Neuropsychologist: (1) Study abnormalities in humans in unis/labs/pharmaceutical companies/institutional (2) Ph.

D in clinical
neuropsyc/ Neurochemical analysis/functional neuroimaging technologies (3) Application of brain behavior principles to the
evaluation/treatment of brain damageABI & TBI assessment in patients with brain damage (e.g., learning disabilities) Clinical
Psychologist: (1) Clinically application to human problems in priv. practice/hospitals/rehab clinics through diagnosis/rehab for
abnormal brain-behavior relationships (2)The scientific study of the relationship between brain&behaviour (3) Diagnosis, Rehabilitation
planning, psychotherapy
TOPIC 2 - NEUROANATOMY
Central Nervous System: brain, spinal cord (tract=collection of axons)
Peripheral Nervous System: somatic nervous system (sensorimotor connections via spinal cord&cranial nerves/ autonomic ns:
balances internal organs through parasympathetic&sympathetic nerves (nerve=collection of axons)
Sympathetic: arouses body for action (fight or fllight) spinal nerves in thoracic lumbar regions e.g., pupil dilation, decreased digestion
Parasympathetic: calms body down (connects with parasympathetic ganglia near target organs) e.g, salivation, decreased <3 rate, blood
Types of neurons: SENSORY: carry info from receptors to the brain MOTOR: carry signals from brain to muscles INTERNEURONS:
convey info between diff. types of neurons
Glial cells: ASTROCYTES: most abundant in brain, associated w neuronal synapses/regulate transmission of electrical impulses
MICROGLIA: main active immune defense in CNS EPENDYMAL: nervous tissue cells that line the cerebrospinal fluid-filled ventricle in
brain/spinal cord OLIGODENDROCYTES/SCHWANN: provide support/insulation to axons in CNS by creating myelin sheet (80%lipid /
20%protein)
Golgi (Visualizing neurons): Golgi staining technology provided first clear images of neurons, allowing to see structure of nerve cells
(bodies, dendrites, axons), how neuron shapes differ, challenging the prevailing notion that the nervous system was a continuous,
filamentary system LEADING TO the proposal of the Neuron Doctrine w/ Ramon Cajal
-Pterion - junction of sphenoid, frontal, parietal & temporal bones (injury=middlemenengiala artery rupture-> epidural hematoma
Cribriform plate - vulnerable (lacerate brian structure)
-Subarachnoid hemorrhage: bleeding of bridging veins in between brain and arachnoid membrane (intracranial pressure)
-Subdural hematoma: blood accumulates between brain and dura mater, tough outer membrane (head trauma)
-Epidural hematoma: bleeding of meningeal arteries (talk and die)
Circle of Willis: circular network of arteries at base of brain that provide backup supply of blood/pressure. Advantage: allows brain to
receive blood if one of the major arteries is damaged (protection against stroke)
-Main parts of brain; telencePhalon,dienceP, mesenceP, metenceP, myelenceP
Neocortex - 6 cortical layers (newer areas of cortex) higher order functioning, decision making
Allocortex - 3 cortical layers (more ancient/primitive areas or cortex) role in limbic system, less developed/complex
*remaining 99% connect to other regions o=within the cortex
Columnar Organization of the cerebral cortex refers to the structured arrangement of neurons in vertical columns that extend through
the layers of cortex: each column represents functionally related neurons that share properties so the brain can integrate/process
sensory, motor and cognitive info more effectively
Limbic system: amygdala (emotion), hippocampus (memory/spatial nav.), mammillary bodies (memory consolidation), septum
(emotion), cingulate cortex (emotion formation,learning)
Cranial Nerves:Olfactory (S), Optic (S), Oculomotor (M), Trochlear (M), (Trigeminal (B), Abducens (M), Faical (B), Auditory (S),
Glossopharyngeal (B), Vagus (B), Spinal Accessory (M), Hypoglossal (M)
Bell-Magendie Law: sensory afferent/motor efferent, dorsal afferent/ventral efferent (same dave)
Dermatomes vs Myotomes: dermatomes control sensation/myotomes control movement
Cervical/lumbar enlargement: high degree of neural input due to increase complexity/demand
Central Pattern Generator: network that generates rhythmic movements located in the brainstem/spinal cord e.g., walking
(altering leg movements) breathing (automatic inhale/exhale)
3 functions of inhibition: signal processing/filtering (regulate flow of info), balance excitation (stability of neural networks), pattern
formation/control (shaping patterns of neural activity)
Blanks: (Sensory, dorsal, motor, ventral, bell-magendie law)(Ligands, bind, activate, inhibit, effector receptors)
(Hypothalamus, midbrain, axon, dendrites, astrocytes, endoplasmic reticulum, caudate nucleus, thalamus, putamen)(3,
cranial, hindbrain midbrain, forebrain, myelencephalon, metencephalon, mesencephalon, diencephalon,
telencephalon)(Coronal, sagittal, sagittal, coronal, sagittal)
TOPIC 3 - NEURAL DEVELOPMENT AND NEUROPLASTICITY
Experience-expectant: resulting from hardwired genetic programs eg, critical periods (time window where brain is especially receptive
to stimuli from environment) Experience-dependent: represents how the environment/experience impacts the biological organization
of the brain, e.g., development of visual cortex of a cat with a sutured eye
Last areas to myelinate: anterior cingulate cortex, inferior temporal cortex, dorsolateral prefrontal cortex
Neuroplasticity inferred (7): experience, behavior, brain anatomy, functional brain maps, synaptic organization,physiological
