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84 Cards in this Set

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From DNA to proteins
1. Nucleus contains chromosomes
2. Chromosomes hold DNA
3. Genes produce mRNA
4. mRNA attaches to ribosomes produced by nucleolus
5. Ribosomes use mRNA info to produce proteins
6. Enzymes (proteins) catalyze reactions
Anterograde transport/Fast axoplasmic transport
kinesin molecules transport molecules from soma to terminal end
Retrograde transport
dyenein molecules transport molecules from terminal end to soma
-can pick up toxins
7 Functions of glial cells
1. Provide nutrients for neurons (neuroglia)
2. Provide structure to brain (neuroglia)
3. Myelinate neurons
4. Provide scaffolding during development (radial glial cells)
5. Function as phagocytes (engulf waste/damage, perform immune fuction; neuroglia)
6. Form scar tissue in brain (astrocytes)
7. Potassium buffering
Properties of the action potential
1. All or nothing event (RMP either passes threshold or not)
2. Propogated down axon membrane
3. Fixed amplitude--do not change in height in relation to signal info
4.Has conduction velocity (m/sec)
5. Has refractory period in which stimulation will not produce an AP--limits firing rate
2 forces acting on ions across axon membrane
1. diffusion--want to go from high to low concentration
2. electrostatic pressure--opposite forces attract
Ion Phases of Action Potential
1. Sodium channels open, sodium begins to enter cell
2. Potassium channels open, potassium leaves cell
3. Sodium channels become inactivated, leads to refractory period, no more sodium enters cell
4. Potassium continues to leave cell--causes membrane to return to resting potential
5. Potassium channels close, sodium channels reset
6. Extra potassium outside membrane diffuses away
Saltatory conduction
In myelinated axons, AP jumps from node to node, depolarizes membrane at each node

-speeds up conduction velocity
Neurotransmitter release
1.Vesicles lie docked near pre-synaptic membrane
2.Arrival of AP at axon terminal opens voltage dependent calcium channels
3. Calcium ions change structure of proteins that bind the vesicles to the pre-synaptic membrane
4. Fusion pore is opened, results in merging of vesicular and pre-synaptic membranes
Postsynaptic receptors
1.Molecules of neurotransmitter bind to receptors located on postsynaptic membrane
2. Receptor activation opens postsynaptic ion channels
3. Ions flow through membrane, either produce depolarization or hyperpolarization
4. resulting postsynaptic potential depends on which ion channel is opened (excitatory/inhibitory)

--Postsynaptic receptors alter ion channels either directly (ionotropic, GABA, glutamate) or indirectly (metabotropic,using 2nd messenger=G-protein)
Termination of Postsynaptic Potentials
1. Binding of neurotransmitter to postsynaptic receptor results in a postsynaptic potential
2. Terminations of PSP accomplished via
A. Reuptake--> NT molecule transported back into cytoplasm of presynaptic membrane, NT molecule can be reused
B. Enzymatic deactivation--> enzyme destroys NT molecule
C. Reuptake by astrocytes
CNS
brain, spinal cord
PNS
cranial/spinal nerves, peripheral ganglia

1. efferent nerves= motor nerves, project to target organs/muscles
2. afferent nerves= carry sensory info to brain
Divisions of PNS
Autonomic (Involuntary), Somatic (Voluntary)
Divisions of Autonomic Nervous System
Sympathetic and Parasympathetic
Sympathetic Nervous System
1. Thorasic lumbar region
2. Fibers arranged short-long (ganglion in between spinal cord and organ)
3. Uses ACh at ganglion,Post-synaptic ganglion=norephinephrine secreting, Pre-ganglionic fibers=cholinergic
4. Concerned with energy expenditure because uses skeletal muscles digestion, automatic functions
Parasympathetic Nervous System
1. Cranio and Sacral regions
2. Long presyn fibers, short postsyn fibers
3. Presynaptic fibers cholinergic (use ACh), Post-ganglionic fibers also secrete ACh
4. Concerned with energy conservation
Divisions of the Adult Human Brain
Forebrain
Midbrain
Hindbrain
Forebrain
Diencephalon
Telencephalon
Midbrain
Mesencephalon
Hindbrain
Myelencephalon
Metencephalon
Telencephalon
Cerebral cortex
Basal ganglia
Limbic system
Diencephalon
Thalamus
Hypothalamus
Mesencephalon
Tectum tegmentum
Metencephalon
Cerebellum
Myelencephalon
Pons
Medulla oblongata
Medulla
controls vital reflexes
Pons area
many axons cross from one side of brain to other
Reticular formation
control motor areas of spinal cord, sends output to cerebral cortex, increasing arousal and attention
Raphe system
sends axons to much of forebrain, increases/decreases brain's readiness to respond to stimuli, has collection of cell bodies responsible for releasing serotonin in different parts of brain

