Reduction of endoplasmic reticulum internal calcium stores via BHQ decreases EJP amplitude

Abstract

Synaptic transmission requires Ca²⁺ to initiate the release of neurotransmitters. While the mechanism that allows this is not known, we do know that Ca2+ allows the vesicles containing these neurotransmitters to fuse with the neurons membrane. Ca²⁺ is released from internal Ca²⁺ stores like the endoplasmic reticulum when a signal is sent to the nerve terminal. This Ca²⁺ re-enters the endoplasmic reticulum internal stores through SERCA pumps. These pumps can be inhibited by the chemical butylhydroquinone (BHQ). This causes a depletion of Ca²⁺ within the internal stores and reduces the removal of free Ca²⁺ from the cytosol. The inhibition of these internal stores has both an immediate and long-term effect on the amplitudes and duration of the EJPs. In the present work we found that amplitude initially fell after the inhibition, but eventually rose until it reached the values from before the BHQ was added. Duration grew steadily longer after the BHQ was added. These results show that the role of endoplasmic reticulum as internal Ca²⁺ stores is important in maintaining both functional amplitude and duration.