524 exam 2.4
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nervous system CNS vs PNS???
- CNS: central nervous system
- - neurons are INSIDE OF the brain and spinal cord
- PNS: peripheral nervous system
- - neurons are OUTSIDE OF or CONNECTING TO the brain and spinal cord
- cranial nerves: not in brain but come off of brain
- peripheral nerves: come off of spinal cord
describe the nervous system organization
- receptors --> afferents --> brain --> efferents --> effectors
- fox has RABEES!!!
- notice all the small details!!!
what are the 3 types of neurons?
- sensory neurons
- motor neurons
afferent neurons, 10 million, 5 senses, for balance, temperature and pain
aka associated neurons, 20,000 million, most within CNS, coordinate input, all higher functions
aka efferent, 0.5 million, muscles, glands and adipocytes
neurons can be a meter long... how does it overcome the challenge of transport???
- using the molecular motors and microtubles in the axoplasmic transport: factory + railroad system
- axons are long! so he has to communicate over long distances
- answer is using this mini railroad
- it's all about the molecular motors and microtubules (polymerized chains that molecular motors are attached to)
- can transport mitochondira, large NTs, ezymes, etc
axoplasmic transport: ANTEROGRADE TRANSPORT
- from cell body to the end of the neuron
- mitochondria, large (peptide) NTs, and enzymes for small NT synthesis
axoplasmic transport: RETROGRADE TRANSPORT
- from the end of the neuron to the cell body
- transports old mitochondria and maybe viruses! (RABIES!!!)
- rabies gets into the end of the neuron and through retrograde transport, gets into brain and not through the blood!!!
describe the structure of a basic neuron: dendrite, soma/cell body, axon/fiber, telodendria, synaptic terminal/knob, synapse/synaptic cleft
- dendrites: receive signals like chemical or pressure (ex sitting down)
- soma (cell body): also receives signals (directly!); generates action potential; large neurotransmitters are created here and then transported down axon to the end
- axon (fiber): propagates action potential
- telodendria (distant tree): branches at the end of the axon
- synaptic terminal/knob: small neurotransmitters created and stored here, all neurotransmitters released here
- synapse/synaptic cleft: gap between neuron and neuron/muscle/gland/adipocyte... space where the neurotransmitter will cross
- notice that not all synapses are neurons
- you'll always have a presynaptic cell (before synapse) and a postsynaptic cell (after synapse)!
neuron structure in sensory v motor neurons???
- common to sensory neurons: cell body is in the middle to protect cell body... ex. if it's on the surface of skin, can loose cell body and neurons can die
- common to motor neurons: more traditional structure
viral disorders and the neural highway???
- rabies and herpes and shingles can be transported in the neuron
- infection is though motor nerves in rabies
- manifestation is in sensory nerves in cold sores and shingles
- cold sores hang out in sensory neurons so when it gets triggered (ex stress), can increase reproduction and come out of neurons (normally maintained by immune system)
- shingles hides in spinal nerves, red rash = where spinal nerve is infected
terminology: single axon vs multiple axons???
- single axon: axon, fiber
- multiple axons: axons, fibers, fiber bundle
- CNS: tract, pathway, column (all means bundles of axons)
- PNS: nerve
notice that name is dependent on location... PNS vs CNS
terminology: single cell body vs multiple cell bodies???
- single: cell body
- multiple: cell bodies
notice that name is dependent on location... PNS vs CNS
neuron vs nerve???
- neuron: like the solid wire, a single axon
- nerve: strand wire, a bundle of axons... when you want to send out a lot of signal, send ore neurons, not make neuron thicker!
just a summary of the terminology of single vs multiple and CNS vs PNS cell bodies and axons:
- pink is sensory, green is motor and blue are interneurons
- rabies virus: learned if fat cells had nerves.... injected rabies in fat tissues to map out pathway nerves traveled from brain to adipose... doesn't jump synapse! goes up one but doesn't travel parallel
a junction between two cells the propagates an electrical impulse
- ~100 billion neurons in brain
- ~100-1000 synapses per neuron
- rabies travel through motor/efferent neurons, can jump across synapse and go to other neurons
what cell types have synapses?
- neuron - neuron
- neuron - muscle
how do they propagate electrical impulses?
- chemical: through some type of neurotransmitter
electrical vs chemical synapse???? which is faster? which is most common???
- electrical if faster but chemical is more common
- electrical synapses takes ions and flushes them through gap junctions... great fast signaling... no space! just go directly from one cell to another... used in heart muscle cells
- organized by size... by how many atoms they're made of
- most hormones in the body are close to the size of peptides
- hormones = lots of amino acids
- most neurotransmitters = 1 amino acid... why are they smaller?
- you need them often, it takes more energy and time to make big things and use big things!
- need to be quick, you don't want to spend time making chains of amino acids
- neurotransmitters are small bec you need them quickly for processing information
- hormones = larger = slower changes
neurotransmitter vs neuromodulator???
- both are released from terminal ends of neurons
- neurotransmitter (NT): has effect by itself
- neuromodulator: modulates effect of NTs, postsynaptic neuron is already doing something, this neuromodulator just alters what it's doing
- peptides and gas molecules are mostly just neuromodulators
- many common NTs can do both
- Seratonin - can be a NT and modulate effect of NT
- Epinephrine (catecholamine)
- Norepinephrine (catecholamine)
- Dopamine (catecholamine)
- catecholamine = subgroup of monamines
for each neuron type, what NT does it release??? cholinergic, dopaminergic, seratonergic, noradrenergic, adrenergic, GABA(n)ergic, glutamanergic???