-projection system
Cerebellum
controls movement, shifts of attention, balance and coordination
Superior and inferior colliculi
important in routes of sensory info
Thalamus
contains nuclei that receive sensory info and transmit it to cortex, all senses meet in thalamus
Hypothalamus
contains nuclei involved in integration of species typical behavior e.g. fighting, feeding, sexual behavior
Meninges
series of membranes that protect brain and spinal cord

3 layers
dura mater
arachnoid
pia mater
Ventricular system
1. Travels through brain and along spinal column
2. Helps to get rid of waste
3. Epidemal cells line 3rd and 4th ventricles, help move along and produce CSF
4. Assists in cushioning brain
Cerebrospinal fluid
1. Produced by choroid-plexus of ventricle
2. Brain floats in pool of CSF, reduces its weight from 1400 g to 80 g, increases its bouyancy
3. CSF also contained within 4 brain ventricles
Limbic system
involved in learning, memory, and emotional states, involves olfactory system
Structures of limbic system
hippocampus
amygdala
mammillary bodies
fornix
Hippocampus
involved in learning, memory
Amygdala
involved in emotion e.g. fear conditioning
Fornix
fiber bundle that interconnects the hippocampus with mammillary bodies
Basal ganglia
globus pallidus, caudate nucleus, putamen
-involved in control of movement
Pharmakinetics
study of drug absorption/administration:
1. absorption
2. distribution
3. metabolism of compound
4. elimination
Depot binding
drugs have a tendency to bind to various tissues in the body that are not necc. the site of action, prevents drug from binding to receptors at site of action in the same concentrations as it otherwise might
Effects of depot binding
1. Slows down rate of accumulation of the drug at the site of action
2. diminishes the concentration of the drug at the site of action
3. delays onset of the drug
4. prolongs action of drug
Common sites for depot binding
1. Albumin in blood
2. Fatty tissues
3. Bone
4. Muscle
5. Liver
6. Kidneys
Dose-Response Curve
relation between drug dose and magnitude of effect
-drugs can have more than one effect, vary in effectiveness
Therapeutic index
effectiveness of drug relative to its safety
Margin of safety
area between dose-response curve for positive effect and dose-response curve for negative effect
Tolerance
1. Repeated drug administration results in diminished drug effect, or requires increased dosage to maintain constant effect
2. Withdrawal effects=opposite effect, often accompanies tolerance
3. Tolerance can reflect decreased drug receptor binding or reduced postsynaptic action of drug
Sensitization
Repeated drug administration results in heightened drug effectiveness
Direct agonist
drug that binds to and activates a receptor
Antagonist
drug that binds to but does not activate, and can block, a receptor
Indirect agonist
drug that attaches to a binding site (not necc. the same as the neurotransmitter) and interferes with the normal action of the receptor
Agonist actions on Synaptic Transmission
1. Act as precursor, facilitate synthesis (e.g. LDOPA)
2. Stimulates release of NT (e.g. black widow spider venom)
3.Stimulate postsynaptic receptor (e.g. nicotine)
4. Blocks autoreceptors
5. Block reuptake
6. Inactivate enzyme
Autoreceptors
receptors on cell releasing NT, bind to NT being released, involved in self-regulation of presynaptic cell
heteroreceptors
can exist on both pre and postsynaptic cells, tends to bind to NT that cell is not releasing

e.g. glutamate receptors on serotonin cell allow membrane potential to be depolarized
Antagonist actions on Synaptic Transmission
1. Drug prevents storage of NT in vesicles (reserpine--monoamines)
2. Inhibits release of NT (botulinum toxin--ACh)
3. Blocks postsynaptic receptors (curare, atropine--ACh)
4. Inactivates synthetic enzyme (PCPA--serotonin)
5. Stimulates autoreceptors (apomorphine--dopamine)
Competitive binding
Drug binds to same place as ligand, likelihood depends on affinities
Noncompetitive binding
Drug binds to site other than ligand, explains how drug can have additive/multiplicative effect
-keeps channel open more often and longer
-bigger effect ultimately
Neuromodulators
have longer, more distal, prolonged effects
-use metabotropic receptors, tend to have bigger effect on brain as a whole

