Physiology Exam 1

BYU CELL 362 with Dr. Woodbury Ch. 1-10

combinaation biomolecules

lipoprotein: blood transport molecules

glycoprotein: membrane structure

glycolipids: membrane receptors

cell membrane

structure: fluid mosaic model, phospholipid bilayer

function

• physical barrier

• gateway for exchange

• communication

• cell structure

mass balance in the body

(mass balance) = (existing body load)

+ (intake & metabolic production)

- (excretion & metabolic removal)

homeostasis and equilibrium

\*homeostasis NOT EQUAL to equilibrium

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**homeostasis**: the ability of the body to maintain a relatively constant internal environment

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equilibrium in cells:

* __osmotic equilibrium__: water goes in and out
* __chemical disequilibrium__: differential solute concentration
* __electrical disequilibrium__: inside of cells is negative to extracellular fluid

body fluid compartments

**Intracellular Fluid (ICF)** = 2/3 of fluid volume

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**Extracellular Fluid (ECF)** = 1/3 of fluid volume

* **Plasma** = blood, 75% of ECF
* **Interstitial fluid** = between cells, 25% of ECF

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barrier between ICF and ECF: cell membrane

barrier between plasma and interstitial: “leaky” epithelium

chemical disequilibrium in ICF vs ECF

ECF

• high Na+ (~145 mM)

• low K+ (~5 mM)

• high Cl- (~108 mM)

• proteins only in plasma, not interstitial fluid

ICF

• low Na+ (~ 15 mM)

• high K+ (~150 mM)

• high Cl- (~10 mM)

• high proteins

E for each ion at resting:

• Na+: +60 mV

• K+: -90 mV

• Cl-: -63 mV

osmosis, osmotic pressure, and osmolarity

**osmosis**: movement of water across a membrane in response to a solute concentration gradient

* aided by aquaporins

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**osmotic pressure**: pressure required to exactly oppose a given concentration gradient

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**osmolarity**: concentration of solute in particles per liter of solution

tonicity

tonicity: volume change of a cell placed in solution

• based on concentration of non-penetrating solutes

hypotonic solution = cell swells

isotonic solution = cell remains the same

hypertonic solution = cell shrinks

osmolarity and tonicity problems

Use a table with solute, volume, and osmolarity.

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Work out total body first. Remember that osmolarity of ECF and ICF will be equal to total body.

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If working with both non-penetrating and penetrating solutes, start with non-penetrating solutes to figure out water movement (volume of ICF and ECF).

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Then add penetrating solutes back in to figure out solute (keep volumes the same).

common body fluid scenarios

IV

• IV fluid enters plasma (ECF)

• 0.9% NaCl is isosmotic to cells

• NaCl is non-penetrating, glucose (dextrose) is penetrating

sweating

• lose water by evaporation, leaves salt behind

• sweat comes from plasma (ECF)

• increases osmolarity of the ECF so that water leaves the cells

measurement of body fluid

dilution method: add a known amount of dye/molecule and then measure concentration when diluted in whole body

• use c1v1 = c2v2

measurements:

• plasma volume: Evan’s blue

• ECF volume: inulin

• total body volume: D20 (heavy water)

• interstitial volume: ECF - plasma

• ICF volume: total body - ECF

dehydration

danger of large decrease in ECF volume: plasma volume drops, so blood pressure drops

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**dehydration**: loss of fluids in excess of 1% or more of body weight

* __caused by__: excess sweating, evaporation from burn surface, chronic hyperventilation, vomiting/diarrhea, etc.
* __leads to__: ECF hypovolemia, **hypotension**, inability to sweat (hyperthermia)

simple diffusion properties

* passive (no ATP)
* high to low concentration
* net movement until concentration is equal

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__faster when__:

* short distance
* higher temperature
* smaller molecular size
* more permeable membrane
* larger surface area of membrane
* thinner membrane
* larger concentration gradient