organization, molecular structure of nervous tissue
Focal hand dystonia: loss of independent control of one or more fingers (repetitive synchronous movements) results in expansion of
cortical areas associated with each finger - functional fusion
Neurogenesis 2 locations: interneurons of the dentate gyrus of the Hippocampus & interneurons of the granular cell layer of the
Olfactory bulb Recovery of function: stage 1 (acute) stage 2 (long-term) e.g., stereoblindness
3 criteria: cortical damage accompanied by loss of behaviors, recovered behavior must be the same as was previously lost, if
treatment produces recovery, then recovery is attributable to treatment and would not have occurred without it (Phineas Gage rod
through head lost inhibition)
Ischemia: loss of blood supply to an area of cortex Closed head injury: traumatic brain injury in which skull remains intact, but there's
damage to the brain due to external forces Stroke: interruption of blood flow to the brain Encephalitis: inflammation of the brain often
caused by viral infection
TOPIC 4: SIGNALING WITHIN THE NEURON
-Neurons generate and transmit signals within themselves by briefly varying the neuron's membrane potential
-Difference in the electric charge across the cell membrane (by differences in ionic concentration inside/outside the cell
-Resting membrane potential is -70mV
-Depolarization; adding + ions (closer to 0)
-Hyperpolarization; adding - ions (further away from 0)
-Graded potentials: found in dendrites (Excitatory depolarization or Inhibitory hyperpolarization) sum of EPSPs and IPSPs
-Action potentials: found in axons/terminal boutons (ballistic/same) SOLUTION for long distance signaling (unlike graded potential, it
will propagate without decrement) using changes in the production rate
-What causes an action potential? Sum of all the EPSPs and IPSPs (must be depolarized to about -55mV for an action potential to
be produced)
Cations: sodium & potassium
Anions: chloride & organic anions
Quantal release: neurotransmitters are stored in discrete amounts within synaptic vesicles. When they release their contents, it
happens in integer multiple which ensures precise and reliable synaptic communication.
TOPIC 6 - NERVOUS SYSTEM AGENTS
11 ways that CNS agents affect synaptic neurotransmission
1. Drug substitutes for one of the dietary precursor chemicals involved in production of NT
(agonist) e.g., L-DOPA
2. Drug inhibits production of NT by a precursor chemical (antagonist) Fenclonine
3. Drug prevents storage of NT in vesicles (antagonist) Reserpine
4. Drug stimulates release of NT in vesicles (agonist) Latrotoxin
5. Drug inhibits release of NT (antagonist) Botulinum toxin: prevents vesicles containing
the NT from fusing with interior surface of presynaptic membrane (nerve impulses
blocked)
6. Drug stimulates postsynaptic receptors (agonist) Nicotine
7. Drug blocks postsynaptic receptors (antagonist) Atropine
8. Drug stimulates autoreceptor action (antagonist) Apomorphine
9. Drug blocks autoreceptor action (agonist) Clonidine
10. Drug blocks reuptake of NT in synapse (agonist) Cocaine; prevents reuptake of
dopamine
11. Drug inactivates acetylcholinesterase (agonist) Physostigmine
Delivery: oral, intramuscular/iv injection, inhalation, transdermal, anal suppositories, intrathecal
Blood brain barrier: barrier composed of tightly connected endothelial cells and astrocytes that restricts the passage of large
molecules from exiting the intravascular space. GAPS: pituitary gland, area postrema, pineal gland
CNS agents: analgesics, anorexiants, anticonvulsants, antidepressants, antiemetic, antiparkinsonism, antipsychotics, anxiolytics,
cholinergics, muscle relaxant
Mechanisms of hormonal secretion: endocrine (hormones secreted directly into bloodstream, borne to target tissues in blood),
exocrine (hormones secreted via ducts), paracrine (hormones diffuse through the interstitial space to nearby target tissues),
pheromone (hormones broadcast into the environment)
TOPIC 8 - THE VISUAL SYSTEM Misleading: Visual information processing engages a large portion of the cerebral cortex in all of the major
lobes (frontal, parietal, temporal, occipital), and terminates in all of the lobes, including occipital poles.
Two Cortical Visual Stream Project from the Occipital Lobe: Ventral: associated w object perception and recognition (agnosias)
e.g., familiar faces Dorsal: associated w object manipulation & visually-guided reaching (apraxias) e.g., mailing
MEN: genes responsible are located on X chrom., men only have one X chrom. making them more susceptible to inheriting mutations
Action potentials are brief electrical signals that transmit info along the axon of a neuron. They involve a rapid change in the
membrane voltage. EPSPs are sub-threshold, graded depolarizations of the postsynaptic membrane in response to NT binding, which
increase the likelihood of an action potential. IPSPs are sub-threshold, graded hyperpolarizations of the postsynaptic membrane,
making it more difficult for an action potential to occur by moving the membrane potential away from the threshold.
Common excitatory: Glutamate & Epinephrine / Common inhibitory: GABA & Serotonin
Narcan: competitive inhibitor for opioid od, binding to same receptors that opioids target & displaces opioid from receptor, temporarily
reversing symptoms such as respiratory depression, inhibition is short-lived (seek medical help)