Ian D. Forsythe

TL;DR: Agonists of mGluRs suppressed a high voltage-activated P/Q-type calcium conductance in the presynaptic terminal, thereby inhibiting transmitter release at this glutamatergic synapse and identifying a target ion channel is a first step toward elucidation of their molecular mechanism.

TL;DR: The authors summarize the current understanding of this subtle signaling pathway, discuss the evidence for nitrergic modulation of ion channels and homeostatic modulation of intrinsic excitability, and speculate about the pathological consequences of spillover between different nitrerGic compartments in contributing to aberrant signaling in neurodegenerative disorders.

TL;DR: It is concluded that mitochondria are the major organelle regulating presynaptic calcium at central glutamatergic terminals, and their role in maintaining transmission by accelerating recovery from synaptic depression after periods of moderate activity.

TL;DR: It is suggested that the available conductance generating the slow EPSP may be sufficient, even at low firing rates, to influence excitability on both a short‐term and more long‐lasting basis.

TL;DR: An in vitro brainstem slice preparation of the superior olivary complex has been developed permitting patch recording from a presynaptic terminal and from its postsynaptic target‐‐the principal neurone of the medial nucleus of the trapezoid body, and whole‐cell recording from the MNTB neurone shows evoked EPSCs preceded by a prespike.