Fick’s law of diffusion

rate of diffusion ∝ (membrane surface area)(membrane permeability)(concentration gradient)(membrane thickness)⁻¹

membrane permeability ∝ (lipid solubility)/(molecular size)

functions of membrane proteins

1. structural proteins
2. enzymes
3. membrane receptor proteins
4. transporters (channel or carrier)

channel membrane proteins

* water channel (aquaporins)
* open channel
* gated channel
* **mechanical**: responds to pressure changes (blood pressure)
* **voltage**: responds to electrical state (nerve/muscle contraction)
* **chemical**: responds to molecules that bind to channel protein

carrier membrane proteins

carrier proteins have specificity to their substrates

• uniport: 1 substrate, 1 direction

• symport: 2 substrates, same direction

• antiport: 2 substrates, opposite directions (ATP)

glucose facilitated diffusion

“diffusion trapping”

* glucose goes into cell through GLUT transporter (down concentration gradient)
* glucose is phosphorylated to glucose-6-phosphate
* keeps concentration of glucose inside cell low so that glucose continues to flow in

primary active transport

uses ATP to go up concentration gradient

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__ex__: Na+ K+ ATPase antiporter

* maintains high Na+ outside cell and high K+ inside
* 3 Na+ go out, 2 K+ go in
* inside of cell is slightly more negative than outside

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__mechanism__:


1. 3 Na+ from inside cell bind
2. ATPase is phosphorylated
3. Protein changes conformation
4. 3 Na+ released into ECF
5. 2 K+ from ECF bind
6. Protein changes conformation (dephosphorylated)
7. 2 K+ released inside cell

secondary active transport

uses potential energy of Na+ gradient to transport a different molecule against its concentration gradient

ex: sodium glucose transporter (SGLT)

1. Na+ in ECF binds to carrier, creating a binding spot for glucose

2. Glucose from ECF binds to carrier, changing carrier conformation

3. Na+ and glucose are released inside cell

carrier protein competition and saturation

**saturation**:

* transport reaches a maximum rate
* once all carriers are full, a higher concentration of substrate doesn’t increase rate

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**competition**:

* ex: maltose or galactose can compete with glucose
* inhibitor can get to active site first

phagocytosis

cell engulfs bacteria or other particle into phagosome


1. bacteria binds to cell membrane
2. cell uses **cytoskeleton** to extend membrane around bacteria
3. bacteria is engulfed into **phagosome**
4. phagosome fuses with lysosomes

endocytosis

can be non-selective (pinocytosis) or highly selective

* **receptor-mediated** uses **clathrin**-coated pits
* **caveolae** use **lipid rafts** for endocytosis without clathrin

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__receptor-mediated process__:


1. ligand binds to receptors on cell membrane and migrate to clathrin-coated pit
2. vesicle forms and is pinched off
3. clathrin coat is lost
4. receptors are recycled to cell surface
5. ligands go to lysosome

epithelial transport

__components__:

* **apical membrane**: faces the lumen of intestine/kidney (“outside”)
* **basolateral membrane**: faces the ECF (“inside”)
* **tight junctions**: form connections between cells and limits movement of materials across cell layer

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__processes__:

* **absorption**: movement from lumen to ECF
* **secretion**: movement from ECF to lumen

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__types of transport__:

* **paracellular**: through tight junctions
* **transcellular**: through epithelial cells themselves

transcellular absorption of glucose

1. **Na+ glucose symporter**: apical, secondary active transport
2. **GLUT transporter**: basal, facilitated diffusion
3. **Na+ K+ ATPase**: basal, primary active transport

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Na+ is high outside cell, low inside cell

glucose is low outside cell, high inside cell

resting membrane potential

**resting membrane potential**: the electrical gradient between the ICF and ECF

* the body is overall neutral
* the ICF is slightly negative and the ECF is slightly positive

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The resting membrane potential of a cell is relative to the outside of the cell

* outside of cell is 0mV
* inside is usually around **-70 mV**

electricity basics

* energy is required to separate positive and negative charges
* opposite charges attract
* **conductor**: material that allows electrons to travel through
* **insulator**: matierial that does not allow free movement of electrons

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**Ohm’s law**: I = Vg

* I is current
* V is voltage
* g is conductance

Nernst equation

tells us what voltage to apply to prevent diffusion of an ion down its concentration gradient

* specific to a particular ion
* at what charge inside cell will the ion stop diffusing across membrane

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z is the charge on the ion

changes in membrane potential

*outside of cell is always reference point (0 mV)

hyperpolarization: membrane potential becomes more negative than baseline (resting)

depolarization: membrane potential becomes more positive than resting

Na+ and K+ membrane potential

**Na+**: assume only Na+ can cross membrane

* E(Na) will approach **+62 mV** inside cell

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**K+**: assume only K+ can cross membrane

