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Identification of the neurotransmitters involved in modulation of transmitter release from the central terminals of the locust wing hinge stretch receptor



The flight motor system of the locust represents a model preparation for the investigation of neuromodulation. At the wing hinges are stretch receptors important in generating and controlling the flight motor pattern. The forewing stretch receptor (fSR) makes direct cholinergic synapses with depressor motor neurons (MN) controlling that wing, including the first basalar MN (BA1). The fSR/BA1 synapse is modulated by muscarinic cholinergic receptors located on γ-aminobutyric acid (GABA)-ergic interneurons (Judge and Leitch [1999a] J. Comp. Neurol. 407:103–114; Judge and Leitch [1999b] J. Neurobiol. 40:420–431). However, electrophysiology has shown that fSR/BA is also modulated by biogenic amines (Leitch et al. [2003] J. Comp. Neurol. 462:55–70). We have used electron microscopic immunocytochemistry (ICC) to identify the neurotransmitters in neurons presynaptic to the fSR and to determine the relative proportion of these different classes of modulatory inputs. Approximately 55% of all inputs to the fSR are glutamate-IR, indicating that glutamatergic neurons may also play an important role in presynaptically modulating the fSR terminals. Anti-GABA ICC confirmed that over 40% of inputs to the fSR are GABA-IR (Judge and Leitch [1999a] J. Comp. Neurol. 407:103–114). Labelling sections with an antioctopamine antibody revealed neurons containing distinctive large, electron-dense granules, which could reliably be used to identify them. Aminergic neurons that modulate the synapse may have very few morphologically recognizable synaptic outputs. Although putative octopaminergic processes were found in close contact to horseradish peroxidase-filled fSR profiles, no morphologically recognizable synaptic inputs to the fSR were evident. Collectively, these data suggest that most inputs to the fSR are from either glutamatergic or GABAergic neurons. J. Comp. Neurol. 502:794–809, 2007. © 2007 Wiley-Liss, Inc.