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Effects of Alverine on electrical properties of vagal afferent neurons in isolated rabbit nodose ganglion

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image of Primary Sensory Neuron
For more content, see Sensory Neuron.

The possibility for Alverine to change the activity of primary afferent neurons was investigated in rabbit nodose ganglion in vitro. Alverine, applied by pressure ejection or by superfusion, depolarized 92% of the C-type neurons and had no effect on the membrane potential A-type neurons. These results were not correlated with the values of input resistances which could be unchanged, increased or decreased. Alverine induces a strong increase (up to 100%) in the duration of the action potentials, due to a decrease of the voltage-dependent outward K+ current. Using a higher dose, this effect is followed by an important decrease in the amplitude of the action potentials, resulting in a change of the full somatic spike into a smaller axonic one, called an 'A spike'. The application of tetrodotoxin (TTX 10-6 M) revealed the presence of a TTX-resistant component. Alverine decreased the amplitude and increased the duration of this component, which depends on Ca2+ channels as it persists in Na+ reduced Krebs solution. Some C-neurons in the nodose ganglion have a slow after-hyperpolarization following the fast one; Alverine completely suppresses the slow after-hyperpolarization. Voltage-clamp experiments showed that Alverine has no immediate effect on the inward currents but progressively decreased the late potassium outward currents, which were maximal at positive membrane potentials. It is concluded that Alverine has powerful effects on different gNa, gK and gCa conductances of the vagal afferent neurons. Depending on the doses injected, Alverine has excitatory or inhibitory influences on these visceral afferents. If the same channel equipment is present at the terminal level, Alverine can positively or negatively affect the synaptic transmission of vagal afferents in the nucleus of the solitary tract.


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