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PubMed · 6233844

Pain.

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1984. Pain.. https://pubmed.ncbi.nlm.nih.gov/6233844/

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Expression of m1-m4 muscarinic acetylcholine receptor immunoreactivity in septohippocampal neurons and other identified hippocampal afferents.

Muscarinic cholinergic transmission plays an important role in modulating hippocampal activity and many higher brain functions. Many of the modulatory effects of acetylcholine on hippocampal function result from direct effects in the hippocampus or from actions on the hippocampal afferent neurons. At each site, the differential expression of a family of five distinct but related receptor subtypes governs the nature of the response. The aim of the present study was to identify the subtypes expressed in the hippocampal afferent neurons by combining retrograde tracing with immunocytochemistry. The retrograde tracer, wheat germ agglutinin conjugated to horseradish peroxidase, was injected into the hippocampus unilaterally to label afferent neurons, and was combined with muscarinic (m) acetylcholine (ACh) receptors (mAChRs) with immunocytochemistry to identify the m1-m4 subtypes expressed. The retrogradely labeled cells in the basal forebrain that contribute to the septohippocampal pathway were found to express m2, m3, and, to a lesser extent, m1. Commissural/associational pathway neurons, which were identified by retrogradely labeled cells in the ipsi- and contralateral dentate gyrus, expressed m1, m3, and m4. The retrogradely labeled cells in the entorhinal cortex of the perforant pathway expressed predominantly m1 and m3, with fewer neurons expressing m2 and m4. Raphe-hippocampal cells were found to express m1. Thus, this study provides evidence for the diversity of mAChR subtypes expressed in neurons that project to the hippocampus. The complex modulation by acetylcholine of hippocampal function, therefore, is governed not only by the variety of mAChRs expressed in the hippocampus but also by their differential expression in extrinsic hippocampal afferents.

Afferent Pathways

Central distribution and peripheral functional properties of afferent and efferent components of the superior laryngeal nerve: morphological and electrophysiological studies in the rat.

The central distribution of the afferent and efferent components of the superior laryngeal nerve (SLN), which in the rat is ramified into the three branches of the rostral branch (R.Br), middle branch (M.Br), and caudal branch (C.Br), was examined after application of horseradish peroxidase conjugated with wheat germ agglutinin (HRP-WGA) to the proximal cut end of each branch. In addition, the afferent and efferent neural activities of each branch were recorded to investigate the functional properties. The present study provided several new findings as to the distribution of each branch and the functional properties of the SLN. The following conclusions were drawn: 1) the R.Br, containing only afferent fibers projecting to the ipsilateral lateral region of the nucleus of the solitary tract (NST), extends between slightly below the obex and the region approximately 0.6 mm rostral from the obex, and it corresponds to the interstitial subnucleus of the NST; 2) the M.Br, innervating the cricothyroid muscle, contains only efferent fibers originating ipsilaterally from the motoneurons localized within the ambiguus nucleus (Amb) and in the area ventrolateral to the Amb; and 3) the C.Br, which innervates the inferior pharyngeal constrictor muscle, contains both efferent and afferent fibers. HRP-WGA-labeled cells are distributed within both the Amb and the dorsal motor nucleus of the vagus nerve, ipsilateral to the injection site. Afferent proprioceptive fibers project to the ipsilateral interstitial subnucleus of the NST. The present results provide evidence that each branch of the SLN has distinctive functional properties and contributes to the laryngeal functions.

Afferent Pathways

Activation of oxytocin neurones by systemic cholecystokinin is unchanged by morphine dependence or withdrawal excitation in the rat.

1. Morphine inhibits supraoptic nucleus oxytocin neurones directly and presynaptically via inhibition of afferent noradrenergic endings. 2. We studied whether morphine tolerance/dependence (induced by intracerebroventricular (I.C.V.) morphine infusion) alters the responsiveness of oxytocin neurones to systemic cholecystokinin (CCK), a stimulus which activates oxytocin neurones via the release of noradrenaline. 3. CCK (20 micrograms kg-1, i.v.) increased plasma oxytocin concentrations similarly in urethane-anaesthetized morphine-naive and -dependent rats. In naive rats, I.C.V. (10 micrograms) and i.v. morphine (0.5 mg kg-1) reduced CCK-induced oxytocin secretion by 95 +/- 4 and 49 +/- 10%, respectively. In dependent rats, i.v. morphine reduced CCK-induced release by only 8 +/- 9%, indicating tolerance. 4. In urethane-anaesthetized rats, i.v. CCK increased the firing rates of oxytocin neurones similarly in morphine-naive and -dependent rats (by 1.2 +/- 0.2 and 1.4 +/- 0.3 spikes s-1 maximum, respectively, over 5 min). Naloxone did not alter spontaneous or CCK-induced activity in naive rats but increased activity in dependent rats (by 3.4 +/- 0.5 spikes s-1), indicative of withdrawal excitation; however, the response to CCK remained unchanged after naloxone. 5. Systemic CCK did not trigger withdrawal, nor did it have a greater excitatory effect in dependent rats. Thus, morphine withdrawal excitation of oxytocin neurones does not involve supersensitivity to the noradrenergic input, or hypersensitivity of this input to i.v. CCK. Tolerance apparently occurs both at the cell bodies of oxytocin neurones in the supraoptic nucleus and in their noradrenergic input. However, dependence is apparent only at the cell bodies.

Afferent Pathways