e.g. norepinephrine, dopamine, serotonin
Paracrine transmission
You can release NT/neuromod in synapse but it escapes the synapse and can have effects on other cells in the surrounding area

e.g. serotonin acts on cells in surrounding area, not enough at synapse; Prozac works to change amount of serotonin available and thus change the system as a whole
NMDA receptors
Important for learning induction, but not necessarily learning expression
Carl Lashley
1950s
-believed could find location in brain that had to do with memory (endogram)
-taught rats to run mazes, looked at cortex to find location using cuts
-tried to get rats to forget maze learning-->FAILED
Why Lashley failed
1. Assumed memories started in cerebral cortex
2. Assumed memories stored in discrete location
3. Assumed all memories physiologically the same
Richard F. Thompson
1980s
-Studied eyeblink response in rabbits, used classical conditioning (pair air puff with tone)
-Figured out that lesioning nucleus in cerebellum (lateral interpositus nucleus) has an effect on conditioning
-can interrupt learning
-lesioning causes permanent loss of eyeblink response to tone
Effect of Red Nucleus on Eyeblink Response
red nucleus= part of motor system, connected to cerebellum
-if you block activity of the red nucleus during training, rabbits do not show eyeblink response
-after you let red nucleus recover, show very strong response

dilemma=rabbit did not appear to learn behavior
Result of Thompson studies
there is a location where a specific type of learning takes place

red nucleus=expression of learning
interpositus nucleus=induction of learning
Donald Hebb
1949
-at least 2 types of memory
-short term and long term
-brain damage effects both types
-short term memory=self-activating circuit

-memory=about how cells behave and the circuits they form
-if circuits stabilize long enough, a permanent change occurs, either chemical or physical
Later evidence for Hebb's theories
It is not length of time that strengthens memory, but emotional impact of the event
Why emotional impact strengthens memory
Emotional events cause a sympathetic reaction underlied by peripheral changes such as the release of adrenaline, increased conversion of glycogen to glucose
-stimulation of vagus nerve when something dramatic happens sends message to brain
-increased loc. coer. activity, stimulation of amygdala (helps you remember negative events)


-events that are emotionally arousing are underlied by a system to create memories esp. negative mechanism
Patient HM
1950s
destroyed medial temporal lobes
-anterograde amnesia (never able to form new memories)
-temporary retrograde amnesia
-removed amygdala, hippocampus
-impaired declarative memory (hippocampus important in)
Hippocampal formation
dentate gyrus
subiculum/subicular complex
Cornu ammonis regions, CA3 and dentate gyrus (hippocampus proper)

-hippocampus important for explicit memory
Hippocampal inputs
1. entorhinal cortex-projects to CA1, CA3, dentate gyrus
2. perirhinal cortex-important for est. associations between pairs of stimuli
Hippocampal projections
1. entorhinal cortex
2. perirhinal cortex
3. gyrus around hippocampus
Hippocampus important in
1. explicit long term memory
2. spatial memory
3. retrieving info you have already learned
Patient RB
Suffered cardiac arrest
Left CA1 regions damaged
Caused severe anterograde amnesia, some retrograde amnesia

-showed CA1 region important for forming new memories, somewhat important for retrieving old memories
Tseing
created mice with knocked out NMDA receptors in hippocampus
-bad spatial memory
-tried giving knocked-in NMDA receptors, but vulnerable to hypoxia, metabolic disturbances
condition most likely to produce retrograde amnesia
damage to medial temporal lobes extending to hippocampus but not CA1 region
Role of serotonin in hippocampal activity
suppressive effect on LTP in hippocampal formation because decreases dendritic spines on parametal cells (release glutamate)
Role of norepinephrine in hippocampal activity
activation of norepinephrine beta receptors in dentate gyrus facilitates LTP
Role of dopamine in hippocampal activity
Facilitates LTP, blockage of dopamine can disrupt learning and memory tasks
Role of ACh in hippocampal activity
Faciliates LTP, generates a lot of theta waves