs
Pure Autonomic Failure
*
-report same emotions as others
-can identify emotions in others
-Report feeling emotions less intensely (cognitive aspect)
3 Responses of Emotions
*
1)Behavioral

2)Autonomic
-SNS increases, PNS decreases

3)Hormonal
-Nor/Epinephrine released
-Adrenal glands secrete steroid hormones
Cannon-Bard Theory
-Cognitive Appraisal
1)Feel Emotions
2)Physiological Change
3)Behavior
Central Nucleus
-Most important part of brain for expression of emotional responses
-Expression of emotions
Serotonin & Emotions
-Inhibits aggressive behaviors
-inhibits risky behaviors
-Problem:linked with depression, not all depression is aggressive
Happiness
Heredity & Neural Mechanisms
-50% momentary happiness=genetic
-80% set point for happiness
Neural Mechanisms
-Amygdala
-Prefrontal Cortex
--Right Ventromedial Prefrontal Cortex=appreciating humor
HPA Axis & Stress
Hypothalamus

Pituitary

Adrenal Glands
Types of Memory
*
1)Sensory Store

2)Working Memory

3)Long-Term Memory
Sensory Store
*
250-500msec

1.Iconic Store

2.Echoic Store

3.Haptic Store
Working Memory
*
1.Central Executive-directs attention toward 1 stimulus or another & determines which items will be stored in memory

2.Phonological Loop-auditory & words

3.Visuospatial Sketchpad- visual info
Long Term Memory
*
1)Explicit
-conscious & intentional
-1.Semantic-general facts
-2.Episodic-events/episodes
2)Implicit
-unconscious & Unintentional
-priming, emotional response, procedural memory

3)Declarative-recall of factual info
4)Nondeclarative-recall of proceudres
Theories of Forgetting
*
1)Decay Theory

2)Interference Theory

3)Context Theory
Decay Theory
*
-older memories will always be more decayed than newer ones
-all memories decay at same rate-some start out stronger
Interference Theory
*
1)Retroactive Interference- New memories interfere with old memories

2)Proactive Interference- Old memories interfere with new memories
Retrograde Amnesia
*
-Forgot what you used to know
Anterograde Amnesia
*
-Unable to form new memories
-More common
-frozen in time
Cortical Dementia
*
-Alzheimer's-50% of all dementia

-Lewy-Body Dementia
Subcortical Dementia
*
-Parkinson's
-Huntington's
-Wilson's
Alzheimer's Disease-Deficits
*
1)Memory-working & recent
-intact implicit & remote
2)Language-Anomia-1st sign-word finding problems
AD Neuropathology
*
1)Plaques-formed from degenerating axons & dendrites - Produces by Amyloid
2)Neurofibrillary Tangles- formed from degenerating structures within cell bodies- produced by Tau
3)Neuronal Loss
AD
*
Alzheimer's Disease
-characterized by memory loss, confusion, depression, restlessness, hallucinations, delusions, sleeplessness, loss of appetite
Mild-Cognitive Impairment
-Transitional stage between cognitive changes of normal aging & more serious problems caused by AD
Characteristics:
-Aware of deficits
-1 cognitive domain
-doesn't interfere with social/occupational function
-"Risk Stage"
Long-Term Potentiation
Plasticity
-learning
1)Synapses activated at high frequencies
2)Leave synapse more responsive to new input
-Specificity-only active cells become strengthened
-Associativity-pairing weak input with strong input enhances later response to weak input
-Cooperativity-simultaneous stimulation produces stronger long-term potentiation
Broca's Aphasia
*
Language Production
-Nonfluent Aphasia
-Inability to produce meaningful speech
-location of grammar
-loss of fluent speech
-impaired use & understanding or prepositions, word endings
Wernicke's Aphasia
*
Language Comprehension
-Fluent Aphasia
-Dissociation between words and meanings
-Location of meaning
-Poor language comprehension & difficulty remembering names of objects
-Difficulty understanding speech
Dyslexia & Brain Structures
-Underactivation of: Angular Gyrys & Wernicke's Area
-Decreased volume in Broca's Area
ADHD Neurotransmitters
*
-Dopamine
-Norepinephrine

Brain Structures:
-Basal Ganglia
-Smaller Prefrontal Cortex
-95% or normal brain volume
Schizophrenia Neurodevelopment Hypothesis
*
-Based on abnormalities in prenatal or neonatal development of nervous system which lead to subtle abnormalities of brain anatomy and major abnormalities in behavior
Schizophrenia Brain Abnormalities
1)Enlarged Ventricles

2)Smaller Prefrontal Cortex
-less gray matter

Causes:
-seasonality effect
-Virus
-famine related
-Thiamine deficiency
-Toxin build up
Schizophrenia Dopamine Hypothesis
*
-High levels of dopamine lead to positive symptoms
-More dopamine receptors
-Twice as many D2 receptors
Schizophrenia Glutamate Hypothesis
*
-Less than normal glutamate release (especially in prefrontal cortex)
-Stimulating NMDA receptors trigger insertion of dopamine receptors into membrane
-Increased dopamine produces same effects as decreased glutamate
Depression & Sleep Patterns
*
-More REM Sleep
-Fall asleep but awaken frequently and early
-Enter REM within 45min & have more eye movements
-Sleep deprivation relieves depression
Depression & Genes
-Family 10x greater chance
-Twins 70% increase
-Moderate degree of heritability
-Elevated with relatives of women with early onset before age 30
-One gene showed 80% decrease in brains ability to produce serotonin
--Serotonin transporter gene