Structure and Function of the Nervous System Flashcards

1
Q

Describe soma dendrites axons and glial cells

A

Soma: cell body, processing plant

- Proteins that need to be made are made HERE. 
- Processing, make receptors, microtubules transport them to dendrites or axon 

Dendrites: extensions off cell body, inputs come here

- Shafts (long main branches and tertiary branches) 
- Spines (where the synapses are re-mostly) 

Axon: conduct electrical signal to terminal buttons

- One neuron can have multiple axon collaterals. 
- One neuron could effect lots of axons at the same time 

Glial cells: no electrical properties, play roles in neural activity

- Structural support
- Blood brain barrier 
- Regulate ion concentrations around cells (needed for electical activity)
- Reuptake of certain neurotrasmitters
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2
Q

Describe the two main types of neurons we will discuss in this class?

A

Classes based on how they’re connected
1. Projection neurons (principle)
Main integrating and processing info coming from other cells (other cells/brain regions)
Send axons that project outside of that brain region (long axons that go to another region)
Send axons that go to local neurons.
Can be built differently/different properties/different transmaters
Cortical pyramidal cells (glutamate)
Striatal spiny: smaller, very spiny. Found in striatum. (GABA)

	2. Interneurons: reside between sensory and motor. But also to cells whos axon remain within a particular brain regions. Very localized. Make connections to interneurons or projection neurons. 
		Smaller than projection 
		High firing rates
		Inhibitory (mostly) 
GABA or ACH
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3
Q

Describe neuronal cell membranes and proteins within them.

A

Phospholipid bilayer with proteins
1. Receptors (initial sites of action of neurotransmitters/drugs)
2. Enzymes: catalyze, etc.
3. Ion channels and pumps (transporters, active) that allow charged molecules to pass through, amino acids/glucose
Ion channels are crutial to the cell.
Sodium, Potassium, Chloride and Calcium
Polarized, need ion channels
Ion channels are typically specific to an ion.
Gated channels are closed, open in response to a specific stimuli. Stay open for a brief period. The way they open up allows neurons to behave the way that they do.

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4
Q

Describe gated ion channels?

A

When ion channels open: excite (Na or Ca to pass) or inhibit (K+ Cl+ to pass) (depolarize/hyperpolarize)

Ionic conductance: ex: if it conducts calcium or sodium, it is excitatory
If it conducts potassium or chlorium its inhibitory.

Voltage gated: voltage of the membrane/electrical potential across the membrane (alters configuration so that they open up)
Ex: potassium: the inner positive proteins in the ion channel to shift towards the negative charge and opens the pore in the center (see image)
Most open when its depolarized, and close at hyperpolarize but some time it’s the other way around.

Ligand Gated: when something binds to it it opens up.
- Ionotropic is a type of ligand gated receptor!

2nd messenger ion channels: closed at rest, but when 2nd messenger adds a group (phosphate group) changes it shape.

Some are ligand and voltage gated: molecule sticks to a part of the channel and the membrane voltage is correct. NMDA glutamate receptors.

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5
Q

Describe the electrical properties of neurons

A
  • Difference in positive vs negatively charged particles.
    • At rest: it’s negative (more negative inside than outside)

In a normal cell: its -100mv (negative inside proteins, positive outside ions)

Potassium channel (non-gated): potassium can get inside! 
Sodium channel (voltage gated): when cell is at rest, they're closed. 

When potassium comes in, its about -70mv before it reaches equilibrium. More potassium inside compared to outside.

Resting potential: ready to change.
When a cell fires action potential…

If something depolarizes the cell a little (a few more positive things go in the cell)

- Goes from -70 to -50. 
- The process is started. 

Voltage gated sodium channels OPEN.
Na+ move inside, so much that the membrane potential changes to +45.
- So so fast! <1 ms.
- Positive membrane potential.

Voltage gated potassium channels open when its +45
This allows potassium ions to go out of the cell, repolarizes and overshoots it at -90 mV

Now everything is messed up :(
Sodium potassium pump use active transport (O2 and ATP) takes sodium out, takes potassium in. (3 sodium out, 2 potassium in)
If brain doesn’t get oxygen, neurons can’t repolarize after they fire an action potential, the ions will be in disarray.

