1) Cell Body

2) Dendrites

3)Axon

Details about axon

what organellels are not found here

1) Boutons/ synaptic end feet

 2) Varicosities

Types of Axons

 Golgi Type 1

Golgi Type 2

Type 1 are long and projection

Type 2 are short, interneurons, and more prevelent.

Dendrite VS. Axon

 Organelles that they do not contain

Dendrites- do not contain golgi bodies

 Axon- do not contain golgi bodies, RER, and ribosomes

Dendrite VS. Axon

 Physical characteristics

Dendrites- Tapers as it goes away from soma, have spines where bulk synaptic reception occurs, Branch profousely

Axon- cylindrical, varicosities, and boutons at terminal end of axon

Dendrite VS. Axon

Mylination

Dendrite- never

Axon- can be

Dendrite VS. Axon

where do ramification occur

Dendrite- close to cell body

 Axons- close or far away

Dendrite VS. Axon

electrical activity

Dendrite- No action potentialm, only graded depolarization and hyperpolarization

Axon- Action potentials

Dendrite VS. Axon

synaptic activity

Dendrite- mostly postsynaptic, but also may be presynaptic in ( dendro-dendrity synapse)

Axon- Presynaptic mainly, but postsynaptic in (axo-axonal synapse)

Dendrite VS. Axon

Energy consumption

Dendrites- most energy consumption, to bring back to Em of cell after each depolarization or hyperpolarization

Axon- low in axon trunck, but may be high in terminals

RER found where?

RER is also known as?

cell body, and dendrites. NOT found in axonal hillock.

AKA: Nissel Substance

Microfilaments

1) diameter

2) single molecule subunit 

3) role

4) how are they assembled

1) 5-8 nm diameter

2) actin

3) helps to change cells shape.

4) are assembled in a single helix

Neurofilaments

1)diameter

2)  how are they assembled

3) Associated with with which disease

1) 10 nm

2) Polar diamer-> non-polar tetramer-> Protofilaments-> Protofibril -> 10 nm neurofilament

3) Alzheimer's Disease

Microtubules

1) diameter

2) how is it polar in axon?

3) subunits?

4) how is assembled?

 5) importance

1) 20-25 nm

2) possitive end goes toward axon terminus

3) alpha and beta tubulin

4) 13 protofilaments form a hollow tube, and they are polar.

5) Filament important in support for dendrites and axons.

1) soma is site of synthesis of protiens, macromolecules, and organelles -> to get them to Axon

2) Axons are long and stuff won't diffuse there fast enough

3) degraded protiens and vesicules need to come back to soma

4) diffusion to slow

Slow axonal transport:

1) moves in which direction

2) two components and what do they move

1) anterograde only

2) a) slow- moves microtubules, nuerofilaments and soluble protiens

b) faster component- moves actin, metabolic protiens, and calmodulin.

Fast antergrade axonal transport

two protiens that allow this to happen?

which way do they move?

What do they move?

A) Kenisin (+). Moves subcellular organellels

B) dynein (-), moves lysomes with stuff that needs to be degraded, recycled membranes, growth factors, viruses, and toxic chemicals

1.  impermeable to ions
2. functions as a capcitor
3.  creates mebrane potential
4.  ions flow through channels.

1) Voltage gated

2) Ligand gated

3) Thermally gated

4) Mechanically gated

Ex=-RT/zF*ln([Xi]/[Xo])

Ex=-0.058/z*ln([Xi]/[Xo])

1) Electrochemical Gradient

 2) Conductance of the Channel

1) threshold

2) All-or-none response

3) latency - time between ap and depolarization starts

4) refractory period

Intracellular- tells you Em

Patch clamp- gives you currents of each ion.

• What is myotonia
• 2 diseases with these symptoms
• physiological reason why it happens?

• difficulty in relaxing a contracted muscles.
• Thomsen's Disease and Becker's Disease.
• Cl- channel abnormality, that prevents the channel from opening. This makes the muscle cells very excitble, because hyperpolarizing effect of Cl- is lost.

1) A's dendrite has a larger diameter than B.

2) A is more excitable than B.

3) A has a higher longitudinal resistance than that of B.

4) A has less density of voltage-gated Na channels along its axon than Neuron B.  

1) true

2) true; (See curves of excitability; this means that it would need less de-polarization to fire an A.P..  So yes.)

3) False

4) Flase (More Na channels means it is more excitable.)

Epilepsy is an inherited condition caused by increased electrical activity (like increased A.P. firing rate).  30% have a known acquired cause (like head trauma, stroke, tumor).  70% are idiopathic.  Genetic factors are believed to be central.  Which of the following genetic mutations can contribute to epilepsy?

Mutation in channels resulting in…

1) …increased gNa?

2) …decreased gK?

3) …increased gCl?

1)Yes 

2) Yes

3) No; (Since there's more chloride outside, this means more would come inside, which leads to hyper-polarization!)

Which is true about voltage-gated Na channels?

1. -it is a transmembrane protein (yes)
2. -self-inactivate
3. -glutamate activates it
4. -blocked by TEA

1. yes
2. yes; leads to refractory period
3. no, voltage gated
4. no, only potassium channels

1. Glutamates role in mind?
2. Where is it found?
3. What type of sypnapse is used?
4. What type of neurons?

1. Primary excititory neurotrasmiter of CNS
2. found all over spine and brain
3. Asymetrical synapse
4. Principle outflow nuerons from a brain region

1. How is Glutamate synthesized in CNS? Major pathway
2. Minor Pathway
3. Does it cross blood brain barrier?

1. Glutamine is converted to Glutamate by glutaminase
2. glutamate dehydrogenase allows NH3 and alpha-ketoglutamate combine to form glutamate.
3. NO

1. What intiates Glutamate relese?
2. How does Glutamate get into its vessicle?
3. How is its activity inhibited?

1. Ca+2
2. VGluT protien uses energy to put glutamate into the vessicle
3. Inhibited by auto-regulators such as mGluR2 and mGluR3

1. How is Glutamate inactvated?

1. Glutamate is taken up into astrocytes from synaptic space by EAAT.  This channel uses a sodium symport system.
2. Then glutamate converted to glutamine via glutamate synthetase.
3. Glutamamine then becomes transported into neuron where it becomes Glu

Three types of Glutamate receptors and describe them.

