What are the four main components of the brain stem?

What do they each consist of/do?

1.diencephalon: hypothalamus, thalamus (vision), epithalamus(hormones)

2. Mesencephalon: routes sensory info to the brain and sends out motor info

3. pons: ponteine centers deal with cardiovascular and respiratory nerves

4. medulla oblongata: continuous/ connector to the spinal

1. microglial cells: type of white blood cells that eliminate pathogens

2. oligodendrocytes: mylenate neurons in CNS

3. Schwann cells/neurolemmocyte: myelinate neurons in PNS

4. astrocyte: transports glucose across the blood brain barrier and into the brain

a RMP is a baseline charge difference between intracellular and extracellular compartments

it represents potential energy and energy that is stored with the potential to do work

regular cells: -40--> -90 mV

neurons: about -70mV but between -60 and -90 mV

high Na+ concentration outside of the cell

high K+ concentration inside the cell

K+ has higher differnce between it's concentration inside the cell and its concentration outside of the cell

Na+ wants in

K+ wants out

When dealing with values of "driving force" what does the positive or negative sign indicate?

In a neuron, how do the driving forces of Na+ and K+ differ? What does this mean?

A positive driving force means that the ion wants to move INTO the cell. A negative diving force means it wants to move OUT of a cell.

K+ has a driving force of -20mV while Na+ has a driving force of 130mV. This means that Na+ wants in more than K+ wants out.

1. K+ wants to move out of the cell, but because it is a + ion it attracts negative ions. So, as K+ moves towards the plamsa membrane, it brings along negative molecules that end up getting stuch on the inside of the plasma membrane when the K+ moves out.

2. Na/K pump, pumps out 3 Na+ and only lets in 2 K+ creating a charge difference across the membrane

3. K+ can easily leak out of channels which, as stated above creates a negative charge on the inside of the plasma membrane. As a result of that negative charge, Na+ is attracted to the outside of the plasma membrane.

RMP: baseline charge difference between intra and inter cellular compartments

Diffusion Potential: the electrogenic diffusion potential that accounts for most of the RMP

Action Potential: series of diffusions of Na+ and K+ down the axon of a neuron

Electrochemical equilibrium potential: Electrochemical equilibrium is the theoretical voltage that would be attained when an ion is at equilibrium inside and outside of the cell. The electrochem equil. potential is the difference between the equilibrium state and the current state of an ion. An ion that is far from being at equilibrium will have a higher electrochemical equilibrium potential.

It is used to estimate the equilibrium potential

Equil. Pot.=-60log(ion conc inside/ion conc ouside)

1. K+ is super permeable

2. There is a great

why is the magnitude of any successful action potential a constant number?

what is that number?

APs are all or nothing things. They are nondecremental meaning that they do not degrade as they move down an axon. Once there is a large enough charge difference created for an action potential, it will go all the way.

40mV

Na+ voltage gated channels have both inactivation and active gates...So:

1. When the channel going through the gate is closed and the hole on the inside is still open the channel is resting

2. when the channel going through the gate is open and the hole on the inside is open as well, then the channel is activated

3. When the channel is open and the hole is plugged by the inactivation gate, then the channel is inactivated

Ultimately what is the source of energy for an action potential?

During the action potential, what source of energy drives it onwards?

Ultimately the energy comes from the RMP

During the AP, it is driven forwards the changes in ion concentrations due to the opening and closing of voltage gated channel.

absolute: the peak of an AP where an AP cannot be initiated because all the local Na+ VG channels are already open, so you can't open more. Basically an AP can not happen when one is already in progress.

relative: this is during the undershoot/hyperpolarization phase. APs can be started but the threshold is high because some of the K+ channels are still acitvated and some of the Na+ channels are still inactivated.

in an action potential diagram where are the following:

slow rising phase

depolarization phase

repolarization phase

hyperpolarization

slow rising phase is the little hump before the large spike

depolarization is the rapid rising phase

repolarization is the rapid decrease

hyperpolarization is the undershoot

what is a graded potential?

what type of conduction is this?

it is a failed attempt at an action potential.

when this happens there is a small influx of Na+ but not enough to create and AP so the little graded potential moves along the axon but while it does so it gets smaller and smaller and eventually fades out.

decremental conduction

sub threshold potentials

little influxes of Na+ that are not enough to create and action potential. they are usually graded potentials that are decremental.

1. inactivation of the Na+ VG channels prevents reverse propagation

2. The inside negative charges on the anterograde side of the AP pull the positive charge on the retrograde side forward

What are two mechanisms by which the membrane in the anterograde direction of the action potential becomes less inside-negative prior to the initiation of an action potential at that location.

