topic 8 Flashcards
compare the structure and function and location of the sensory, motor and relay neurones
motor, sensory and relay neurones all have dendrites, an axon, cell body and myelin sheath. however the cell body is found in different locations. sensory neurones conduct action potentials from receptors to the central nervous system. relay neurones conduct action potentials within the central nervous system and the motor neurones conduct action potentials from the CNS to an effector, which is usually a muscle or gland. Relay neurones are found in the central nervous system. both sensory and motor neurones are found in the peripheral nervous system , however the cell body of the motor neurone are found within the CNS, whereas the axon is found within the peripheral
what is the myeline sheath
the fatty insulating layer around the axon, it influences the speed of conduction, making it faster
the pupil increases in diameter in dim light. how does this occur
an action potential is generated in the sensory neurone, the action potential is transmitted to the co ordinator via the optic nerve, action potentials are generated in relay neurones in the central nervous system and the motor neurone. the motor neurone are connected to the dial muscles in the iris. resulting in the contraction of the radial muscles and an increase in the diameter on the pupils
how does resting potential occur
when there is no action potential being generated then it is at -70mV
the SODIUM POTASSIUM PUMP will establish a CONC GRADIENT required for the K+ IONS to diffuse OUT of the neurone (DOWN TH CONC GRADIENT BY FACILLITATED DIFFUSION)
the movement of the potassium ions out of the neurone causes the outside of the neurone positive and the inside negative
the membrane is permeable to k+ ions and almost impeccable to Na+ ions as their channel is closed
the potential difference in charge is -70mV
the speed of conduction
the myeline sheath and the nodes of ranvier ensure that there is SALTARY CONDUCTION ( where depolarisation only occurs at the nodes of ranvier)
the speed of conduction. can also be affected by the diameter of the axon ( increase in diameter increases the speed of conduction)
and the temperature
what is the refractory period
this is when you over shoot (hyper polarisation) during this period no action potential can pass a long the axon, this lasts until the sodium potassium pump can establish the conc gradient to return to the resting potential.
this is needed so the action potential travels in 1 direction and allow each action potentials to be separate
treatments for prakinsons disease (inefficient dopamine)
- selegiline ( enzyme inhibitor)
- L-Dopa (precursor)
- dopamine antagonist (mimic the role of dopamine)
- gene therapy
- cell therapy
how does the drug selegiline work for parkinsosns
it is an enzyme inhibitor
it slows down th loss of dopamine from the brains
allowing sufficient levels of dopamine in the synaptic cleft and this allows it to bind to the receptors on the post synaptic membrane allowing the membrane to depolarise
it does this by inhibiting the enzyme MONOAMINE OXIDASE, it will compete with the dopamine and bind to the dative site,
therefore not allowing the dopamine to bind and break down.
how does the drug L-Dopa work in treating parkinsosns disease
it is a precursor
dopamine cannot pass through the blood brain barrier
L-Dopa can pass through the blood brain barrier as it is small enough
one it passes it is then converted into dopamine in the brain by the enzyme DOPA DECARBOXYLASE
how does the drug dopamine agonist work in treating Parkinson’s
they mimic the role of dopamine in the brain
they bond to the dopamine receptors on the post synaptic neurone and enable to movement of Na+ into the post synaptic neurone
this causes depolarisation of the membrane, causing an action potential to be generated
how is gene therapy and cell therapy used in treating parkisnsons
genes for the protein that increase the dopamine production and that promote the growth and survival of nerve cells are inserted into the brain
the proteins themselves are injected into the cell
what is the cause of depression
it is multifactorial
there are genetic lelemst with e a genetic pre disposition, triggered by traumatic events.
there is insufficient levels of serotonin , or the serotonin produced is not remaining the in the synaptic cleft for long enough
how do the drugs SSRIs work in the treatment of depression
selective serotonins reuptake inhibitor
they inhibits the enzymes that break down serotonin and this means the serotonin remains in the synapse for longer
how does the synapse transmit an action potential
an action potential arrives at the presynaptic membrane
the membrane of the pre sysnaotcic membrane becomes depolarised
the causes the synaptic vesicles containing the neurotransmitter (acetylcholine) to migrate towards and fuse with yeh pre synaptic membrane
neurotransmitters are released into the synaptic cleft through exocytosis
the neurotransmitters diffuse across the synaptic cleft
the neurotransmitters binds to the protein receptors on the post synaptic membrane
the sodium channels open, sodium ions flow through the channels
the membrane if the post synaptic membrane depolarises and and action potential is generated
the reuptake of the neutransmitter by the presynaptic membrane
how do CT scans work
they emit thousands of NARROW BEAMS X-RAYS
the final pictures are more details than x-rays
each of the narrow beams are reduced in strength according to the density of the tissue (usually soft tissue)
the x rays are used to produce images
dis
- they produce still images
- patients need to remain still which may be uncomfortable
