ionotropic receptors and synapses

excitatory neuronal synapses

- generate EPSP
- smaller than NMJ end plate potential
- glutamate = NT that diffuses across synapse
- excitatory receptors allow na to enter neurone (glutamate binds receptor)

what is EPP

- end plate potential
- depolarisation of muscle

what is IPSP

inhibitory post synaptic potential

inhibitory synapses

- generate IPSP (hyperpolarisation - mp moves further from threshold)
- NT = glycine (spinal cord) and GABA (brain)
- ionotropic receptors = GABAa and glycine receptors (chloride channels)

what are the 2 types of GABA receptors

- GABAa = fast and ionotropic (allow ion passage)
- GABAb = not ion channels (metabotropic) so effects through activation of g protein signalling system

IPSC

- inhibitory postsynaptic current
- at RMP (-65mV) there is cl influx
- Vm hyperpolarised

NT in stretch reflex

- fast synaptic connections
- sensory fibres = glu
- motor neurone = ach
- 1a interneurone = GABA

what does fast inhibition via GABAa r modulate

- excitatory activity
- IPSP modulate or suppress effects of excitation
- IPSP reduces magnitude of EPSP which helps regulate activity of synaptic function

what are the excitatory receptors

ionotropic glutamate receptors

ionotropic

channel once activated allows passage of particular ions

two types of glutamate receptors

AMDA and NMDA

AMDA and NMDA channels

- activated by ligands
- present in excitatory synapses
- permeable to na and k
- na influx and k efflux
- when activated, open and na influx = depolarisation

what do NMDA channels also allow permeability to

- Ca2+
- ca influx mainly through this channel
- blocked at RP by extracellular Mg2+

what removed mg block in nmda channels

- depolarisation
- removes block allowing nmda channel to bind, open and allow ion passage

properties of typical nmda channels

- ca permeable
- block by extracellular mg and drug APV (blocked at -80mv - not blocked in absence of mg)
- voltage sensitive
- unblocked by depolarisation

how to study excitatory synapses

- voltage clamp post synaptic cells
- stimulate fibres to make/fire AP
- EPSC
- influx of + ions moving through channel counter acted by hyperpolarising current

what glutamate receptor opens rapidly during depolarisation

AMPA

evidence for mg channel block

- patch clamp
- patch of mem containing individual receptor is voltage clamped
- glutamate (agonist) in micropipette
- recordings made in presence of mg2+

Hebb's rule

- neurons that fire together wire together
- neurones must contain a molecular mechanism for co-incidence detction

co incidence detection by NMDARs

- strong depolarisation unblocks NMDAR channel (removes mg block so glutamate can bind)
- NMDAR suited to job as highly permeable to ca, strong synaptic input activates channels, ca influx can activate various pathways and is a powerful signal for many plasticity related processes

what glutamate receptors act as coincidence detectors

- NMDAR

what does repeated synaptic activation lead to

- summation of EPSP
- leads to depolarisation
- mg block of nmda channels partially relieved
- now nmda channels contribute to EPSP
- ca influx into cell
- influx leads of activation of intracellular signalling pathways


- larger EPSP and stronger depolarisation