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6
Q

Describe how an action potential can happen? And the difference between EPSPs and APS

A

The action potential is caused by EPSP or ISPS

- If enough connections come it, it can SUM UP inputs and cause an AP 
- Local potentials driven by synaptic inputs that cause EPSPs or IPSPs (slight depolarizations, slight change triggered by ion fluxes that occur through ligand gatd ion channels, and this can trigger threshold potential to be reached and fire. 

Graded: vary in magnitude. Larger stimulus, more nt released, the greater the depolarization/hyperpolarizatoin.
- Lots of small little ones can SUM together to make an AP. 1 input will not cause it to fire, but summing it will.

Probabalistic: pushing it to go one way or another: balance of power over exitatory vs inhibitory inputs.

Aps are all or none: size is unrelated to amount of depolarization

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7
Q

Describe the organization of the nervous system

A

Organization of Nervous system
CNS (brain and spine)
PNS (nerved in the body) - good for side effects
- Somatic: volunary muscles/movements do stuff. Delivering sensory input from body to brain
- Autonomic: internal environment, organs, not under volunary control without jedi powers, smooth muscles (intestines bladder), cardiac muscles , glands (adrenal, salivary, hormone release)
Digestion, blood pressure, body temp and other functions.

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8
Q

Describe the sympathetic nervous system and parasympathetic nervous system

A

Sympathetic: fight or flight, stress, excitement. Turns on when you need to exert. Be more alert, have energy reserves ready to go.
Sympathetic, im in trouble, have sympathy for me
- Increased heart rate, need more stuff to muscles, increase blood pressure, blood flow to muscles, increase in adrenaline, pupillary dilation (more light to get into your eyes),
- Turns off digestion and other hormones

Parasympathetic: energy reserved conserved (peace time)
- Increase in salivation, digestion, store of glucose, slows heart rate, decrease respiration. Body maintenance and repair.

Antagonistically.

ANS usues: noepinephrine (NE) or ACH acytlcholine as transmitters
- Many psychoactive drugs effect these systems.
Blood goes in entire body. Leads to side effects (blood pressure, dry mouth, pulillary dilation, urinary issues, digestive issues)

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9
Q

Describe the smypathetic nervous system and its neurotransmitters in more detail.

A

Spinal cord sents ach to sympathetic ganglia (and adrenal glands)

  • exitatory
  • nicotinic receptors (ionotropic)

Sypmathetic ganglion send NE inputs to organs
NE is secreted in bloodstream from adrenal glands.
NE is excitatory or inhibitory (exitatory on heart, inhibitory on stomach)

*Drugs that increase/decrease NE activity increase/decrease sympathetic activation (antidepressants can increase sympathetic activation)
• Drugs may block NE receptors, turn down sympathetic NS.
• Drugs can effect Nicotinic receptors (nicotine)
○ Drusg that incrase ACH or stimulate nicotinic receptors, have effect on sympathetic functioning (fire more)
Cholenergic drugs have lots of effects (activate sympathetic NS, stimulating sympathetic ganglia so they release NE.

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10
Q

Describe the parasympathetic system in more detail.

A

ACH only. at parasympathetic ganglion and then to glands

  • first with nicotinic
  • then with muscarinic receptors (metabotropic). (depending on subtype, have different effects)
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11
Q

What are the effects of cholenergic drugs on the (para)sympathetic NS?

A

Muscarinic antagonists slow para function (resembling sympa function) looks like you’re increasing NE release.

Muscarinic agonists do the opposite.

When ACH levels are increased, fluids are often secreted.

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12
Q

What happens to drugs that stimulate nicotinic receptors or increase ACH release more generally?

