vert phys ch7 fsu

Central nervous system: brain and spinal cord
Peripheral nervous system: cranial and spinal nerves

neurons which conduct impulses and GLIAL CELLS which support the neurons. (glial cells are also called neuroganglia sometimes)

cell body: cluster in groups called nuclei in the CNS and ganglia in the PNS

dendrites: recieve signals

axon: conduct impulses

no! sometimes signals do not go through dendrites and instead go straight on to the cell body or axon

vary from a few millimeters to a meter

it is the region closest to the cell body and its where the MOST action potentials are generated. therefore, there is a HIGH density of Na+/K+ pumps

sensory neurons- conduct impulses from sensory receptors to the CNS

motor neurons- conduct impulses from the CNS to target organs (muscles/glands)

association/interneurons- located COMPLETELY within the CNS and intergrate functions of the nervous system

somatic- responsible for reflexes and VOLUNTARY control of SKELETAL muscle

autonomic- innervate involuntary targets such as smooth muscle, cardiac muscle and glands

sympathetic- fight or flight
parasympathetic- rest and digest

pseudounipolar- single short processes that branches like a T to form 2 longer processes. ex: sensory neurons

bipolar neurons- have 2 processes, 1 on either end (dendrite and axon) ex: retina of the eye

multipolar neurons- several dendrites and 1 axon, *most common type*

bundles of axons located outside the CNS. composed of both SENSORY and MOTOR neuron axons (called mixed nerves).

old factory nerve

a tract

Schwann cells- (aka neurolemmocytes) they form mylein sheaths around peripheral axons

Satellite cells- (aka ganglionic gliocytes) support cell bodies within the ganglia of the PNS

Oligodendrocytes- form mylein sheaths around the axons of the CNS neurons

Microglia- migrate around tissue and phagocytize foreign and degenerated material (help clean things up!)

Astrocytes- regulate the external enviorn. of neurons

Ependymal cells- line the ventricles and secrete cerebrospinal fluid. *have cilia*

neurilemma (also called sheath of Schwann) is a sheath of Schwann cells that surrounds all axons in the PNS. they wrap to form the myelin sheath in the PNS

-small axons (2 micrometers in diameter) are usually unmyelinated. ex: pain fibers!
****even unmyelinated axons in the PNS have neurilemma****

ogliodendrocytes

white matter- myelinated tissues

gray matter- cell bodies and dendrites

PNS! because PNS can form a regeneration tube which is created by Schwann cells.

CNS cant regenerate bc ogliodendrocytes hurt regeneration by forming scar tissue

1. they promote neuronal growth in fetal brain.

2. in adults they help maintain sympathetic ganglia and in the regeneration of sensory neurons.

astrocytes! :)

its the most abundant glial cell and it processes with END FEET that associate with blood capillaries and axon terminals

-take up K+ from the extracellular enviorn. to maintain ionic enviorn. for neurons

-take up extra neurotransmitter released from axon terminal. *Chemicals are recycled.

-the end feet around the capillaries take up glucose from blood for use by neurons to make ATP. **convert glucose to lacate.

an excitatory neurotransmitter

1. formation of synapses in the CNS

2. regulate neurogenesis in regions of the adult brain.

3. form the brain blood barrier.

4. release transmitter molecules that can stimulate or inhibit neurons.

NO!!

They are excited by changes in entracellular Ca2+ concentration

-when neurons get excited they release ATP, which in turn increases the Ca2+ of the adjacent astrocytes. this makes the astrocyte release prostaglandin E2 from the end-feet on a blood capillary which increases blood flow. this increase in blood flow brings more glucose and O2 to the brain.

tight junctions!

they can affect the production of ions channels, tight junctions, and enzymes that can destroy toxic substances by secreting glial-derived neurotrophic factor

-70 mV

-inside the cell theres a much higher concentration of K+

yes, known as excitability.

caused by changes in permeability to certain ions

ionic current

their electrochemical gradient, which is a combo of concentration gradient and electrical attraction to opposite charges.

polarized: when the inside is more negative than the outside

depolarized: when membrane pot. inside cell is more positive than outside

repolarized: returning to resting potential

hyperpolarized: when membrane pot inside becomes more negative.