* E(K) will approach **-95 mV** inside cell

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**overall membrane potential**: both K+ and Na+ cross

* membrane potential is about **-70 mV** inside cell
* mostly due to K+ (cell more permeable to K+)

insulin secretion

__components__:

* **ATP-gated K+ channel**: closes with ATP
* **voltage-gated Ca2+ channel**: opens with more positive membrane potential

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__with high glucose levels__:

* glucose flows into cell and metabolism increases
* increase in ATP causes K+ channel to close
* K+ no longer leaves cell
* membrane potential **depolarizes** (more positive)
* voltage-gated Ca2+ channel opens
* Ca2+ enters cell and triggers exocytosis of insulin

cell-cell communication: local

1. **Gap junctions**: connect cytoplasm of neighboring cells
2. **CAMs (cell adhesion molecules)**: interaction between membrane molecules on two cells

cell-cell communicaton: chemical signals

1. **paracrine signals**: secreted by one cell and diffuse to adjacent cells
2. **autocrine signals**: act on the same cell that secreted them

cell-cell communication: long distance

1. **Hormones**: released into bloodstream by endocrine cells
2. **Neurohormones**: released into bloodstream by neurons
3. **Neurotransmitters**: sent from neuron directly to target cell

intracellular and extracellular signal receptors

1. lipophilic molecules can cross the cell membrane

   • bind to cytosolic or nuclear receptors

2. extracellular signal molecules bind to the cell membrane receptor and trigger a response

four groups of membrane receptors

1. receptor-channel (fast-acting)
2. G-protein coupled receptor
3. receptor-enzyme
4. integrin receptor (cytoskeletal response)

signal transduction

basic pattern:

1. Signal molecule (first messenger) binds to…

2. Membrane receptor protein (transducer) activate…

3. Intracellular signal molecules (second messenger) alter…

4. Target proteins create…

5. Response

ion receptor channels

Four ways they work:

1. Receptor channels open or close in response to signal molecule binding

2. Some channels are directly linked to G proteins (when ligand binds G protein couple receptor, ion channel opens/closes)

3. Some channels respond to intracellular second messengers

4. Electrical or mechanical signals open or close ion channels

G protein coupled receptor example: adenylyl cyclase

1. Signal molecule binds to GPCR

2. G protein is activated, activates adenylyl cyclase

3. Adenylyl cyclase converts ATP to cyclic AMP (cAMP)

4. cAMP activates protein kinase A

5. Protein kinase A phosphorylates other proteins

G protein couple receptor example: phospholipase C

1. Signal molecule binds to GPCR

2. G protein is activated, activates phospholipase C (PLC)

3. PLC cuts membrane phospholiplids into a head group (IP3) and diacyl glycerol (DAG).

4. IP3 opens a channel in the ER, releasing Ca2+

5. DAG activates protein kinase C

6. Protein kinase C phosphorylates other proteins

receptor-enzymes

• A ligand binds the receptor portion

• The attached enzyme (cytoplasmic side) changes conformation to carry out its enzymatic function

  • usually kinase or guanylyl cyclase

• example: tyrosine kinase

integrin receptor

• outside cell: bind to ligands or extracellular matrix proteins

• inside cell: integrins attach to cytoskeleton through anchor proteins

signal transuction summary

intracellular signals: Ca2+

• inside the cell - stored in endoplasmic reticulum

  • released from intracellular compartments through second messengers

• enters the cell through gated channels

• binds to other proteins - calmodulin, etc.

intracellular signals: gases

three main ones: nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S)

Nitric Oxide

• produced by endothelial cells, diffuses into smooth muscle cells

• causes dilation of blood vessels

• reactive with H20 and O2, short half-life = local control

intracellular signals: lipids

phospholipase 2: cuts off 2nd fatty acid to make arachidonic acid (2nd messenger)

signal pathway modulation: receptor ligands

ligand: activates receptor

agonist: activates receptor, competes with ligand

antagonist: blocks receptor activity

signal pathway modulation: receptors

one ligand can bind different receptors with different responses

• epinephrine binds alpha receptor in intestine → blood vessel constricts

• epinephrine binds beta2 receptor in skeletal → blood vessel dilates

• epinephrine binds beta1 receptor in cardiac → stimulate contractility

downregulation: decrease number of receptors

desensitization: binding to chemical modifier

upregulation: increase number of receptors

ways to terminate signal: transport away, breakdown signal, endocytosis

tonic control

signal is always present, but changes in intensity

• intermediate signal, can go up or down

• ex in neurons: increase signal rate means constriction of blood vessel, decrease signal rate means dilation