A
  • Body is a mess. When artificially.
    • Nicotinic recpeotr activated on parasympatheic and sympa ganglia. Both systems are turned on.
    • Sympatheic and parasympatheic
    • Increase in heart rate and increase in gastro motility.
      Normally when one turns on one turns off, drugs can turn both systems on at the same time. Very uncomfortable.
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13
Q

Describe the my/met/mesencephalon

A
  • Nuceli that have cell bodies that hold NT (dop, NE, opiods)
    • Neurons that use those NT, those cell bodies (located in areas in the back of the brain )
    • Send long axons to the whole brain
      Broadcast signal (neuron fires in back of the brain, axons release DOP in multiple brain regions)
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14
Q

Describe the basal ganglia

A
  1. Basal Ganglia: 5 nuceli for motor coorniation and action
    Striatum (projections are medium spiny neurons)
         DORSAL STRIATUM (Caudate/Putamen, in rats they're mushed). Motor learning, refine actions. 
         Receives excitatory inputs from all brain and sensory motor cortex specifically. And dopamine from sub nigra
         Some motor signals go to spinal chord, other parallel signals go to dorsal striatum and make the movements more automatic (habitual behavior) 
         Learning the best way to move your body. 
         Damage: huntingtons lose med spiny neurons
         Parkinsons: lose dopamine input to stritaum 
         Can't do motor movement coordinations. 
    
         VENTRAL STRIATUM. (nucleus accumbens (septi)) 
    
         - Reward and motivated behaviors 
         - Limbic regions and dopamine from VTA (mesencephalon)
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15
Q

Describe the limbic system

A

Limbic system: emotion, memory, motivation, learning

- Lots of nuclei, from Papes (dogs who had rabies had damage here, same for humans in post mortem) 
- Olfactory bulb, amygdala, hipopocampus, mammillary body, thalamus, cingulate cortex, fornix.
- Four Fs

Limbic: anatomical locations relative to cortex. Limbic means edge. Reside on lower border of the cerebral cortex.
KEY REGIONS:
- Hippocampus: LT memory, identify relationship between stim, spatial memory. Target for antidepressants.
- Amygdala: various compoenents of emotional response (fear and anxiety, connections to other regions). Sounds downward projections and regulate endocrine responses. Target for anti-anxiety drugs. Reward Learning.
○ Both connected to each other, and frontal lobes and nucelus accumbens.
- Hypothalamus (Regulatory), Nucleus accumbens, Recieves projections from hippo and amyg, and PFC. Large region. Prefrontal cingulate cortex: cingulate cortex is connected to other aspects of the limbic system. Most similar to cells and connectivity with other animals.

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16
Q

Describe the cerebral cortex and brodmann’s areas.

A

Largest structure: cerebral cortex
- Most relevant for us: frontal lobes.

Brodmann: looked at different regions and divided them based on how cells worked. Or other functions. Or how they were organized.
50 areas: Brodmann’s areas. Distinguish one part of the cortex from another. Numbered these regions.

PFC has a lot of functions

- Planning, choices, strategies, decisions, emotional response, connections to amygdala. 
- Many disorders are impaired here. 

Frontal lobes also have motor cortex and some sensory.

- But since we're more complex, we have this prefrontal cortex cause we are so fun. 
- Humans: frontal cortex devoted to PFC, bigger than any animal.
17
Q

Describe the connections of the PFC to the rest of the brain.

A

PFC
Connections to the rest of the brain.
Different regions: connected to different nuceli.

- Hippocampus 
- Amygdala reciprocal connections 
- Striatum, influence motor output/action selection 

PFC as a whole: not a decision or anything “Center”
It coordinates and integrates info to solve more complex problems
- Surprise, ambiguous
- Not for simple functions (association areas)

Can help you distinguish between memories, but doesn’t store memories
Doesn’t generate emotinoal responses, but can use emotions to identify threats/relevance
Coordinate activity in amygdala (descending projections)
Coordinate actions due to striatum.

18
Q

Convince me that the telencephalon has a lot of receptors we will be talking about (give an example.

A

Drugs can effect dop, serotonin, ach, opiod, noep are targets.
RELATIVE AMOUNT OF DIFFERENT NT AND RECEPTORS CAN DIFFER BETWEEN BRAIN REGIONS.
EXAMPLE: Striatum and PFC both have DOP and NE. Concentrations of these things + receptors differs between them. Striatum has more dopamine, PFC has more NE than dop. Same with receptors.
When you give a drug that targets a receptor in more than 1 brain region, dose will be exerted where there is a region where there are more receptors.