Na+

depolarization is when Na+ returns into the cell causing the inside to become more positive

when K+ leaves the cell causing the cell to be more negative or when negative ions (such as Cl-) enter the cell, which would also cause the cell to become more negative.

depolarization- excitatory

hyperpolarization- inhibitory

by changes in flow of ions through the channels

1. not gated (always open). sometimes called "leak" channels

2. voltage gated K+ channels, which open when a particular membrane potential is reached

only 1 type... voltage gated channels that remain closed at rest

open when membrane potential depolarizes to -55mV- which is known as the threshold.

work by Na+ rushing in due to the electrochemical gradient. then the membrane potential climbs more positive (towards the Na equilibrium potential). the channel is inactivated at +30 mV

along with depolarization, these channels open slowly and K+ will rush out of the cell. this follows the electrochemical gradient.

this will make the cell repolarize back toward the K+ equilibrium potential

at the threshold membrane potential (-55mV) the voltage gated Na+ channels open and Na+ rushes in. the cell depolarizes and more Na+ channels open and cell gets more and more positive. (positive feedback loop)

then membrane potential reaches +30mV

well, hyperpolarization is when K+ rushes out of the cell and possibly Cl- rushes in. This happens to try to bring down the membrane potential after it reaches +30 mV back to its resting potential of -70mV. but, REPOLARIZATION occurs while this is happening. repolarization is the overshooting of resting potential to something more negative. however, membrane pot wont go all the way down to K+ resting pot (-90mV) bc the volatge gated K+ channels will quickly close and the Na+/K+ pumps will help to reestablish ion gradients

it means that once the threshold as been reached (-55mV) an action potential WILL be generated.

also refers to the fact that the size of the stimulus has no affect on the size of the action potential.... it always goes to +30mV and then back down... and it has no affect of the duration of the action potential... its always roughly the same amt of time... however the stronger the signal, the faster the action potential will be evoked.

it will make action potential happen more frequently and may also activate more neurons in a nerve... this is called RECRUITMENT (bc it's recruiting new axons)

the fact that after an action potential happens there is an amount of time where the neuron cant become excited again. **action pot can only increase in frequency to a certain point!

occurs during action potential when Na+ channels are INactive

when K+channels are still open. only a VERY strong stimulus can overcome this

the ability of neurons to conduct charges through their cytoplasm.

-its poor due to high internal resistance to the spread of charges through the membrane

-therefore neurons cant rely on cable properties to move an impulse down the length of an axon

Na+ channels open as a wave down the length of an axon

the axon potentials are produced down the entire length of the axon and the conduction rate is slow bc so many action potentials are generated and there is leak of charge through the membrane

the action potentials leaping from one node of ranvier (unmyelinated part) to another. these nodes allow Na+ and K+ to cross the membrane every 1-2mm

1. increased diameter of the neuron. (this reduces resistance to the spread of charges via cable properties)

2. decrease in the number of leak channels

3. myelination (because of saltatory conduction)

synapse = functional connection btwn a neuron and cell its signaling.
-cns the cell = another neuron
-pns the cell = muscle or gland

neuromuscular junctions

neuron one = presynaptic neuron
neuron two= postsynaptic neuron

a PRESYNAPTIC neuron

respectively, axodendric, axosomatic, axoaxonic synapses

smooth muscle and cardiac muscle, btwn some neurons of the brain and btwn glial cells

joined by gap junctions

the are the presynaptic axon endings where the neurotransmitter is released

separated by synaptic cleft and held together by cell adhesion proteins. (CAM's) these ensure that rapid chemical transmission will be possible

connexin = connector proteins
connexon = 6 connector proteins together

enclosed in synaptic vesicles in the axon terminal

in order for neurotr. to get into synaptic cleft, the synaptic vesicles need to bind to the PM and exocytosis must occur. This process is triggered by action potentials that stimulate the entry of Ca2+ into the cell through voltage gated channels. **greater freq of action pot results in more stimulation of postsynaptic neuron

synaptotagmin!! this forms Ca2+ protein complex

through use of SNARE proteins!! they bridge the synaptic vesicles and PM

the Ca2+ protein complex is what displaces part of the SNARE protein complex and allows for complete fusion of vesicle membrane to plasma membrane and formation of the pore which the neurotransmitter gets released from

1. action potentials reach axon terminals
2. voltage gated Ca2+ channels open
3. Ca2+ binds to synaptotagmin protein
4. Ca2+ protein complex stimulates complete fusion of vesicle w PM and exocytosis of neurotransmitter happens.

it goes across synaptic cleft and binds to specific receptor protein. **neurotransmitter is called LIGAND
this binding causes opening of ligand gated ion channels

the membrane pot changes depending on which channel is open
Na+ or Ca2+ : channels have DEpolarization called Excitatory Postsynaptic Pot (EPSP)
K+/Cl- : have HYPERpolarization called inhibitory postsynaptic pot. (IPSP)

EPSP's: memb pot moves closer to threshold required for action potential (enough EPSP's = action potential)

IPSP's: move memb pot farther from threshold. it can counter EPSP's from other neurons

if an action potential will occur and how frequently which they are fired with. ***note: once first action pot is generated, they will regenerate themselves along the axon like they always do

its an exitatory or inhibatory neurotrans. that can directly or indirectly open ion channels upon binding to its receptor on postsynaptic neuron.