What process pushes the membrane at that location to become more inside-negative?

1. At the place of the AP there is a positive inside charge so that charge tends to move towards the anterograde side reducing the negativity of the anterograde side.

2. Also, on the outside there is a positive charge that is being drawn away towards the outside negative at the AP point. This causes the inside negative at the anterograde to want out as well.

Also anterograde positive is always leaking through the channels which actually increases inside negative.

What is the significance of the spacing of neurofibril nodes on an axon?

1. Causes a saltatory conduction which is much quicker than carrying charge in and out at every point along the axon

2. It also prevents positive charge leakage that results from the increase in inside posi charges that repel eachother

spatial summation is when two influxes of a positive stimulus from different places on the soma add up

temporal summation is when several positive stimuli from the same presynaptic terminal add up

Explain how temporal and spatial summations of neurotransmitter activity cause the initiation of an action potential at the axon hillock.  In your explanation, include the terms EPSP and graded potential.

IPSP: Inhibitory Postsynaptic Potentials are an influx of negative charge that cause hyperpolarizations that inhibit APs

EPSP: Excitatory Postsynaptic Potentials are influxes of positive charge that can initiate an AP at the axon hillock

Brain: gray outside 6 layers of soma, white inside

Spinal cord: white outside grey inside

Dorsal roots: afferent pathway, sensory

Ventral Roots: efferent pathway, motor

grey= soma

white= dendrites and axons

1- NT made in the somae

2- anterograde NT vesicle transport

3- docking

4- action potential propagation allows for

5- activation of CA + (Ca+ influx)

6- quantum is released

7- binds to post synaptic cell receptors

low molecular weight, Amine

uses cholinergic receptors: nicotinic (ligand gated) and muscarinic (g-protein)

synthesized in axon terminals

CNS and PNS

secreted by cholinergic fibers, requires acetytransferase

Acetyl CoA derivative

ADH

high molecular weight neuropeptide

made in soma

modulates low molecular weight activity

peptide

 G protein linked metabotropic

made in hepatocytes

amino acid/ monoamine

ligand gated (ionotropic)

CNS

low molec. wght synthesized in axon terminal

uses adrenergic receptors

high molecular weight synthesized in soma

inhibitory NT of the CNS
Endogenous opioid; pain supression, analgesic

OPIUM HEROIN & LSD

catecholamine (tyrosine derivative)

secreted by cerebral dopaminanergic fibers

mediates emotions

lack of= parkinsons, schizophrenia

CNS

Low molecular weight synthesized in axon terminals

metabotropic

monoamine

tryptophan derivative

low molecular wght synthesized in axon terminal

ionotropic ligand gated (some versions metabotrophic)

CNS

secreted in the brain stem

Endogenous opioid

inhibitory of the CNS

analgesic

Agonists: lsd opium morphine heroin

high molecular wght sythesized in the soma

Gamma Amino Butyric Acid

GABA

amino acid

inhibitory CNS

ligand gated ionotropic

low molecular weight made in axon terminals

peptide

hi molecular wght (made in soma)

secreted from pancreas

amino acid

ligand gated ionotropic

low molec wght sythesized in axon terminals

CNS

EPSP NT

Amino acid

ligand gated

low molecular weight

inhibitory CNS

high molecular weight

peptide

induces cell uptake of glucose

metabotropic

are metabotropic!

ADH Glucagon insulin oxytocin and gastrin

catecolamine (tyrosine derivative)

Secreted by adrenergic fibers in the CNS and PNS

secreted by chromaffin cells

metabotropic G protein linked

Beta 1 - activate EPSPs to increase heart rate

Beta 2 - activate/ inactivate EPSP, decrease Heart activity (Beta blocker, grandpa's drug) smooth muscle relaxer

       - both Beta 1&2 activate adenylate cyclase

Alpha 1- increases intracellular CA++ smooth muscle contraction, uses phospholipase C

Alpha 2- inhibits adenylate cyclase (antagonistic to Beta receptors) uses the GI protein

peptide

hi molec wght

metabotropic

made in the soma

ligand gated channel

ACh from the ISS binds to the nicotinic receptors

this activates them allowing Na+ influx and K+ efflux

ACh can be reused later

 Explain the difference between an m₁ and an m₂ receptor in terms of whether they are iontropic or metabotropic and whether they cause EPSPs or IPSPs

M1- muscarinic cholinergic receptor, receives acetylcholine, EPSP. Decreases K+ activity creating inside positive environment

M2- muscarinic cholinergic receptor, receives acetylcholine, IPSP. Increases K+ activity creating an inside negative environment

Both use G protein IP3 pathway

Which of the following are agonists?

