Journal: Neuropharmacology

Article Title: Roles of K + and Cation Channels in ORL-1 Receptor-mediated Depression of Neuronal Excitability and Epileptic Activities in the Medial Entorhinal Cortex

doi: 10.1016/j.neuropharm.2019.04.017

Figure Lengend Snippet: Activation of ORL-1 receptors depresses the AP firing frequency in entorhinal neurons. A1-A3, Application of NOP inhibited the AP firing frequency of layer II stellate neurons. A1, Voltage responses (upper panel) generated by current injection at an interval of 0.1 nA (lower panel) recorded from a stellate neuron in layer II. The RMP of this neuron was shown on the left. A2, AP firing recorded before, during and after application of NOP from the stellate neuron. The membrane potential elevated by continuous injection of a positive current to induce stable firing was shown on the left. A3, Pooled time course of AP firing frequency from 10 stellate neurons in response to NOP. B1-B3, Application of NOP inhibited the AP firing frequency of layer III pyramidal neurons. B1, Voltage responses (upper panel) generated by current injection at an interval of 0.1 nA (lower panel) recorded from a pyramidal neuron in layer III. The RMP of this neuron was shown on the left. B2, APs recorded for the layer III pyramidal neuron before, during and after the application of NOP. The membrane potential elevated by continuous injection of a positive current to induce stable firing was shown on the left. B3, Pooled time course of AP firing frequency from 8 layer III pyramidal neurons before, during and after the application of NOP. C1-C3, Application of NOP significantly inhibited the AP firing frequency of layer V pyramidal neurons recorded by perforated patches. C1, Voltage responses (upper panel) generated by current injection at an interval of 0.1 nA (lower panel) recorded from a pyramidal neuron in layer V. The RMP of this neuron was shown on the left. C2, APs recorded for the layer V pyramidal neuron before, during and after the application of NOP. The membrane potential elevated by continuous injection of a positive current to induce stable firing was shown on the left. C3, Pooled time course of AP firing frequency from 10 layer V pyramidal neurons in response to NOP. D1-D3, NOP depressed the excitability of layer III pyramidal neurons assessed by injecting a series of positive currents. D1, Overlays of voltage responses (upper) evoked by injection of currents from 0 to 210 pA at an interval of 30 pA with a duration of 600 ms (lower) in a layer III pyramidal neuron in control condition. The RMP of this neuron was −60 mV. Note that injection of current at +30 pA began to evoke AP firing in this condition. D2, Overlays of voltage responses (upper) evoked by injection of currents from 0 to 210 pA at an interval of 30 pA with a duration of 600 ms (lower) in the same layer III pyramidal neuron in the presence of NOP. Note that NOP hyperpolarized the RMP of the neuron and injection of positive currents >+90 pA began to evoke AP firing. D3, Relationship of the numbers of APs and the corresponding currents injected from the same population of layer III pyramidal neurons (n=12) before and during the application of NOP. Note that the current-AP curve shifted to the right in the presence of NOP suggesting that NOP decreases neuronal excitability.

Article Snippet: Recordings of action potentials, resting membrane potentials and holding currents from entorhinal neurons Whole-cell patch-clamp recordings using a Multiclamp 700B amplifier (Molecular Devices, Sunnyvale, CA) in current- or voltage-clamp mode were made usually from the pyramidal neurons in layer III of the medial EC visually identified with infrared video microscopy (Olympus BX51WI) and differential interference contrast optics unless stated otherwise.

Techniques: Activation Assay, Generated, Injection