- excitatory in CNS and in all somatic motor neurons
-inhibatory in some autonomic motor neurons (but excitatory in others)

nicotinic Ach receptors: stim by nicotine and found in motor end plate of muscle cells in autonomic ganglia and in parts of CNS

muscarinic Ach receptors: stim by muscarine and found in CNS and PM of smooth/cardiac muscle innervated by autonomic motor neurons

agonist= drugs that can stimulate a receptor (ex muscarine and nicotine)

drugs that can inhibit a receptor ex= atropine for muscarinic receptors
curane for nicotinic receptors

1. ligand gated ion channels
2. g-protein coupled channels

this means that the receptor protein is also an ion channel and that the binding of the nuerotransmitter DIRECTly opens ion channel

ex: nicotinic Ach receptors

when Ach binds to a nicotinic receptor, a channels opens that permits both Na+ into the cell and K+ out of the cell. The inward flow of Na+ creates depolarization of postsynaptic cell and an EPSP, however the diffusion of K+ prevents depolarization from going about 0mV **diff from action pot bc with AP, the Na/K channels are different and the K channel doesnt open til AFTER the Na one closed.

these also are opened by the binding of Ach, but are diff from ligand gated bc the receptor protein and the ion channel protein are NOT the same protein, they are separate. Thus, binding of neurotrans to its receptor can open the ion channel only INDIRECTly.

ex muscarinic ach receptors

g proteins have 3 subunits: alpha, beta and gamma. sometimes alpha is active and sometimes beta is active

binding of Ach results in dissociation of alpha and beta subunits

either alpha or beta diffuses through cytoplasm to the ion channel and will open the channel for a short period.

opening K+ channel would cause hyperpolarization (IPSP). happens in the heart to slow heart rate

closing K+ channel would cause depolarization (EPSP). happens in the stomach to increase peristalsis and contraction

an enzyme that inactivates Ach activity shortly after it binds to the receptor.
-one way of inactivation is breakdown of Ach into acetate and choline which are then taken back to the presynaptic cell for reuse

neuromuscular junctions

motor end plate
EPSP's formed here are called are called end plate potentials.

end plate potentials open voltage gated Na+ channels which result in action potenial!! this produces muscle contraction!! **so action potential produced by muscle fibers stimulates muscle contraction**

if its blocked it can lead to paralysis or death.
ex is curare. its an antagonist of Ach and will block its receptors so muscles wont contract. leads to paralysis and death bc of paralyzed diaphram. can be used as muscle relaxant.

neurons that use Ach as a neurotransmitter. found in CNS.
alzheimers disease is assoicated w loss of cholinergic neurons that synapse on the brain areas responsible for memory (hippocampus)

regulatory molecules derived from amino acids
1.catecholamines: derived from tyrosine ex= dopamine, norepinephrine/epinephrine
2.serotonin: derived from tryptophan
3. histamine: derived fr histidine
**serotonin, dopamine and norep/epineph are neurotransmitters**

made in presynaptic axon (like Ach), released via exocytosis, diffuse across synapse and bind to receptor

degraded by monoamine oxidase (MAO) and can be taken back to the presynaptic cell (called reuptake)

once catecholamine binds to its receptor the g protein dissociates and alpha subunit is sent to an enzyme called ADENYLATE CYCLASE which converts ATP to cAMP

almost all use 2nd messenger system... ex: cAMP

cAMP then activates PROTEIN KINASE which phosphorlyates other proteins and an ion channel opens

in the raphe nuclei (middle region of brain stem).
implicated in mood, behavior, appetite, cerebral circulation
LSD might be agonist

serotonic specific reuptake inhibitors. they inhibit the protein that reuptakes serotonin so that more of it stays in your brain. used to treat depression

no! there are over a dozen receptors which make for diverse function of serotonin
(appetite, headaches, anxiety control)

the MIDBRAIN! two main areas:
1. nigrostriatal dopamine system- for motor control
2. mesolimbic dopamine system- emotional reward

