Dendrites
Receptive area
Afferents synapse here
Axon
Electrical signaling via action potentials
Terminals
Release transmitter to send signal to next neuron
Primary route for ions to cross membrane
Ion channels
*also pumps, transporters
Deficient in long QT syndrome - cardio
K+ channel ion channel
Deficient in Cystic Fibrosis
Chloride transporter
Cell connection = cardio
Gap junction
Direct electrical coupling
Neuron connection
Chemical = hormone/neurotransmitter
What increases Gaba-A flux (Cl)?
Post synaptic =
Sedatives, anti-anxiety, anti-epileptic, ETOH
Gaba-b receptor = presynaptic
function
Reduce Ca2+ flux
Ionotropic vs Metabotropic
Ionotropic
Metabotropic
Ca2+
concentration/movement/storage
outside = [Low] Inside = [high]
Store = mitochondria/ER
Glutamate/NMDA receptor
What goes in?
Ca2+
One type
Excess Ca2+ damage in:
Ex; Memantine = blocks NMDA
Uneven ion distribution/RMP
Due to:
*Large anions in cytoplasm
(Balance elect charge/osmolarity)
*Ion pumps - Na/K atpase
(Na high outside
K high inside)
Electrogenic Na+/K+ Atpase pump
Current flow
Net outward. (Small hyperpole)
Reversal potentials
Na/K
Na+ = +57 mV
K+ = -85 mV
RMP = equilibrium?
NO = STEADY STATE
Rest = inward Na flow
Outward K flow
Constitutively active channels
+
Ion selectivity mech
K+ leak, no stim needed
Barrier to depole
Pore loops = K selectivity
Voltage-gated K+ channel
How open?
How selective?
Open = voltage sensor
Selective = pore loops
*essential for Act Potential
Channelopathies (Rxs enhance)
Epilepsy
Cardio arrythmia
Hyperekplexia (startle disease)
Epilepsy = K/nicotinic
Hyperekplexia= glycine receptor mutations
Cardio arrythmias = Na/K
OD lidocaine = seizure
Why?
* targets inhibitory neuron
AP involves (channels)
* Slower voltage-gated K+
AP initiation:
Positive feedback cycle with
Na+ influx
By end almost all Na channels open