1) neurons

2) glial cells AKA glia

Number and fxn of neurons?

" " of glia?

100 billion neurons; fxn: communication

1 trillion glia (10x more than neurons); fxn: support system

Astrocytes

Oligodendrocytes

Schwann Cells

Microglia

Myelin in the CNS is provided by?

in the PNS?

CNS myelin - Oligodendrocytes

PNS myelin - Schwann Cells

Astrocytes form tight junctions with the endothelial cells that line capillaries and venules

Insulate axons with myelin in the CNS

*** Note: you should review the diagram on slide 4; it's very clear and provides a perspective that will help your mental image of myelination.

1) structural & metabolic support

2) Help clean up extracellular ions and neurotransmitterrs

3) Guide the migration of neurons during development

They examined the shapes of neurons under the microscope  (examined 'neuronal morphology')

Santiago Ramon y Cajal:

- The _________ Doctrine (year: ____)

- Using the Golgi stain they discovered that: ____________ .

The Neuron Doctrine (1889)

they discovered that the brain is a bunch of individual nerve cells linked by long extensions

(so NOT Golgi's  continuous mass model)

Neurons receive inputs from ________, pass info down the ______ toward the ______  ________ .

*Note: lots of variety in ___________ .

Neurons receive inputs from dendrites, pass info down the axon toward the nerve terminals

Lots of variety in MORPHOLOGY

What approximate range is the # of synapses cortical neurons make?

Is the upper limit of that range higher or lower for subcortical neurons?  (Name an example and give its approximate upper limit)

cortical: 1000-5000 synapses

 subcortical: many more

ex: cerebellar Purkinje cells make 200,000 synapses

Divergent: one neuron branches out to connect to many other neurons

Convergent: a neuron has inputs coming in from many other neurons

"Connections are many to many."

"Observed at all levels: molecular, cellular, operational, systems levels"

The above to statements are explaining the property of neurons known as ____________.

Where are NTs synthesized?

Where are they released from?

Where do they bind the post-synaptic neuron?

synth'd: in the cell body OR synaptic terminals

released: from synaptic vesicles by the presynaptic neuron

post-release: bind receptors on post-syn. neuron

glutamate (Glu)

acetylcholine (Ach)

Gamma-aminobutyric acid (GABA)

glycine (Gly)

Dopamine (DA)

Norepinephrine (NE)

Serotonin (5-HT)

Volume transmission

Acetylcholine facilitates _________ & _________

and is affected in this illness/disease/disorder: 

Ach facilitates learning and memory

and is affected in Alzheimer's Disease

vigilance

&

preparation for action

3 functions of dopamine (as a neuromodulator):

1) facilitates movement

2) reinforces behaviors

3) keeps info in short-term (working) mem.

low DA levels in:

high DA levels in:

low DA = Parkinson's Disease

high DA = schizophrenia

serotonin inhibits some behaviors

and is affected in depression

When elec. impulses carry signal within a neuron:

inputs from other neurons elicit _____s (aka _______ _______s) that travel down the neuron _________ly and decay __________ly.

When elec. impulses carry signal within a neuron:

Neuron Anatomy

Place where inputs received:

Cell body / basic cell functions carried out:

Where passive currents are summed:

Place where APs are transmitted:

Where NT-filled vesicles released into synapse:

Fatty substance insulating the axon to facilitate conduction:

Place where inputs received: dendrites

Cell body / basic cell functions carried out: soma

Where passive currents are summed: axon hillock

Place where APs are transmitted: axon

Where NT-filled vesicles released into synapse: nerve terminals

What is the first, most immediate next step that occurs after an AP travels down the axon?

 And after that?

1) voltage-gated calcium channels open

2) calcium triggers 'cascade of events' causing vesicles to fuse to membrane and release NT into synapse

The NT binding to the receptor leads to a second messenger signaling cascade (involving second messengers and G-proteins) that results in an ion channel opening.

Unnecessary note: the simplification here is that a metabotropic pathway is NOT always just another way to get an ion channel to open. The 2nd messenger/G-protein pathway can have many steps and lead to many other things.

- The drug is a precursor to the NT being synthesized

- Drug prevents packing of NT into vesicles

- Drug [in]activates enzyme that synths NT

- Drug blocks NT reuptake

- Drug inactivates acetylcholinesterase

- Drug stimulates/blocks post-synaptic receptors

- Drug blocks/stimulates autoreceptors

problem = low serotonin levels

treatment = SSRIs

(selective serotonin reuptake inhibitors)

SSRIs block the reuptake of 5-HT into the presynaptic cell

Example: Fluoxetine (aka Prozac)

Describe the concentrations and locations of Na+ and K+ at resting membrane potential.

How is this polarization maintained?

high Na+ outside and high K+ inside

maintained by Na+/K+ ion pumps (in the cell membrane)

[obviously Na is pumped out and K is pumped in]

Cl- concentration is higher outside the cell.

Negative charges from proteins are inside the cell.

Know where the following are: resting membrane potential, EPSP, AP, hyperpolarization, return to resting potential

 [image]

Synaptic potential or receptor potential -->

1) Depolarization of membrane -->

2) Opening of voltage-gated Na+ channels -->

3) Na+ flows into neuron --> BACK TO STEP 1

1) Passive (nongated) - are open ALL THE TIME

2) Gated (their opening is triggered by something, for example, a voltage change)

Which ion channels are open to the outside and inside of the membrane and which ions are flowing in or out at each of the following phases of the AP:

- resting

- depolarization

- repolarization

- hyperpolarization (refractory period)

[next phase is resting again]

**Note: the pic this is based on (slide 35) shows the K+ channel with no 'gate' on the interior side of the channel (so it would always be open to the inside of the cell)

Resting: Na & K closed to outside, Na open to inside, no ion flow

Depolarization: K closed to outside, Na open to in & out, Na flowing in

Repolarization: Na closed to inside, K open to outside, K flowing out

Hyperpolarization: Na closed to outside, Na open to inside, K open to outside, K still flowing out

Myelin on axons increases ____ ____ and has what effect on signal speed and signal decay?

What is the transmission speed of the signal in saltatory conduction?

electrical insulation

speed = maximized

signal decay = minimized

speed = 120 m/s (meters/sec)

What disease results in demyelination of nerve fibers?

What effect does this have on nerve conduction?

multiple sclerosis (MS)

demyelination slows OR COMPLETELY DISRUPTS nerve conduction

(Note: symptoms of MS depend on the site of nerve damage, ie, which part of brain, which part of PNS, whether sensory or motor neurons are damaged...)

1) genetic AND environmental factors

2) abnormal neural development

3) abnormally high DA levels