K+ Accumulation and Clearance in the Calyx Synaptic Cleft of Type I Mouse Vestibular Hair Cells.

Vestibular organs of Amniotes contain two types of sensory cells, named Type I and Type II hair cells. While Type II hair cells are contacted by several small bouton nerve terminals, Type I hair cells receive a giant terminal, called a calyx, which encloses their basolateral membrane almost completely. Both hair cell types release glutamate, which depolarizes the afferent terminal by binding to AMPA post-synaptic receptors. However, there is evidence that non-vesicular signal transmission also occurs at the Type I hair cell-calyx synapse, possibly involving direct depolarization of the calyx by K+ exiting the hair cell. To better investigate this aspect, we performed whole-cell patch-clamp recordings from mouse Type I hair cells or their associated calyx. We found that [K+] in the calyceal synaptic cleft is elevated at rest relative to the interstitial (extracellular) solution and can increase or decrease during hair cell depolarization or repolarization, respectively. The change in [K+] was primarily driven by GK,L, the low-voltage-activated, non-inactivating K+ conductance specifically expressed by Type I hair cells. Simple diffusion of K+ between the cleft and the extracellular compartment appeared substantially restricted by the calyx inner membrane, with the ion channels and active transporters playing a crucial role in regulating intercellular [K+]. Calyx recordings were consistent with K+ leaving the synaptic cleft through postsynaptic voltage-gated K+ channels involving KV1 and KV7 subunits. The above scenario is consistent with direct depolarization and hyperpolarization of the calyx membrane potential by intercellular K+.

A fast transient outward current in layer II/III neurons of rat perirhinal cortex.

The perirhinal cortex (PRC) is a supra-modal cortical area that collects and integrates information originating from uni- and multi-modal neocortical regions, transmits it to the hippocampus, and receives a feedback from the hippocampus itself. The elucidation of the mechanisms that underlie the specific excitable properties of the different PRC neuronal types appears as an important step toward the understanding of the integrative functions of PRC. In this study, we investigated the biophysical properties of the transient, I (A)-type K(+) current recorded in pyramidal neurons acutely dissociated from layers II/III of PRC of the rat (P8-P16). The current activated at about -50 mV and showed a fast monoexponential decay (tau(h) >> 14 ms at -30 to +10 mV). I (A) recovery from inactivation also had a monoexponential time course. No significant differences in the biophysical properties or current density of I (A) were found in pyramidal neurons from rats of different ages. Application of 4-AP (1-5 mM) reversibly and selectively blocked I (A), and in current clamp conditions it increased spike duration and shortened the delay of the first spike during repetitive firing evoked by sustained depolarizing current injection. These properties are similar to those of the I (A) found in thalamic neurons and other cortical pyramidal neurons. Our results suggest that I (A) contributes to spike repolarization and to regulate both spike onset timing and firing frequency in PRC neurons.