Low-threshold spikes

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Low-threshold spikes (LTS) are brief, large depolarizations in neurons caused by T-type calcium channels. They happen when the cell is hyperpolarized (made more negative) and then slightly depolarized, often after inhibitory input. When the T-type channels recover from inactivation during hyperpolarization, a small depolarization can open many channels and produce a big, rapid depolarization—the LTS. This usually ends with a short burst of 2–7 action potentials, called a low-threshold burst. LTS are voltage-dependent: if the resting membrane potential is too depolarized (above about −60 mV), they inactivate and cannot occur.

LTS are mainly driven by calcium (Ca2+) entering through T-type channels, though several other currents shape them. Early there is a leak current of K+ and Na+, then a hyperpolarization-activated sag helps bring the membrane toward threshold, and finally the inward Ca2+ current dominates and creates the large spike. The size of the LTS depends largely on how much Ca2+ conductance there is and how hyperpolarized the cell was before the spike.

These channels are common in the brain, especially in thalamic relay neurons, where they support two firing modes: tonic (no LTS) and burst (LTS with a rapid spike train). LTS often follow inhibitory inputs, and their timing (latency) gets shorter as the initial depolarization grows.

Blocking T-type channels can help treat absence seizures, which involve characteristic spike-and-wave discharges. LTS also play a role in rhythmic activity in several brain regions, including the inferior olive and thalamus, and they can be modulated by neurotransmitters such as serotonin.

LTS were described in the 1980s by Llinás and colleagues. They are an important part of how neurons generate bursts and rhythms, helping explain sleep rhythms and motor control signals.