Electrotonic current represents the passive flow of charge along the dendrites and axons of neurons due to the movement of ions.
It spreads in all directions but tends toward the axon terminal in the case of neurons.
This current weakens as it moves further from the source due to leakage of positive charges through the membrane.
Positive charges can leak through the membrane, often represented by potassium ions.
Lower internal resistance (Ri) means a higher likelihood for ions to encounter others and transmit current. Larger axons or dendrites, having more cytoplasm, facilitate easier current flow due to increased ion presence.
Dendrites initially have a resting membrane potential around -60 mV.
Action potentials start with an excitatory post-synaptic potential (EPSP) which may not always reach threshold alone; hence, summation is necessary.
Temporal Summation: Repeated action potentials arrive quickly in succession, leading to a cumulative effect where they increase the likelihood of reaching threshold together.
Spatial Summation: Synaptic input from multiple sources occurs simultaneously, aggregating EPSPs across different locations on the neuron.
The membrane must be sufficiently depolarized at the axon initial segment to activate voltage-gated channels and propagate an action potential.
The axon initial segment (AIS) serves as a crucial integration point where excitatory and inhibitory signals (IPSPs) are summed.
Strong IPSPs can inhibit the transmission of sensory information if they outbalance EPSPs.
Signals are integrated regardless of their source, leading to a potential action that dictates whether to proceed with the signal transmission or not.
Once threshold is reached, sodium channels open, causing rapid depolarization (voltage steps up to +30 mV).
After reaching +30 mV, sodium channels inactivate, and potassium channels begin to open, triggering repolarization, which overshoots resting potential, creating a hyperpolarization phase.
The sodium-potassium pump restores the resting potential by moving sodium out and potassium in, preparing for the next action potential.
Continuous propagation in unmyelinated axons requires frequent regeneration of action potentials. As sodium ions rush in, they affect adjacent segments, triggering further depolarization.
This process is akin to a domino effect where the current travels along the axon, and if it drops below threshold, the action potential will cease.
In contrast, myelinated axons exhibit saltatory propagation, where action potentials jump between nodes of Ranvier, significantly increasing transmission speed and efficiency (up to 30 miles/hr).
Myelination decreases leakage of ions and increases the length constant, allowing action potentials to travel further.
Only the nodes of Ranvier contain sodium channels which reduce the need to open channels along the entire length of the axon, thereby enhancing conduction speed.
The body selectively myelinates certain motor and sensory neurons for fast response and efficiency in signaling.
Loss of myelin disrupts normal signaling, causing erratic transmission as signals fail to reach the synapse effectively due to increased leakage and slower conduction.
Demyelination results in symptoms related to motor control and sensation as the axon cannot conduct signals as quickly or efficiently as before.
Following depolarization, the cell enters a refractory state where sodium channels remain inactive, preventing immediate reactivation.
The refractory period ensures one action potential follows another without overlap.
It is crucial for directional signal propagation as it prevents the backtracking of signals to the soma, funneling action potentials towards the synapse.