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M Brunelli

Publications and source records attributed to M Brunelli.

At least 55 records · Page 3Linked to original sources

Serotonin and Retzius cell depress the hyperpolarization following impulses of leech touch cell.

Intracellular recordings from T mechanosensory cells of Hirudo medicinalis showed, as previously demonstrated, that repetitive firing is followed by a long-lasting hyperpolarization. Serotonin application at two concentrations (1 microM and 50 microM) depressed this hyperpolarization by up to 2/3; the effect was dose-dependent, long-lasting and reversible. Intracellular stimulation of giant serotonergic neurons (Retzius cells, Rz) mimicked serotonin perfusion: the effect was proportional to the number of spikes fired by Retzius cells. The combined use of intracellular iontophoretic injection of horseradish peroxidase and lucifer yellow indicated the possible sites of contact between Rz and T cells. The effect of serotonin, released by Rz cells, is discussed with respect to its possible physiological significance.

Animals↗

Heterosynaptic facilitation and behavioral sensitization are inhibited by lowering endogenous cAMP in Aplysia.

An adenylate cyclase inhibitor, RMI 12330A, is able to depress cAMP synthesis stimulated by serotonin in the abdominal ganglion of Aplysia depilans and punctata. This substance reversibly blocked the heterosynaptic facilitation, induced by activation of serotonergic pathways, of the EPSP recorded from L7 motoneuron in abdominal ganglion after electrical stimulation of the siphon nerve. RMI 12330A, injected into whole unrestrained animals, inhibited the short-term dishabituation of the siphon withdrawal reflex. These findings demonstrate that the increase of endogenous cAMP in the sensory neurons mediating the gill and siphon withdrawal reflex is an essential step in the mechanism of potentiation of the transmitter output underlying heterosynaptic facilitation and short-term behavioral sensitization.

Adenylyl Cyclase Inhibitors↗

Role of serotonin and cyclic AMP on facilitation of the fast conducting system activity in the leech Hirudo medicinalis.

In the nervous system of the leech Hirudo medicinalis it has been possible to study short-term plastic changes. Depression and facilitation have been demonstrated in the fast conducting system (FCS) activity; this pathway consists of a chain of electrically linked neurons present in each ganglion. In semi-intact animals or in preparation of nerve cord and segments of body wall, both electrical stimulation of peripheral roots and tactile stimulation of the skin induced, after repetitive stimulation (0.1/s) a prolonged decrement of FCS response. Strong nociceptive stimulation applied onto the head or the body wall produced a sustained facilitation of the waned response. The same potentiation has been observed by perfusing the isolated ganglion with serotonin (5 x 10(-5) M). Such a potentiation is abolished by preincubation with methysergide, an antagonist of serotonin, and with imidazole, a cAMP-phosphodiesterase activator. Such an effect is mimicked by an analog of cAMP, db-cAMP. Simultaneous recordings of both T neurons (intracellularly) and FCS firing discharge showed that, during FCS response decrement, the T cell activity remained unchanged and no modification of conductance occurred, excluding therefore a detectable involvement of sensory neurons in the depression. These results suggest that short-term plastic changes of the FCS of the leech are due to a prolonged potentiation of synaptic transmission as a result of serotonin-mediated increase in cAMP.

Animals↗

Synaptic facilitation and behavioral sensitization in Aplysia: possible role of serotonin and cyclic AMP.

The neural changes accompanying sensitization of the gill-withdrawal reflex in Aplysia are associated with presynaptic facilitation at monosynaptic connections between sensory neurons and motor cells. To analyze the molecular mechanisms underlying the facilitation, the pharmacological actions of serotonin, octopamine, and dopamine were examined. Only serotonin enhanced synaptic transmission between the sensory and the motor neurons. A serotonin antagonist, cinanserin, reversibly blocked the synaptic facilitation. The action of serotonin may be mediated by adenosime 3',5'-monophosphate (cyclic AMP). Exposing the ganglion to dibutyryl cyclic AMP or injecting cyclic AMP into the cell body enhances the synaptic action of a sensory neuron. The mechanism of presynaptic facilitation, therefore, may include activation of one or more serotonergic neurons, which enhance the release of a neurotransmitter by increasing the intracellular concentration of cyclic AMP in the terminals of the sensory neurons.

Action Potentials↗

The neuron of the fast conducting system in hirudo medicinalis: identification and synaptic connections with primary afferent neurons.

A single neuron, located in the center of each segmental ganglion of H. medicinalis is antidromically activated by electrical stimulation of the ventral cord anteriorly and posteriorly to the ganglion, at the same threshold as the fast conducting system (FCS) and with a latency equal to the FCS conduction time. This neuron is activated trans-synaptically by tactile and photic stimulation of the skin and by stimulation of high-threshold fibres running along the cord. A spike evoked by intracellular stimulation of this neuron propagates along the FCS. Intracellular staining shows that this neuron sends two axonal branches in the anterior and posterior median connectives. Direct electrical stimulation of touch cells (T cells), as well as mechanical stimulation of the skin, lowers the threshold of and may eventually fire, the FCS neurons, not only at the level of the ganglion to which they belong, but also at the level of the neighbouring ganglia. This effect is mediated by bilateral pathwasy located in the lateral connectives. It is concluded that the FCS consists of a chain of single neurons, located in each ganglion and electrotonically coupled to each other. Touch cells project with excitatory synapses on the FCS neurons.

Animals↗

Apomorphine pecking in the pigeon.

Pecking activity elicited by apomorphine was studied quantitatively in intact and thalamic pigeons. While apomorphine pecking is easily observed in the intact pigeon, it is absent in the acute thalamic animal. I reappears, however, in the chronic preparation simultaneously with the recovery of spontaneous pecking. Apomorphine pecking is described by satiation and increased by fasting. Reticular stimulation produces reversible blockade of both apomorphine and spontaneous pecking with the same parameters, without increase in heart rate. Apomorphine pecking can be observed only in the presence of visual contrast, and is always aimed at the contrast points or edges. A decrease in contrast produces a decrease in the number of pecks delivered to the contrast points and an increase in those missing the target, while the total number of pecks delivered in a unit time is unaffected. A lowering of the background luminance is followed by a decrease in the total number of pecks, which is mostly due to a reduction of those aimed at the contrast points. All these findings are discussed and it is concluded that: i) apomorphine exerts an excitatory action (direct or indirect) on the hypothalamic feeding centers; hence apomorphine pecking can be considered as a pharmacologically motivated behavior; ii) visual contrast exerts a dual action on apomorphine pecking, namely it acts both as triggering stimulus and goal object; iii) the decrease in apomorphine pecking induced by lowering the ambient light intensity is probably due to a decrease in the level of the general arousal.

Animals↗