neurochemistry
- Created by: lw121x
- Created on: 08-12-15 19:10
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- Neurochemistry
- within neurones electrical flow across membranes
- Synaose is chemical!
- Loewi
- frog heart beating, nerves hang out. Stimulation = beat faster. If chemicals squirted chemicals of slow into other jar it should slow it down
- Chemical communication
- synaptic cleft, precynaptic cell constantly makes vessels, they wait in an axon until released
- they then go out and bind to receptor site excite or inhibit it
- PRE VS POST, relative lavel can be pre synaptic to one cell but post synaptic to another
- synaptic cleft, precynaptic cell constantly makes vessels, they wait in an axon until released
- What triggers an AP in a neurone?
- vestricles full of neurotransmitters held in axon teminal
- Change in concentration levels of calcium causes ventricles to come down neurotransmitters and merge to post synaptic membrane
- Channels sensitive to certain chemicals, if neurotrans binds to on up.
- this releases neurochemicals
- Channels sensitive to certain chemicals, if neurotrans binds to on up.
- Lock and key
- each neurotransmitter has a shape, attach to those that compliment
- once neurotrasnmitters has change in ligand/ transmittergated ion channel this opens. Closes ion channel.
- can only happen to post synaptic cell
- Everytime stimulated = chemical
- not every tiem pos can inhibit the effects of post synaptic cell. If channel negative already further depolarised from excitation threshold = AP less likely
- summation synapses
- just one is not enough! to cause AP
- if you put a lot of AP all releasing neurones you can get a temporal summation, must be close enough to sum up
- spatial summation: if a + b + c across neurone many diff points they will add up to get AP, causes local AP
- Inhibition
- not always pos
- effect post syn mem further polarises cell
- moves away threshold
- make neg
- input less likely fire
- if pos enough to exceed neg = still pos AP
- Drugs
- agonist help aid neuro function
- Neurotransmitters
- 100 types some only work with other neurotrans, have effect inhibition + excitation 'lock + key'
- The receptor site has a name for each neurotrans it accepts ie. acetecholine> 'cholingenic'
- Direct- bind other protein men, change in cell effect ion channel + Indirect- directly ion channel, change shape channel, pos neg
- Transient effect
- only effect certain amount of time, only as long as in synapse- active processes to empty synapse
- some inactivated after being dischanrged by 'clean up' enzymes
- if not reuptake or destroyed
- only effect certain amount of time, only as long as in synapse- active processes to empty synapse
- DRUGS
- agonists - enhance neurotrans function GABA SSRI help it have effect,
- antagonist impede its effect
- drugs work by block synaptic reuoptake, counteract clkeaning or mimicking action
- We can affect synthesis in a cell being made, release turnover how long allowed to stay there to effect reuptake
- ALCHOL
- GABA normally binds pos + neg choride ions. Alchol bind and keeps channel open for longer more enter. Binds on GABA receptor, alchocol keeps open = neg ions in cell = further inhibition
- Cannabis more complex
- indirect effect GABA neurones reduce GABA
- less inhibition of post synaptic dopamine neurones> more dop released dopminergeric neurone> extra dop = firing cells these linked to reward
- Brain is protected from many chemicals...
- 1900s dyes affecta ll organs but brain
- blood brain barrier keeps things out
- LDOPA go to brain convert dop
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