When singing was in full swing (Fig. 9A), the membrane potential during the chirp intervals was up to 5 mV below the resting potential, and in addition, every chirp started with a pronounced compound IPSP of up to −5 mV amplitude. More insight into coupling

of membrane hyperpolarization and subsequent excitation was provided by spontaneous synaptic activity, as well as hyperpolarizing current injection. After a singing episode, we recorded a continuous train of IPSPs (Fig. 9D). The individual IPSPs had amplitudes between −2 and −5 Inhibitors,research,lifescience,medical mV (average: −3.1 mV; N = 1, n = 30; asterisk in Fig. 9D inset), occurred at a rate of 15–20 Hz, and were followed by transient postinhibitory selleck chemicals depolarization of 10–20 msec duration and peak amplitudes of 0.3–1.1 mV (average: 0.6 mV; N = 1, n = 30; arrowhead in Fig. 9D inset). Similarly, hyperpolarizing current injection of −2 nA for 500 msec elicited a Inhibitors,research,lifescience,medical subsequent rebound depolarization of 4 mV (peak amplitude), which triggered an immediate spike response and rhythmic singing activity starting about 300 msec after the stimulation (Fig. 9D). Short (125 msec) hyperpolarizing current pulses

of −4 nA also entailed Inhibitors,research,lifescience,medical rebound depolarization that reliably triggered a single spike that was frequently followed by 1–3 IPSPs after 100–200 msec (Fig. 9E). When hyperpolarizing pulses (−4 nA; 125 msec) were injected repetitively at 2 Hz, corresponding to a slow chirp rate, they eventually triggered brief episodes of rhythmic membrane potential oscillation accompanied by singing motor activity. To quantify the relation between hyperpolarization and subsequent rebound depolarization, the closer type 2 diabetes interneuron Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical was stimulated with hyperpolarizing current pulses of different amplitudes but with a constant duration of 125 msec. No depolarization or spike response occurred after stimulation with −1 nA (N = 1, n = 5), whereas pulses of −3 nA (N = 1, n = 5) evoked 1–3 mV poststimulus depolarizations that

occasionally triggered a single action potential. Current pulses of −4 nA (N = 1, n = 5) elicited rebound depolarizations Brefeldin_A of 2–4 mV that reliably triggered 1–2 spikes (see average responses in Fig. 9F). The post-hyperpolarization spike response was frequently accompanied by consecutive IPSPs occurring after 100–300 msec (Fig. 9E). Figure 9 Postinhibitory rebound activation of a morphologically nonidentified closer interneuron recorded in A2. (A–E) Singing motor activity (top trace) and intracellular dendritic recordings of the interneuron (lower trace). A dashed line marks the resting … In another cricket, a recording from the dendrite of a closer interneuron in the unfused abdominal ganglion A3 (data not shown) showed very similar characteristics.