LTS is mediated by a Ca2+ conductance When the hyperpolarization of the membrane in these interneurons is maintained at a certain level calcium conductance is reduced, if not completely inactivated. This results in the membrane polarization not being in the right range for single spikes and hence "bursts" result. The LTS therefore is dependent upon the conductance of calcium. Serotonin inhibition of the low-threshold spike The striatum, a nucleus in the basal ganglia, contains low-threshold spike interneurons. The basal ganglia serve many functions, which include involuntary motor control, emotions, and cognition. These interneurons produce nitric oxide and are modulated by neurotransmitters, specifically serotonin, released from the brainstem. Serotonin serves to inhibit these interneurons. This was studied using transgenic mice in which nitric oxide interneurons were labeled green using green fluorescent protein (GFP). Serotonin binds to serotonin receptors on the interneuron (5-HT2c), which increases potassium conductance and subsequently decreases the excitability of the neuron. Research Much of the research done on LTS has examined cells of a cat’s lateral geniculate nucleus. All thalamic relay cells experience these specific voltage-dependent calcium currents, and the cat has proven to be a useful model species to study. Different variations of current clamp methods, in addition to model simulations have shed light on many aspects of the phenomena. Recent research has also been conducted on the T-type calcium channel and how modulation of these channels may allow for the treatment of various neurological and psychological disorders such as schizophrenia, dementia, mania, and epilepsy. This is, however, still a new area of research. T-type calcium channels have been known to play a role in the spike-and-wave discharges of absence seizures. Antiepileptic drugs can control absence seizures by inhibiting the T-type calcium channels which prevents low-voltage calcium currents. Amplitude of the Ca2+ spike The amplitude of LTS has been shown to directly correlate with the size of the transient Ca2+ current that underlies the LTS in certain neuronal cells. They are triggered by a combination of a hyperpolarized membrane, or de-inactivation of Ca2+ channels, and a suprathreshold depolarizing input. The amplitude of the Ca2+ spike is therefore predominantly dependent on the level of preceding membrane hyperpolarization and the depolarizing input. However, it has been demonstrated that the LTS are all-or-none events due to the regenerative nature of the phenomenon. As with the action potentials that follow them, LTS vary little in amplitude or shape at different holding