4

substantia negra (dark substance) in the midbrain. dark bc contains melanin.
send fibers to a group of nuclei called corpus striatum
impt step in control/initation of movement
parkinsons caused by degeneration of these neurons

originates in the midbrain and sends neurons to the forebrain.
involved in emotional reward/addictions
schizophrenia is associated with too much of this.... drugs that treat schizophrenia are dopamine antagonists.

mao inhibitors and L-dopa

in sympathetic neurons of the PNS (fight or flight) (smooth muscle, cardiac and glands are affected)

in some neurons in CNS associated with arousal. ex amphetamines work by stimulating norep. pathways

*major excitatory neurotransmitter in the brain*
produces over 80% EPSP's in synapses of the CNS

3 ion channels:
1. NDMA receptor
2. AMPA receptor
3. Kainate receptor
*NDMA and AMPA work together in memory storgage

and there are 8 known G-protein coupled receptors.

its INHIBITORY... it hyperpolarizes the postsynaptic membrane and causes IPSP's.
-binding of it opens Cl- channels causing influx of Cl- which makes it harder to reach threshold to create act. pot.

in the spinal cord! used for regulating skeletal movement. allows for relaxation of some muscles while contraction of others.
-STRYCHNINE is poison that blocks glycine receptors and produces death bc diaphram cant relax, and you cant breathe.

derivative of glutamate, *MOST prevalent neurotransmitter in the brain*
also inhibitory!! hyperpolarizes memb by opening Cl- channels.
effects involved in motor control

alcohol, painkillers/roofies, barbiturates/anesthesia

has ion channel and g protein coupled receptors

huntingtons disease

polypeptides found in the synapses of the brain. believed to function as hormones secreted by sm intestine and other endocrine glands.

ex:CCK- involved in satiety after a meal

Substance P- mediates sensations of pain

relieve pain by binding with drugs like opium and morphine

endogenous opioids are found in the body naturally and are polypeptides produced by brain and pituitary gland.
ex: B-endorphin, enkephanlin and dynorphin

most abundant neuropeptide in the brain!!
-plays role in stress response, circadian rhythms, and control of cardiovascular system.
-powerful simulator of hunger!!

neurotransmitters that bind to the same receptor proteins in the brain as THC from marijuana.
-lipids! short fatty acids, released from dendrites of cell body *ONLY LIPIDS known to act as NEUROTRANS**
-retrograde neurotrans. :means that they're released from POSTsynaptic membrane and diffuse backwards to PREsyanptic memb and will inhibit the presynaptic memb from further neurotrans. release

they can inhibit IPSP producing neurotransmitters from one neuron so that EPSP producing neurotransmitters from another neuron can have greater effect
-may enhance learning and memory and shown to induce appetite.

NO is FIRST gas to be identified as a neurotransmitter! produced by neurons in PNS and CNS
-can diffuse across plasma membrane w no vesicle needed
-diffuses into target cell and activates production of cGMP as 2nd messenger system

secreted by autonomic neurons onto cells in digestive tract, respiratory tract, penis. *responsible for an erection.
*viagra works by decreasing cGMP production which increases amt of NO

also gas used as neurotransmitter.
also activates production of cGMP
-used in olfactory epithelium and cerebellum.

its a purine neurotrans. and used as a cotransmitter released via vesicles with another neurotransmitter
-binds to purinergic receptors (A/G)
-released w norephinephrine to stimulate blood vessel constriction and w Ach to stimulate instestinal contraction

axons have collateral branches so one presynaptic neuron can form synapses with several postsynaptic neurons

several diff presynaptic neurons (up to 1000) can synape w one postsynaptic neuron.

-occurs due to convergence of signals onto a single postsynaptic neuron. *happens bc unlike action pot's, synaptic potentials are graded and lack refractory periods. this allows them to add together at axon hillock

due to successive waves of neurotransmitter release. results in summation of EPSP's that help to determine if the depolarization that reaches the axon hillock will result is action potenital

its the fact that the strength of synaptic transmission can get stronger or weaker with repeated use

when a presynaptic neuron is experimentally stimulated at a high frequency and the excitability of the synapse is enhanced.
-causes improved efficiency and higher EPSP's
-can last for hours or weeks
-found in hippocampus where memories are stored and associated w NDMA and AMPA glutamate receptors

presynaptic: endocannibinoids inhibit presyn neurons. also endogenous opioids in pain reduction synapses on the axon of the second neuron which inhibits neurotransmitter release

post: GABA and glycine. open Cl- channels