Neuronal integration: dendrites, presynaptic inhibition, electrical synapses and firing rate

Mechanism
For completeness

A neuron adds up thousands of small pushes and pulls on its dendrites; if the sum at the axon start crosses threshold it fires, faster when pushed harder.

Updated Nov 13, 2026

Also called: Electrical synapses, Presynaptic inhibition, Electrotonic conduction

See it in 3D: Grey matter of the cord

Key points

Chemical synapses are one-way, delayed (≈ 0.5 ms), and can amplify or invert a signal; electrical synapses (connexin gap junctions) are fast, usually two-way and synchronize groups of cells.
IPSP: opening Cl⁻ channels (GABA-A, glycine) or K⁺ channels (GABA-B) holds the membrane near or below rest; shunting inhibition works even without hyperpolarization.
Presynaptic inhibition reduces Ca²⁺ entry into the excitatory terminal, so less transmitter is released (GABA on axo-axonic synapses; opioids on C-fibre terminals in the dorsal horn).
Distal dendritic synapses lose much of their effect before reaching the soma (electrotonic decrement); synapses near the soma and initial segment weigh more.
Above threshold, firing rate rises with the amount of net excitation (the excitatory state).

What it is

Each neuron receives thousands of synapses, mostly on its dendrites and soma. Excitatory and inhibitory potentials spread passively and fade with distance, then sum at the axon initial segment, where the decision to fire is made. Inhibition can act on the neuron itself (postsynaptic) or on the terminals that feed it (presynaptic). A minority of neurons are also coupled directly by gap junctions, which pass current with almost no delay.

How it works, step by step

Transmitter opens ligand-gated channels: Na⁺ influx gives an EPSP; Cl⁻ or K⁺ flux gives an IPSP.
Each potential spreads passively along the dendrite and shrinks with distance, set by membrane and axial resistance (length constant).
Potentials summate in space (many synapses at once) and in time (rapid repeats at one synapse).
The axon initial segment has the most voltage-gated Na⁺ channels, so its threshold (≈ −45 mV from a rest of ≈ −65 mV) is reached first.
If net depolarization there stays above threshold, the neuron fires repeatedly; stronger excitation shortens the interval between spikes.
Axo-axonic GABA synapses or opioid receptors on an excitatory terminal reduce its Ca²⁺ entry, cutting release without changing the target's own membrane.

Action potential

Rest −70 mVThreshold −55 mVPeak +35 mVDuration ≈ 1–2 ms

Tap a phase (the pills above or its band) or a refractory period (ARP, RRP) at the base of the plot.

Mainly Na⁺
Mainly K⁺
Rest
Threshold
ARP: absolute refractory period
RRP: relative refractory period

The spike that fires once summed input at the initial segment reaches threshold.

Chemical versus electrical synapses

Feature	Chemical	Electrical (gap junction)
Delay	≈ 0.5 ms or more	Almost none
Direction	One way	Usually both ways
Gain and sign	Can amplify, invert, be modulated	Passive, follows the presynaptic voltage
Typical role	Most CNS signalling, learning	Synchrony: inferior olive, cortical interneurons, retina; heart and smooth muscle

Clinical notes

Benzodiazepines make GABA-A channels open more often and raise inhibition; this is why they stop seizures and why combining them with other depressants is dangerous.
Opioids act presynaptically on primary afferent terminals in the dorsal horn and reduce release of glutamate and substance P, one basis of analgesia.
Strychnine (glycine-receptor block) and tetanus toxin (blocks glycine and GABA release) remove spinal inhibition and cause spasms.

Test yourself

Think of the answer, then tap the question to see it.

Why does an excitatory synapse on a distal dendrite affect firing less than one on the soma?

Its EPSP spreads passively and decays with distance (electrotonic decrement), so a smaller depolarization reaches the initial segment.

How does presynaptic inhibition differ from postsynaptic inhibition?

Presynaptic inhibition lowers transmitter release from one input terminal (less Ca²⁺ entry), leaving other inputs untouched; postsynaptic inhibition changes the target cell's membrane.

How can opening Cl⁻ channels inhibit a neuron even when the Cl⁻ equilibrium potential equals the resting potential?

Shunting: the open channels lower membrane resistance, so excitatory currents produce smaller depolarizations.

What property of gap junctions makes them suited to synchronize neurons?

They pass ionic current directly between cells with almost no delay, often in both directions, so coupled cells tend to fire together.

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Connections

See it in 3D1

The structures of Durgical's 3D anatomy where it happens.

Grey matter of the cord

In Biochemistry1

Glutamate (glutamic acid)

In Pharmacology2

← All of physiology

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: Neuroanatomy, Gray Matter (StatPearls (NCBI Bookshelf), 2024); Neuroanatomy, Spinal Cord (StatPearls (NCBI Bookshelf), 2024).

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Representative model, for educational purposes only.