antagonist control

different signals for two different directions

• like gas pedal and brake pedal

• faster change in response

simple and complex reflex pathways

1. simple endocrine

2. simple neural

3. complex neuro-endocrine

nueral vs endocrine control

nervous system overview

Central Nervous System (CNS): brain and spinal cord

Peripheral Nervous System (PNS):

• sensory (afferent) neurons: send signals to brain

• efferent neurons: receives signals from brain

neuron cell structure

dendrites: receive input signals

cell body: integration center

axon: carry outgoing information

synapse: output signal

types of neurons

sensory: both dendrites and axon separated from cell body

interneurons: CNS neurons, highly branched

efferent: single long axon, dendrites as branches from cell body (classic neuron shape)

fast axonal transport

1. Protein synthesis in ER and packaging in Golgi

2. Motor proteins walk vesicles and mitochondria down axon along microtubule network

3. Exocytosis of vesicles

4. Synaptic vesicle recycling

5. Retrograde fast axonal transport

6. Old membrane components digested in lysosome

Glial cells

astrocytes: help create healthy environment for neurons in CNS

• take up ions, water, neurotransmitters

• help form blood brain barrier

myelin sheath: oligodendrocytes in CNS, Schwann cells in PNS

• multiple layers of phospholipid membrane surrounding axon

• acts as insulation, speeds up signal transmission

• node of Ranvier: section of unmyelinated axon between two Schwann cells

• sometimes after an axon injury axon can reform under myelin sheath

Goldman-Hodgkin-Katz (GHK) equation

membrane potential that results from the contribution of all ions that can cross the membrane

• Na+, K+, and Cl- have the most influence

• P = relative permeability of ion

• denominator and numerator of Cl- is reversed due to negative charge on ion

graded potential

decreases in strength as it spreads out from a point of origin

• variable, can be different levels (intensity)

• occurs in dendrites, cell body

• usually receives a chemical signal

• if signal is above a threshold when it reaches the ‘trigger zone’, it causes an action potential

action potential

depolarizations that travel long distances down axon

• all-or-nothing (frequency)

• occurs in trigger zone through axon

• uses voltage-gated channels (electrical signal)

• fires over and over until graded potential fades

conduction: high speed movement of action potential along axon

action potential (steps)

Depolarization:

• An Na+ gated channel is opened. Na+ enters the cell.

• Voltage-gated Na+ and K+ channels begin to open.

• Even more Na+ enters the cell (positive feedback loop).

Repolarization:

• Delayed opening of K+ voltage-gated channels. K+ exits the cell.

• Inactivation gates close and stop Na+ from entering cell.

Hyperpolarization:

• K+ leaving the cell.

• Na+ channels reset (voltage gate closes, inactivation gate opens)

Resting:

• both K+ and Na+ channels closed.

refractory period

absolute refractory period

• can’t fire another action potential during this time

• reset of Na+ gates (inactivation gate opens, voltage gate closes)

• prevents action potential from going backward or overlapping

relative refractory period

• action potential can fire but requires larger stimulus

• some but not all Na+ gates are reset

• K+ gates are still open

action potential speed

speed of action potential influenced by:

• diameter of axon (larger = faster)

• resistance of axon membrane to ion leakage (myelinated = faster)

  • only Nodes of Ranvier have channels - action potentials “jump” between nodes.

  • saltatory conduction

electrical vs chemical synapses

electrical synapse

• pass electrical signals through gap junctions

• can be bidirectional

• synchronizes activity of a network of cells

chemical synapse

• neurotransmitters cross synaptic cleft

• unidirectional

neurotransmitter release

action potential reaches axon terminal

depolarization of axon terminal opens voltage-gated Ca2+ channels

Ca2+ enters cell, interacts with docked synpatic vesicles to trigger exocytosis

short diffusion of neurotransmitters across synpatic cleft

neurotransmitters bind receptors (ligand-gated) in postsynaptic cell

synaptic vesicles and docking proteins

SNARE proteins drive fusion

• tSNARE and vSNARE wind together

• SNAP-25 and other proteins make 4 helices

• bacterial toxins can target these proteins (botulism, botox, tetanus)

termination of neurotransmitter activity

three ways:

1. Take neurotransmitter back up into axon terminal

2. Break neurotransmitter down with an enzyme

3. Neurotransmitters diffuse out of synaptic cleft

synthesis and recycling of acetylcholine

mechanism:

• acetylcholine is synthesized in pre-synpatic cell

• in the synaptic cleft, acetylcholinesterase breaks down acetylcholine

• choline taken back up into pre-synaptic cell by cotransport with Na+

• choline is recycled to make more acetylcholine

affected by:

• nerve gas: inactivates acetylcholinesterase, muscles constantly activated (spasms)

• curare: antagonist to receptors, die of paralysis

convergent and divergent neuron pathways

divergent: one neuron sends signal to many other neurons

convergent: many neurons sends signals to one neuron

postsynaptic responses

excitatory depolarization (EPSP): makes an action potential more likely

• open Na+ channels (more Na+ in)

• close K+ channels (less K+ out)

inhibitory hyperpolarization (IPSP): makes an action potential less likely

• close Na+ channels (less Na+ in)

• open K+ channels (more K+ out)

• open Cl- channels (more Cl- in)

long-term potentiation and depression

long-term potentiation (LTP): permanent increase in connection

long-term depression (LTD): permanent decrease in connection

glutamate is key:

• has receptors AMPA and NMDA

• NMDA is blocked by a gate and Mg2+ ion

  • Mg2+ ion is released when depolarization occurs through AMPA channel opening

• when MG2+ ion os released, Ca2+ flows in and activates second messenger pathway (LTP)

• sensitivity to glutamate is increased

spatial summation

additive effect of multiple neurons sending a signal to another neuron at the same time (more than one graded potential)

• if several excitatory neurons fire at the same time, they might not individually reach the threshold for an action potential, but together they do

• if excitatory and inhibitory neurons fire at the same time, their effects can ‘cancel out’

temporal summation

additive effect of multiple neurons sending a signal to another neuron close together in time (more than one graded potential)

• if graded potentials are too far apart in time, then no summation occurs

• if graded potentials are close together in time & arrive at trigger zone in short period of time, they may sum and create an action potential

hormones

hormone: chemical signal that goes throughout the body

• half-life = length of activity

classification:

1. Peptide hormones

2. Steroid hormones

3. Amino-acid derived hormones

peptide hormones

storage: made in advance, store in secretory vesicles

release from parent cell: exocytosis

transport in blood: dissolved in plasma

half-life: short

receptor location: cell membrane

response: seccond messenger system, fast

peptide hormone synthesis

proteolytic, post-translational modification

preprohormone: large, inactive precursor

• cleaved in ER to become prohormone

prohormone: smaller, inactive precursor

• cleaved in secretory vesicle to become active hormone

steroid hormones

cholesterol-derived, lipophilic

storage: synthesized on demand, made in adrenal glands and gonads

release from parent cell: simple diffusionbinds

transport in blood: carrier proteins

half-life: long

receptor location: usually cytoplasm & nucleus, sometimes cell membrane

response: usually gene activation (slow), sometimes nongenomic (fast)

amino-acid derived hormones: catecholamines

modify tyrosine R group, behave like peptides

storage: made in advance, store in secretory vesicles

release from parent cell: exocytosis

transport in blood: dissolve in plasma

half-life: short

receptor location: cell membrane

response: seccond messenger system, fast

amino-acid derived hormones: thyroid

made from 2 Tyr and iodine, behave like steroid

storage: made in advance, store in secretory vesicles

release from parent cell: transport protein

transport in blood: carrier proteins

half-life: long

receptor location: nucleus

response: gene activation, slow

example: parathyroid simple endocrine reflex

input: low concentration of blood Ca2+

integrating center: parathyroid cell

efferent pathway: parathyroid hormone released into bloodstream

effector: bone and kidney

response:

• increase bone resporption (release Ca2+)

• increase kidney reabsorption of Ca2+

• produce calcitrol → increase intestinal absorption of Ca2+

increase concentration of blood Ca2+ (negative feedback)

neurohormones

1. Catecholamines (from adrenal medulla)

2. Hypothalamus

3. Pituitary gland (anterior and posterior)

anterior pituitary

endocrine tissue - secretes 6 hormones

• release is controlled by neurohormones from hypothalamus

process:

