PubMed · 5657123
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E de Boer, L B Jongkees. On cochlear sharpening and cross-correlation methods.. https://doi.org/10.3109/00016486809120947
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The neuronal threshold, which can be determined by the level of depolarization immediately prior to spike generation, is different for responses to conditioned and discriminated stimuli after conditioning. However, it is impossible to determine excitability within a response to stimuli that failed to generate a spike. In the present study we examined the role of the AP threshold of two related Helix defensive neurons in the initiation of an AP during elaboration of the neuronal analog of a classical conditional reflex. These neurons fire in a synchronous manner though spikes sometimes are not generated simultaneously. We compared the change in spike threshold within the responses with other parameters of intracellular activity that also affect the neuronal response, but which can be measured without an analysis of the spike waveform (spike latency, slope of excitatory postsynaptic potentials, etc.). We found that the change in slope is not the reason for the change in the threshold during pairing. The thresholds within conditioned and discriminated responses affected spike generation and their values correlated with the spike presence or absence in related neurons. The excitability changed transiently within the responses, since these alterations were selective for the conditioned and discriminated stimuli and applied primarily to the first spike of the response. The firing threshold seems to be a dynamic property of excitable membrane. Neurons appear to evaluate the significance of the input signal, transiently change their own excitability and only after that compare the magnitude of this signal and threshold.
To clarify the functions of nitric oxide (NO) induced by either neuronal NO synthase (nNOS) or endothelial NO synthase (eNOS) after transient cerebral ischemia, we investigated the effects of L-N(5)-(1-iminoethyl)ornithine (L-NIO), a relatively selective eNOS inhibitor, and 7-nitroindazole (7-NI), a relatively selective nNOS inhibitor, on hippocampal dysfunction caused by cerebral ischemia. We measured mean arterial blood pressure (MABP), hippocampal blood flow, direct current (DC) potential, CA1 population spike (PS) and extracellular concentrations of glutamate from rat hippocampus after transient forebrain ischemia, which was induced by four-vessel occlusion for 10 min. L-NIO (20 mg/kg) and 7-NI (25 mg/kg) were administered intraperitoneally 20 min before ischemia. L-NIO, but not 7-NI, increased MABP before, during and after ischemia, compared with the vehicle group. 7-NI, but not L-NIO, reduced the amplitude of anoxic depolarization induced by ischemia. 7-NI recovered the PS amplitude in part 60 min after ischemia. 7-NI, but not L-NIO, reduced the ischemia-induced levels of glutamate. These results indicate that nNOS inhibition with 7-NI improves, at least in part, hippocampal dysfunction after ischemia, while eNOS inhibition with L-NIO worsens it.
The present study examined the correlation between the level of activity neuron B52 and the transition from protraction to retraction phases of buccal motor patterns (BMPs) and the termination of the BMPs. The level of activity in B52 during the protraction phase was positively correlated with the duration of that phase. A second burst of activity in B52 was associated with the termination of the retraction phase. An apparent monosynaptic inhibitory connection from B52 to B64, may mediate the effects of B52. The first burst of activity in B52 delays the onset of activity in B64, thereby prolonging the protraction phase, and the second burst inhibits activity in B64, thereby terminating the retraction phase. These results suggest that activity in B52 may contribute to switching between ingestion-like and rejection-like BMPs by regulating both phase transition and termination of BMPs.