RESUMO

The optic tectum in birds and its homologue the superior colliculus in mammals both send major bilateral, nontopographic projections to the nucleus rotundus and caudal pulvinar, respectively. These projections originate from widefield tectal ganglion cells (TGCs) located in layer 13 in the avian tectum and in the lower superficial layers in the mammalian colliculus. The TGCs characteristically have monostratified arrays of brush-like dendritic terminations and respond mostly to bidimensional motion or looming features. In birds, this TGC-mediated tectofugal output is controlled by feedback signals from the nucleus isthmi pars parvocellularis (Ipc). The Ipc neurons display topographically organized axons that densely ramify in restricted columnar terminal fields overlapping various neural elements that could mediate this tectofugal control, including the retinal terminals and the TGC dendrites themselves. Whether the Ipc axons make synaptic contact with these or other tectal neural elements remains undetermined. We double labeled Ipc axons and their presumptive postsynaptic targets in the tectum of chickens (Gallus gallus) with neural tracers and performed an ultrastructural analysis. We found that the Ipc terminal boutons form glomerulus-like structures in the superficial and intermediate tectal layers, establishing asymmetric synapses with several dendritic profiles. In these glomeruli, at least two of the postsynaptic dendrites originated from TGCs. We also found synaptic contacts between retinal terminals and TGC dendrites. These findings suggest that, in birds, Ipc axons control the ascending tectal outflow of retinal signals through direct synaptic contacts with the TGCs.

Assuntos

RESUMO

We investigate possible interactions between acetylcholine (ACh)- and adenosine 5'-triphosphate (ATP)-induced responses of petrosal ganglion, where the perikarya of most sensory neurons of the glossopharyngeal nerve are located. Experiments were performed on petrosal ganglia excised from pentobarbitone-anesthetized cats, desheathed and perfused in vitro. Separate applications of ACh and ATP to the exposed surface of the ganglion induced bursts of antidromic potentials recorded from the carotid (sinus) nerve branch of the glossopharyngeal nerve, which frequencies were dependent on the dose of the applied agonists. The simultaneous application of previously determined ED50s of ACh and ATP provoked responses corresponding closely to the simple addition of the responses elicited by the separate application of each agent. Responses usually subsided within 1 min of stimuli application but were followed by periods of refractoriness to subsequent application of the same agent. After determining the timing for recovering from desensitization to the ED50s of ACh and ATP applied separately, ACh was applied while the preparation had been desensitized to ATP and then ATP was applied during desensitization to ACh, but responses obtained were similar to control responses induced by each agent separately. In summary, ACh- and ATP-induced responses of petrosal ganglion neurons are simply additive, followed by a few minute lasting desensitization, but cross-desensitization was not observed. Thus, ACh and ATP seem to operate through independent receptors, activating separate ionic channels, whose coincident currents do not interfere each other.

Assuntos

Assuntos

Assuntos

RESUMO

The inhibitory effect of nitric oxide (NO) on carotid chemosensory responses to hypoxia has been attributed in part to an antidromic inhibition of chemoreceptor cells activity. However, NO may also modulate the activity of the primary sensory neurons because NO is produced in the soma of these neurons located in the petrosal ganglion. Since a population of petrosal neurons is selectively activated by acetylcholine (ACh), we studied the effects of NO-donor, sodium nitroprusside (SNP), and the NO-synthase inhibitor, Nomega-nitro-l-arginine methyl ester (l-NAME), on the responses evoked in the carotid sinus nerve (CSN) by ACh applied to the petrosal ganglion in vitro. ACh (1 microgram-1 mg) increased the frequency of action potentials recorded from the CSN in a dose-dependent manner. SNP (10-50 microM) reduced the sensibility and amplitude of the CSN response to ACh, although the maximal response appears less affected. The withdrawal of SNP from the superfusion medium increased the sensibility of the responses to ACh. l-NAME (1-2 mM) slightly increased the sensibility of the ACh-induced responses, effect that persisted after l-NAME withdrawal. These results suggest that NO may play a role as modulator in this autonomic primary sensory ganglion.

Assuntos