Other signalling molecules, such as glutamate and PD153035 hydrochloride nitric oxide, can also be released from astrocytes and contribute to calcium wave propagation. The second is through cell-cell contacts and gap junctions which allow the movement of calcium ions and inositol 1,4,5-trisphosphate into neighbouring cells, thus perpetuating the calcium wave over long distances. As the calcium wave travels further from the point of Ceftiofur hydrochloride stimulation, the amplitude of the i response decays exponentially with distance. A third way in which calcium waves propagate through the hippocampal network is mediated by action potential generation in neurons close to the electrode which synapse on other neurons and glial cells located up to hundreds of microns away from the site of stimulation. This can explain the small number of cells in figure 2B, located 300�C500 mm from the point of stimulation, which display relatively fast ��time-to-first peak�� kinetics. Because the velocity of calcium wave propagation in hippocampal slice cultures appears to increase.150 mm from the point of stimulation, this may represent a transition from gap junction-mediated propagation to release of soluble factors that stimulate neighbouring cells and perpetuate the calcium wave over long distances through astrocyte networks. ATP is also a well-known trigger of i oscillations which could explain the increased number of oscillations at further distances from the point of stimulation. The importance of astrocytes and other glial cells in hippocampal synaptic plasticity is becoming more and more evident in recent years. Astrocytes can release neuromodulatory chemicals that can serve to either enhance or dampen synaptic transmission. The triggering of calcium oscillations in astrocyte networks in the hippocampus could activate the release of neuromodulators from glial cells. Therefore, astrocytes may contribute to the decoding of the initial theta-burst stimulus and likely serve a pertinent role in LTP and synaptic plasticity changes in the hippocampus post-TBS stimulation.Patients with the rapidly progressive and severe ML II exhibit a total or near total loss of GlcNAc-1-phosphotransferase activity mostly due to nonsense or frameshift mutations while ML III a/b patients tend to have missense or splice-site mutations resulting in some residual GlcNAc-1-phosphotransferase activity and a milder clinical course.