In this study, we sought to characterize the effects of focal GABA(A) receptor antagonism on spontaneous and evoked activity in dorsal horn neurons of the alpha-chloralose anesthetized cat. Bicuculline (0.5, 1.0 mM) applied near the neurons through a transparenchymal dialysis fiber resulted in increased evoked activity in nociceptive dorsal horn neurons. Hair deflection was the stimulus most affected, followed by both low and high threshold tonic mechanical stimulation of the receptive field. In addition, neurons displayed increased background discharge and a subpopulation developed an increased afterdischarge to noxious mechanical stimulation. This is in contrast to our previous work with glycine receptor antagonism where only the evoked response to hair follicle activation was significantly enhanced. Subsequent co-administration of an NMDA receptor antagonist (AP-7, 2.0 mM) was without any apparent effect on either basal or bicuculline-enhanced responses. Co-administration of a non-NMDA excitatory amino acid receptor antagonist (CNQX, 1.0 mM) with the bicuculline non-selectively blocked both low and high threshold mechanical input. The inability of AP-7 to reverse the bicuculline-associated hyperreactivity also contrasts with the AP-7 reversal of the strychnine-associated hyperreactivity. These results point out that, while GABA and glycine are frequently co-localized in cells of the spinal dorsal horn and both appear to mediate tonic inhibitory control systems, they are not at all equivalent and are subject to different modulatory pharmacologies. Removal of each influence may model a different component of neuropathic pain.

The normal pattern of breathing movements in Rana pipiens has been studied by recording pressure and volume changes in the buccal cavity and lungs, and electromyograms from the muscles involved in this activity. Two types of breathing movement were obtained, one concerned with ventilation of the buccal cavity (buccal cycles) and the other with lung ventilation (lung cycles). Only in the latter type of movement were the nares and glottis actively involved. During buccal cycles the nares remained open and the glottis closed, so although excursions of the buccal floor were some two-thirds of the magnitude of those occurring during lung cycles, only low pressures were generated. The onset of a lung cycle was signalled by activity in the laryngeal dilator muscle. When the glottis opened, lung pressure and volume decreased, and buccal cavity pressure and volume increased. After closure of the nares, the buccal floor was rapidly elevated by the activity of the breathing muscles and air was forced into the lungs from the buccal cavity. At peak pressure in the lungs and buccal cavity the glottis closed and nares opened. The recovery stroke of the buccal pump was passive. No evidence was found for large pressure differentials between the buccal cavity and lungs when the glottis was open, and air-flow recordings at the external nares showed two phases of flow during each buccal cycle and four phases with each lung ventilation cycle.

Pacing thresholds in most Micra patients with elevated thresholds decrease after implant. Micra device repositioning may not be necessary if the pacing threshold is ≤2 V.

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