potentials. This dictates that suprathreshold depolarizing inputs do not affect the amplitude and only factor into the initial activation of the LTS. The amount of de-inactivation determines the conductance of Ca2+ channels and is the main factor that contributes to the amplitude of LTS. It has also been suggested that the activity of delayed rectifier K+ channels can affect the amplitude of LTS. Burst firing caused by LTS are therefore thought to be used as on/off signaling as opposed to tonic firing which is graded and more responsive to the intensity of depolarizing inputs. Latency of the Ca2+ spike The latency of a LTS is the amount of time between the depolarizing pulse and its peak. It has been shown that unlike amplitude, it is directly affected by the size of the initial depolarizing current. This is derived from the interaction between the initial, outward ohmic response, which is the leakage K+ ions out of the cell in response to change in membrane potential, and the voltage-dependent gating of the T-type calcium channels. Latency is decreased with an increased depolarizing current, which overruns the outward ohmic current and more quickly depolarizes the membrane. This more quickly activates the exponential growth of the Ca2+ spike. This reduction occurs more sharply with depolarizing currents closer to the threshold and more gradually as current injections are increased beyond threshold. Latency cannot be further reduced beyond a certain depolarizing current and becomes nearly uniform with any larger current. This has led to the hypothesis that burst signaling as a result of LTS with stronger activating inputs is more stable than LTS due to near-threshold activating inputs. Parkinson's Disease The thalamus is responsible for relaying sensory and motor signals to the cerebral cortex. Therefore, much research has been conducted on low-threshold spikes in the neurons in the thalamus and how it could relate to Parkinson's disease and the corresponding loss of motor function. Hypo-bradykinesia, as seen in Parkinson's disease, is improved by medial thalamotomy; this suggests that it is caused by interference of thalamic LTS bursts with cortical functions. LTS have been found to occur in the human lateral thalamus during sleep; however, they fade as soon as the patient is awakened. Abnormal LTS bursting activities that have been noted in awake parkinsonian patients suggests a relation between the clinical condition and this neuronal activity. References Electrophysiology Cellular neuroscience