1. hypothalamus neurons realease neurohormones into capillaries of portal system

2. portal veins carry neurohormones directly to anterior pituitary

3. endocrine cells release their peptide hormones into capillaries for distribution to rest of body

posterior pituitary

neural tissue -secretes 2 neurohormones

process:

1. neurohormone made and packaged in cell body of neuron (hypothalamus region)

2. vesicles transported down the cell

3. vesicles containing neurohormone are stored in posterior pituitary

4. neurohormones released directly into the blood

endocrine control

Three integrating centers of hypothalamus-pituitary

1. Hypothalamus: stimulated by CNS

2. Anterior pituitary: stimulated by hypothalamic hormones that travel thru portal system

3. Endocrine gland: stimulated by anterior pituitary hormones

short-loop and long-loop negative feedback

short-loop: a pituitary hormone feeds back to decrease hormone secretion by the hypothalamus

long-loop: the hormone secreted by the peripheral endocrine gland feeds back to suppress secretion of its anterior pituitary and hypothalamic hormones

example: growth hormone

1. Hypothalamus releases growth hormone-releasing hormone (GHRH) into portal system.

2. GHRH acts on anterior pituitary growth hormone cells to release growth hormone (GH) into bloodstream.

3. GH acts on liver cells to release insulin-like growth factors (IGFs) into bloodstream.

4. IGFs act on bone and soft tissue to stimulate growth.

example: cortisol

1. Hypothalamus releases corticotropin-releasing hormone (CRH) into portal system.

2. CRH acts on anterior pituitary to release adrenocorticotropin (ACTH) into bloodstream.

3. ACTH acts on the adrenal cortex to release cortisol into bloodstream.

4. Cortisol feeds back to suppress secretion off CRH and ACTH. (long-loop negative feedback)

exogenous cortisol: will supress secretion in hypothalamus and anterior pituitary, but stimulate target tissue

hormone interactions

synergism: combined hormone effect is greater than sum of the individual effects

permissiveness: need a second hormone for full effect

antagonism: one hormone opposes the action of the other

hormone pathologies terms

hypersecretion: excess hormone production

hyposecretion: insufficient hormone production

hypertrophy: enlargement of organ/gland

atrophy: decrease in size of organ/gland

down-regulation: decreased number of receptors

hormone pathologies diagnosis

diagnose based on relative hormone levels

• primary: issue is with last endocrine gland in pathway

• secondary: issue with pituitary gland

• tertiary: issue with hypothalamus

CNS: meninges

membranes that provide protection and cushioning for brain

• dura mater (outer)

• arachnoid membrane

• pia mater (inner)

CNS: anatomy

CNS: white and gray matter

gray matter: cell bodies

white matter: myelinated axons

ex: cerebral cortex cell layers

CNS: cerebrospinal fluid

water & materials from blood transported through layer of endothelial cells to cerebrospinal fluid (CSF)

• CSF circulates through CNS

• fluid returns to veins through arachnoid villi

blood-brain barrier

usually endothelial cells are ‘leaky’, but in the brain tight junctions prevent solute movement between endothelial cells

astrocytes surrounding blood vessel promote tight junction formation

spinal cord

• afferent tracks go up toward brain: dorsal/back

• efferent tracks go down away from brain: ventral/front

diencephalon

diencephalon = hypothalamus + thalamus

• thalamus: relay station, senses that are coming in

• hypothalamus: homeostasis control center, subconscious

basal nuclei, corpus callosum, & limbic system

basal nuclei (ganglia): control of movement

corpus callosum: communication between hemispheres

limbic system:

• cingulate gyrus: emotion

• hippocampus: learning and memory

• amygdala: emotion, reflexive memory, fear

cerebral cortex

frontal lobe:

• gustatory cortex

• behavior, coordinate info from other association areas

parietal lobe: sensory info from skin, muscluloskeletal system, viscera, taste buds

occipital lobe: vision

temporal lobe: auditory cortex, olfactory cortex

lateralization and crossover

visual field crossover: optic chiasmus

sensory & motor crossover: spinal cord

lateralization: certain functions on one side of brain

• geometry and music on right

• language and symbols on left