1. AMPA- ionotropic; move both K+ and Na+, but mainly Na+; primary excititory receptor of brain.
2. Kainate- ionotropic
3. NMDA- metabotropic.  Needs glycine and AP as well as glutamate to open channel and displace Mg+2 plug to let Ca+2 through. Plays a role in synaptic plasticity.

mGluR's

• metabotropic glutamate receptors
• they are g protien linked
• in post synaptic cells caused more Ca+2 to enter cytoplasm from sarcoplasmic reticulum or by coupled ion channels.
• Presynaptic- modulates glutamate release

Excitotoxicity

1. Define
2. Diseases it can cause
3. When it can occur

1. When the neuron gets to excited it lets too much Ca+2 into the cell which can cause irreprebal harm
2. ALS and Huntington's
3. Also occurs when cell is stavrved for nutrients like O2 and Carbohydrates.

1. Where are noradrenergic neurons found?
2. What role do these neurons play?

1. The hind brain- Pons, medulla oblongate, and midbrain.  AKA ventricular system
2. Important in arousal of mind and autonomic functions.

Synthesis of norepinephrine

1. tyrosine- Tyrosine hydroxylase
2. DOPA- DOPA decarboxylase
3. Dopamine- Dopamine beta hydroxlase (found in secretory vessicle)
4. Norepinephrine

• The rate limiting enzyme is tyrosine hydroxylase. 
• The affinity of tyrosine hydroxylase for BH4 is regulated by phosphyralation on specific serine residues. 
• Increased intracellular Ca+ levels leads PKA to phosphorylate the serines
• Auto receptors cause cAMP break down--> decreased PKA activity.
• Also end product inhibition; Norepinephrine leaks out of vesicles and inhibits tyrosine hydroxylase

1. How does dopamine get into the vessicle?

Three Mechanisms for norepinephrine release

1. Ca+ dependent vesicle fusion
2. Reverse plasma membrane transport
3. Dendridic Release of vesicles that is not Ca+2 dependent.

1. leaking out of vesicles VMAT2
2. what ever is reabsorbed from the synapse

1. How does alpha2 receptor activity affect norepinephrine production?
2. How does beta receptor activation affect norepinephrine production?

1. decreases cAMP levels in cell, leading to less phosphorylation of tyrosine hydoxylase
2. increases Ca+2 concentration in cell-> cAMP levels increase -> PKA activity increases.

1. Diffusion out of synaptic cleft
2. Reuptake into presynaptic neuron by transporters that use sodium as co-transporter.
3. Then it is deactivated by 1) MAO or (2) catechol-O-methyl-transferase (COMT) uses SAM.

1. What does binding of norepinephrine to its receptor result in?
2. diffrence between alpha and beta
3. diffrence between alpha1 and alpha2 receptors
4. What regulates these receptors ability to activate signal transduction and receptor quantity?

1. g-protiens
2. Alpha receptors bind to norepinephrine better than epinephrine.  the opposite is true for beta.
3. alpha1 are postsynaptic receptors in periphery; alpha2 are presynaptic that inhibit norepinephrine release by breaking down cAMP.
4. Changes in activation and amount of norephiephrine in the synapse.

1. What type of transmiter it nuerotensin?
2. What parts of the brain is it found in?
3. Can a neuron co-release it with another neurotransmiter?  If yes, than which ones?

1. peptide
2. prefrontal cortex, hypothalamus, and midbrain
3. yes, only dopamine

1. Peptide is synthesized as a 170 AA chain. The chain also contains another neurotransmiter neuromedin N
2. The neurotransmiter is then taken down the axon in dense core vessicles
3. Ca+2 dependent release, but requires high action potential frequency as well.
4. Release occurs anywhere, not just the active zone
5. Activation of dopamine autreceptor enhances its release.

Inactivation of Neurotensin (3 ways)

1. Nonselective peptidases
2. Diffusion
3. internalization of receptor to cell body of post synaptic cell.

1. G protien coupled

1. Anadamide is made up of which molecules and how are they linked?
2. Where is it found?
3. What is an agonist for the molecule?
4. What does it modulate?

1. arachidonic acid and ethanolamine linked by an amide bond
2. Striatum, limbic cortex, hippocampus, and cerebellum
3. Who got that gonja? THC
4. feeding, sleep, bp, balance and posture, memory, mood, and other neurotransmitters

Made the way you like it, fresh (synthesized on demand)  by two enzymes

1. Transcyclase- it is activated by high intracellular Ca+2 levels. to make NAPE
2.  NAPE cleaved to anandamide by phospholipaseD

Canaboid receptors

• Are g protien coupled
• Almost always presynaptic
• inhibits Ca+2 channel opening, hence inhibits neurotransmitter release. 

How does anadamide work?

when is it increased? 

• it is activity dependent, and retrograde in nature
• made when neuronal activity is high
• binds to a presynaptic receptor that inhibits Ca+2 influx, inhibiting neurotransmiter release
• Increased durng stroke seizures and brain trauma.