LSD

Opium

Mescaline

agonists of Beta endorphines and Enkephalin

ACH agonist of nicotine, muscarine

ACh, acetylcholinesterase, choline, acetate, acetyltransferase, acetyl CoA, CoA

What is the relationship between them?

CoA makes AcetylCoA

AcetylCoA+ choline = ACh

Acetyltransferase transfers the acetyl group of AcetylCoA and puts it with Choline to make ACh.

Acetylcholinesterase breaks apart ACh after its hit post synaptic receptors. When broken apart, it is broken into choline and acetate. Choline gets recycled back into the pre synaptic terminal.

Acetylcholinesterase= AChe

See Slide 25 of slideset 4 for diagram

I D NC

Smooth muscle contraction following increased adrenergic input to an alpha 1 receptor

Increase

The a1 receptors receive adrenergic responses that increase the intracellular CA++ which increases muscle contraction.

Adrenergic Responses: norepinephrine, catecholemines

I D NC

intracellular IP# levels following decreased adrenergic input to smooth muscle alpha 1 receptors

Decrease

Adrenergic responses cause the Gprotein pathway that releases IP3, increases cellular CA++, causing muscle contraction

Cytosolic adenylate cyclase activity following increased adrenergic input  to a₂ receptors.

Decrease

increased adrenergic input to a2 receptors increases a2 receptor activity,

a2 receptors inhibit adenylate cyclase

Increase

b1 receptors cause heart to pump harder and faster once they receive adrenergic input

cAMP concentration following increased adrenergic input to b₁ receptors.

Increase

increase adrenergic input to B1 receptors increases their activity

B1 receptors activate adenylate cyclase

adenylate cyclase makes cAMP

Arteriole constriction following decreased adrenergic input to b₂ receptors of smooth muscle.

Increased

Decreased adrenergic input means decreased b2 activity

b2 relaxes heart

 a₁                        

 a₂                    

b₁

b₂

_{What do they activate or inhibit?}

a_{1      activates phospholipase C (PLC)}                  

 a_{2     inhibits adenylate cyclase}                

b_{1      activates adenylate cyclase}

b_{2     activates adenylate cyclase}

Serotonin

Dopamine

How do funky levels affect mental health?

Serotonin- NT involved with pain perception. Overactive recovery from synaptic cleft leads to depression.

Dopamine mediates emotions and skeletal muscle movement- if the dopaminanergic fibers in ones brain degenerate = Parkingsons/ schizophrenia

What are the two efferent pathway classifications?

explain their differences in terms of direct and indirect innervation and in terms of the effectors of each pathway.

somatic and visceral (autonomic)

Somatic= direct innervation, skeletal mm & skin

Visceral= indirect innervation, smooth mm & glands (heart and adipocytes)

Sympathetic

Parasympathetic

Dual innervation

Parasympathetic and sympathetic divisions both act on the effector

Smooth mm of blood vessels and sweat glands are only innervated by the Sympathetic nervous system

somatic cells- direct innervation

visceral- indirect innervation

BUT the exception is Chromaffin cells of the Visceral Nervous System have direct innervation

Explain the differences between the parasympathetic and sympathetic autonomic nervous systems in terms of origins from the CNS

parasympathetic (craniosacral) comes out of the cranial and sacral vertebrae

sympathetic (thoracolumbar) comes out of the thoracic and lumbar vertebrae

Explain the differences between the parasympathetic and sympathetic autonomic nervous systems in terms of autonomic ganglia location

parasympathetic ganglia follows a long preganglionic neuron

sympathetic ganglia follows a short preganglionic neuron

Explain the differences between the parasympathetic and sympathetic autonomic nervous systems in terms of location of cholinergic and adrenergic fibers

Parasympathetic and Sympathetic nervous systems both have cholinergic fibers pre-ganglion

Parasympathetic NS also have cholinergiv fibers post ganglion

Sympathetic  NS has sdrenergic fibers post ganglion

Which effectors are acted on by the Parasympathetic NS?

pupils constricted

stimulates digestion

slows heart beat

constricts airways of the lungs

vasodialation of blood vessels

clitoral and penile arousal

stimulates salivary glands

slide 4

dialates pupils

ihibits digestion

relaxed airways of the lungs

accelerates heartbeat

stimulates sweat glands

Constricts blood vessels

stimulates an orgasm

slide 10