2. Neurones & glia Flashcards
name the 3 types of glial cells and their general function
- astrocytes (most abundant type) - supporters
- oligodendrocytes - insulators
- microglia - immune response
name 5 functions of astrocytes
- structural support
- help provide nutrition for neurones: glucose-lactate shuttle
- remove neurotransmitters (uptake): control NT conc. (esp. important for toxic glutamate)
- maintain ionic environment: K+ buffering
- help to form BBB
describe the energy supply to neurones
Neurones don’t store or produce glycogen.
- glucose enters interstitial space from blood via GLUT1 and then enters neurone via GLUT3
- glucose supply can be supplemented by astrocytes via glucose-lactate shuttle: take up glucose (GLUT1) and store as glycogen (enough for 10-15min). Can then be broken down to lactate which can be taken up by neurones and converted to pyruvate
how is NT response at pre-synaptic terminal ended and spread of NTs in brain prevented
astrocytes keep NT conc. low: have transporters for NT uptake (e.g. glutamate) and recycling
how do astrocytes buffer brain ECF [K+] when high neuronal activity
astrocytes have very negative resting MP allowing K+ uptake through several channels/transporters:
- K+ channel
- Na/K ATPase
- NKCC2 transporter
name 3 structures that form the BBB
- tight junctions between brain capillary endothelial cells
- basement membrane surrounding capillary
- end feet of astrocyte processes (promote formation of tight junctions)
explain why the CNS is described as ‘immune privileged’
- Immune response is present: microglia act as phagocytes and APCs, and T cells can enter CNS
- but inflammatory response is limited as rigid skull will not tolerate volume expansion (would lead to raised ICP) - CNS inhibits initiation of pro-inflammatory T cell resp.
name the 3 classes of neurotransmitter in the CNS
- amino acids
- biogenic amines - ACh, noradrenaline, dopamine, serotonin, histamine
- peptides - somatostatin, neuropeptide Y, substance P
name the main excitatory amino acid NT and describe its MOA
glutamate: causes excitatory post-synaptic potential (increased neuronal firing) by binding to Na/K ligand-gated channels
describe the generation of initial fast depolarisation at CNS excitatory synapses
i. pre-synaptic terminal releases glutamate which diffuses across cleft…
ii. binds to AMPA Rs (Na+/K+ channels) causing them to open…
iii. Na+ influx and membrane depolarisation
describe the role of glutamate Rs in learning and memory
i. strong, high frequency stimulation/glutamate release at synapse…
ii. activation of NMDA Rs (Na+/K+ and Ca2+ channel) allows Ca2+ entry…
iii. up-regulates AMPA Rs - LONG TERM POTENTIATION (LTP)
why can excess glutamate cause neurone damage
too much glutamate… too much Ca2+ entry through NMDA Rs… excitotoxicity
name the 2 main inhibitory amino acid NTs in the CNS - how do these act?
- GABA - acts in brain
- Glycine - acts in brainstem and spinal cord
GABA and glycine Rs have integral Cl- channels: opening of channel… Cl- influx… hyperpolarisation - inhibtiory post-synaptic potential decreases AP firing
how do barbiturates and benzodiazepines act in the CNS
Both bind to GABA Rs and enhance response to GABA - anxiolytic and sedative actions by decreasing neuronal activity
- barbiturates: sometimes used as anti-epileptic drugs
- benzodiazepines: used to treat anxiety, insomnia and epilepsy
what is the role of glycine in the patellar reflex
i. sensory neurones from quadriceps spindle Rs synapse with interneurones in spinal cord…
ii. interneurone synapses with motor neurone to reciprocal muscle (hamstrings) - releases glycine to inhibit APs
