RESUMEN
Interactions among mechanosensory neurons, sensitive to touch, pressure and nociceptive stimuli in the leech nervous system were studied in isolated ganglia and in body-wall preparations. Pairs of touch-pressure, touch-nociceptive and pressure-nociceptive neurons were tested by suprathreshold stimulation of one neuron while recording the response of the other, in both directions. Pressure and nociceptive stimulation evoked depolarizing and hyperpolarizing responses in touch cells, mediated by interneurons. The relative expression of these responses depended on the stimulus duration. One or two pressure cell spikes produced, predominantly, a depolarization of the touch cells, and increasing number of spikes evoked a hyperpolarization. Nociceptive cells produced primarily the hyperpolarization of touch cells at any stimulus duration. When touch cells were induced to fire by injection of positive current into the soma, stimulation of pressure cells inhibited touch cell activity. However, when touch cells were induced to fire by peripheral stimulation, pressure cell activation failed to inhibit touch cell firing. The results suggest that excitation of pressure and nociceptive cells would not limit the responses of touch cells to peripheral stimuli, but would inhibit the firing of touch cells evoked by their central connectivity network.
Asunto(s)
Red Nerviosa/fisiología , Neuronas Aferentes/fisiología , Animales , Sanguijuelas , Mecanotransducción Celular/fisiología , Potenciales de la Membrana/fisiología , Inhibición Neural , Neuronas Aferentes/clasificación , Estimulación FísicaRESUMEN
The non-spiking neurons 151 are present as bilateral pairs in each midbody ganglion of the leech nervous system and they are electrically coupled to several motorneurons. Intracellular recordings were used to investigate how these neurons process input from the mechanosensory P neurons in isolated ganglia. Induction of spike trains (15 Hz) in single P cells evoked responses that combined depolarizing and hyperpolarizing phases in cells 151. The phasic depolarizations, transmitted through spiking interneurons, reversed at around -20 mV. The hyperpolarization had two components, both reversing at around -65 mV, and which were inhibited by strychnine (10 micromol l(-1)). The faster component was transmitted through spiking interneurons and the slower component through a direct P-151 interaction. Short trains (<400 ms) of P cell spikes (15 Hz) evoked the phasic depolarizations superimposed on the hyperpolarization, while long spike trains (>500 ms) produced a succession of depolarizations that masked the hyperpolarizing phase. The amplitude and duration of the hyperpolarization reached their maximum at the initial spikes in a train, while the depolarizations persisted throughout the duration of the stimulus train. Both phases of the response were relatively unaffected by the spike frequency (5-25 Hz). The non-spiking neurons 151 processed the sensory signals in the temporal rather than in the amplitude domain.
Asunto(s)
Sanguijuelas/fisiología , Neuronas Aferentes/fisiología , Potenciales de Acción/efectos de los fármacos , Potenciales de Acción/fisiología , Animales , Electrofisiología , Ganglios de Invertebrados/citología , Ganglios de Invertebrados/fisiología , Interneuronas/fisiología , Mecanorreceptores/fisiología , Movimiento/fisiología , Venenos/farmacología , Estricnina/farmacología , Sinapsis/fisiologíaRESUMEN
The response of Retzius neurons, the main neuronal source of serotonin in the leech nervous system, to cholinergic agonists has been extensively investigated. In this study, we analyzed the effects of inhibiting the acetylcholinesterase (AChE) activity in the leech midbody ganglion on the electrophysiological activity of the Retzius neurons. Bath application of neostigmine and physostigmine (0.1-100 mumol l-1) produced, after a delay, a strong depolarization of the Retzius neurons with a dose-dependent amplitude and latency. The amplitude of this depolarization increased as the extracellular level of Ca2+ increased and decreased as the extracellular level of Ca2+ decreased. The response to neostigmine and physostigmine was inhibited by curare (100 mumol l-1), nicotine (10 mumol l-1), atropine (100 mumol l-1) and strychnine (100 mumol l-1), but was not affected by mecamylamine (100 mumol l-1) or hexamethonium (100 mumol l-1). Superfusion with solutions containing 100 mumol l-1 strychnine or atropine produced a progressive hyperpolarization of the Retzius neurons, while superfusion with 100 mumol l-1 curare did not. The hyperpolarization induced by atropine was inhibited in the presence of curare. Other neurons in the ganglion showed distinctive responses to the AChE inhibitors that were coincident with their responses to cholinergic agonists. The results suggest the existence of a basal level of acetylcholine (ACh) release in the leech ganglion that is powerfully counteracted by endogenous AChE activity. Under control conditions, this basal release appears to be sufficient to generate an ACh tonus that regulates the membrane potential of Retzius neurons. Since these neurons can support a sustained firing rate, which is dependent on the membrane potential, the results presented in this report suggest that the basal ACh tonus regulates the output of these neuromodulatory serotonergic neurons.