PubMed · 3074500
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J R Mao, Q Z Yin. 1988. [The spinal catecholaminergic neuron system].. https://pubmed.ncbi.nlm.nih.gov/3074500/
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This study proposes a method for the automatic classification of nonlinear interactions between a strictly periodical event series modelling the activity of an exogenous oscillator working at a fixed and well-known rate and an event series modelling the activity of a self-sustained oscillator forced by the exogenous one. The method is based on a combination of several well-known tools (probability density function of the cyclic relative phase, probability density function of the count of forced events per forcing cycle, conditional entropy of the cyclic relative phase sequence and a surrogate data approach). Classification is reached via a sequence of easily applicable decision rules, thus rendering classification virtually user-independent and fully reproducible. The method classifies four types of dynamics: full uncoupling, quasiperiodicity, phase locking and aperiodicity. In the case of phase locking, the coupling ratio (i.e. n: m) and the strength of the coupling are calculated. The method, validated on simulations of simple and complex phase-locking dynamics corrupted by different levels of noise, is applied to data derived from one anesthetized and artificially ventilated rat to classify the nonlinear interactions between mechanical ventilation and: (1) the discharges of two (contemporaneously recorded) single postganglionic sympathetic neurons innervating the caudal ventral artery in the tail and (2) arterial blood pressure. Under central apnea, the activity of the underlying sympathetic oscillators is perturbed by means of five different lung inflation rates (0.58, 0.64, 0.76, 0.95, 1.99 Hz). While ventilation and arterial pressure are fully uncoupled, ventilation is capable of phase locking sympathetic discharges, thus producing 40% of phase-locked patterns (one case of 2:5, 1:1, 3:2 and 2:2) and 40% of aperiodic dynamics. In the case of phase-locked patterns, the coupling strength is low, thus demonstrating that this pattern is sliding. Non-stationary interactions are observed in 20% of cases. The two discharges behave differently, suggesting the presence of a population of sympathetic oscillators working at different frequencies.
Norepinephrine (NE) plays a complex role in the behavioral state-dependent regulation of sensory processing. However, the role of forebrain NE action in modulating high-order sensory activity has not been directly addressed. In this study, we take advantage of the discrete, feedforward organization of the avian song system to identify a site and mechanism of NE action underlying state-dependent modulation of sensory processing. We have developed an experimental paradigm in which brief arousal repeatedly suppresses song system auditory responsiveness. Using pharmacological manipulations in vivo, we show that infusion of alpha-adrenergic antagonists into the NIf (nucleus interfacialis of the nidopallium), an auditory forebrain area, blocks this state-dependent modulation. We also demonstrate dose-dependent enhancement and suppression of song system auditory response properties by NE and adrenergic agonists. Our results demonstrate that noradrenergic release in a single forebrain area is a mechanism underlying behavioral state-dependent regulation of auditory processing in a neural system specialized for vocal learning.
Previous studies showed that nicotine induces adrenergic nerve-dependent vasodilation that is mediated by endogenous calcitonin gene-related peptide (CGRP) released from CGRP-containing (CGRPergic) nerves. The mechanisms underlying the nicotine-induced vasodilation were further studied. Rat mesenteric vascular beds without endothelium were contracted by perfusion with Krebs solution containing methoxamine, and the perfusion pressure was measured with a pressure transducer. Perfusion of nicotine (1-100 microm) for 1 min caused concentration-dependent vasodilation. Capsazepine (vanilloid receptor-1 antagonist; 1-10 microm) and ruthenium red (inhibitor of vanilloid response; 1-30 microm) concentration-dependently inhibited the nicotine-induced vasodilation without affecting the vasodilator response to exogenous CGRP. Nicotine-induced vasodilation was not inhibited by treatment with 3,4-dihydroxyphenylalanine (DOPA) receptor antagonist (l-DOPA cyclohexyl ester; 0.001-10 microm), dopamine D1 receptor-selective antagonist (SCH23390; 1-10 microm), dopamine D2 receptor antagonist (haloperidol; 0.1-0.5 microm), ATP P2x receptor-desensitizing agonist (alpha,beta-methylene ATP; 1-10 microm), adenosine A2 receptor antagonist (8(p-sulfophenyl)theophylline; 10-50 microm) or neuropeptide Y (NPY)-Y1 receptor antagonist (BIBP3226; 0.1-0.5 microm). Immunohistochemical staining of the mesenteric artery showed dense innervation of CGRP- and vanilloid receptor-1-positive nerves, with both immunostainings appearing in the same neuron. The mesenteric artery was also densely innervated by NPY-positive nerves. Double immunostainings showed that both NPY and CGRP immunoreactivities appeared in the same neuron of the artery. These results suggest that nicotine acts on presynaptic nicotinic receptors to release adrenergic neurotransmitter(s) or related substance(s), which then stimulate vanilloid receptor-1 on CGRPergic nerves, resulting in CGRP release and vasodilation.