- each neuron type above releases the stated NT only!!! (for the most part)
- but some of those above may also release neuromodulators (peptide and gas neurotransmitters)
- ex. dopaminergic might also release nitric oxide or peptide neuromodulators BUT it only releases dopamine... and can be under the influence of several things like epinephrine to decrease or increase activity
- neurons may mostly release just one NT, but they are under the influence of several NTs
what happens during basic neurotransmitter release???
- AP activates voltage gated calcium channels
- influx of calcium via channels stimulates vesicles with stored NTs to dock and release NTs
- NTs drift to receptors
what happens during synaptic delay???
- synapse transmission is the slowest part of neuronal signaling
- it's the rate limiting stem, mostly due to the time needed for calcium influx and vesicle docking
- more synapses = slower signal
- fastest reflexes have one synapse: sensory neuron --> (spine) --> motor neuron
vesicle dysfunction: OVER STIMULATION
- black widow spider toxin = latrotoxin
- directly stimulates massive vesicle docking and massive NT release in PNS
- toxin gets to synaptic knob and lots of NTs get released
- we're not clearing NT fast enough and we can't stop
- motor neurons release massive ACh and cause muscle rigidity
vesicle dysfunction: UNDER STIMULATION
- clostridium botulinum bacteria toxin = botunilus toxin
- directly inhibits vesicle docking and inhibits NT release in PNS
- motor neurons can't release ACh, less ACh, and get muscle paralysis
10% of brain cells, functional units of nervous system
90% of brain cells, surrounds neurons, supporting cells of nervous system; separate, protect, support, regulate neurons and ECF
neuroglia (glial cells)
synapse regulation: positive and negative regulation
- NEGATIVE REGULATION
- 1. enzymes break down NTs: inside synaptic space, inside neurons and glial cells, basically metabolizes NTs and found in 3 areas listed
- 2. reuptake transporters: reuptake NTs into neurons and glial cells
- 3. autoreceptors: negative feedback released NTs
- NEGATIVE OR POSITIVE REGULATION
- 4. heteroreceptors: receptors that binds other molecules... chemical binds to this receptor and affects release of NTs
ENZYME: acetylcholinesterase (AChE)
- acts by inactivating ACh through hydrolysis to acetate and choline
- located on postsynaptic membrane
- degrades 50% of ACh prior to reaching receptors!!!
- each molecule of AChe degrades about 5,000 molecules of Ach per second!!!
- degrades other 50% of ACh 20mSec AFTER receptor binding... to terminate signal
- Ach is degraded to acetate + choline
what are the inhibitors of acetylcholinesterase?
- 1. irreversable (mostly) = toxins: insecticides, sarin nerve gas... effect is to cause build up of ACh and get rigidity
- 2. reversible = medications: Aricept (donepezil) for alzheimer's... to help people who have low amounts of ACh
what are the 4 reuptake transporters on presynaptic neuron and the reuptake transporter located on glial cells?
- ON PRESYNAPTIC NEURON
- 1. choline transporter (CHT)
- 2. dopamine transporter (DAT)
- - blocked by cocaine, buproprion (wellbutrin - used for depression/ADHD)
- - reversed by amphetamines
- 3. norephinephrine transporter (NET)
- - blocked by cocaine, burproprion (wellbutrin), atomoxetine - reversed by amphetamines
- 4. seratonin transporter (SERT)
- - blocked by cocaine, buroprion (wellbutrin), paroxetine (paxil) [ssri]
- - reversed by amphetamines
- so ampetamines... instead of just blocking it, it turns it around and causes it to release more NTs
- LOCATED ON GLIAL CELLS
- 4. excitatory amino acid transporters
- - example: transport glutamate
italicized = strong specificity, very selective
ENZYME: monoamine oxidase (MAO)
- causes the inactivation of neurotransmitters by oxidation
- mostly inside presynaptic neurons
- degrades monoamines (shenand... dopamine, epi, norepi, sera)
- increased MAO activity --> less NTs... associated with depression
- decreased MAO activity --> more NTs
- some MAO polymorphisms decrease NT catabolism... associated with antisocial rage behavior, high prevalence in maori people
- MAO inhibiting drugs = used to treat depression!!!
ENZYME: catechyl-o-methyl transferase (COMT)
- causes the inactivation of NTs by methylation
- located inside postsynaptic neuron and astrocytes to clean up 'escaped' NTs
- degrades catecholamines and similar molecules (END of shend... dop, epi, norepi)
- increased COMT activity --> less NTs... some polymorphisms result in increased catabolic activity (breakdown)... associated with schizophrenic behavior, NT not being in proper proportions
- decreased COMT activity --> more NTs... some polymorphisms result in decreased catabolic activity... associated with aggressive behavior... some drugs can directly inhibit COMT... used for parkinsons disease
- presynaptic receptor!
- responds to the same NT released by synapse
- tends to decrease synthesis and release of NT
- examples of autoreceptors:
- glutamate = NMDA receptor
- NE = alpha-2A or 2C
- ACh = muscurinic-2 or 4
- depends on NT it releases!
- some NT binds to autoreceptor and tells cell to decrease prod or release of NT
- presynaptic receptor! (NTs, neuromodulators, neurohormones)
- mechanism: many work by influencing intracellular calcium levels
- mainly effects calcium channel to increase or decrease the amount of calcium uptake
- PRESYNAPTIC INHIBITION
- - GABA can decrease release of NTs
- - NE can decrease release of ACh
- - ACh can decrease release of NE
- PRESYNAPTIC FACILITATION
- - seratonin can increase release of some NTs
- - ACh release decreased by NE binding to noradrengergic receptors (alpha-2A, 2B or 2C) on cholinergic synapses
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