A1-LC is a local closer interneuron in the A1 neuromere of the metathoracic ganglion (Fig. 8A). Its dorsal cell body was located near the ganglion midline and its primary neurite projected toward the contralateral ganglion side. An anterior and a posterior dendritic main branch arose from the primary neurite at the midline of the ganglion and ramified along the dorsal midline of A1 and A2 where they spatially overlapped with the posterior dendrite of T3-DO and axonal branches of A3-AO and T3-DO. During fictive singing, A1-LC was depolarized and generated 2–4 action potentials in each wing-closer phase

and was inhibited during the wing-opener phase (Fig. 8B). For each syllable, the Inhibitors,research,lifescience,medical neuron fired its Inhibitors,research,lifescience,medical first spike 11.4 ± 1.5 msec (mean ± SD; N = 1, n = 20) after the first wing-opener motoneuron spike and 10.2 ± 1.1 msec (mean ± SD; N = 1, n = 20) before the first spike of the wing-closer burst. During the chirp intervals, the membrane potential of A1-LC was up to 3 mV below the resting potential, which drastically reduced its spontaneous spike activity from 23 Inhibitors,research,lifescience,medical Hz before and after GSK2656157 cost singing episodes to a mean spike activity of 8 Hz during chirp intervals. Figure 8 Structure and activity of the local closer-interneuron A1-LC. (A) Morphology of A1-LC

in the fused abdominal neuromeres of the metathoracic ganglion (ventral view). (B) and (C) Singing motor activity (top trace) and intracellular recordings of Inhibitors,research,lifescience,medical A1-LC (lower … In the A2 neuromere, we recorded a morphologically unidentified closer interneuron that received conspicuous inhibition at the beginning of each chirp and indicated postinhibitory rebound as a presumable mechanism contributing to singing pattern Inhibitors,research,lifescience,medical generation. During fictive singing, this closer neuron was inhibited in each opener phase and depolarized by 20–25 mV in the closer phase (Fig. 9A). Every depolarization gave rise to a burst of 5–6 action potentials with a spike frequency of 250–300

Hz. During each syllable, the neuron fired its first spike 12.0 ± 2.3 msec (mean ± SD; N = 1, n = 50) after the start of the wing-opener these motoneuron burst and 8.0 ± 0.4 msec (mean ± SD; N = 1, n = 50) before the first spike of the wing-closer burst. Injection of depolarizing current pulses (+5 nA; 100 msec) reset the ongoing chirp rhythm similar to A3-AO and T3-DO, but in contrast to the reset effect of the opener interneurons, electrical stimulation of this closer neuron did not elicit additional singing motor activity (Fig. 9B). Interestingly, during the chirp intervals following the current pulses (arrows in Fig. 9B), the membrane potential was about 3 mV lower as during the preceding and following chirp intervals. Before the start of each singing episode, this closer interneuron received several volleys of 4–6 individual IPSPs at a time (Fig. 9C).