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Results for “Afferent Pathways”

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At least 145 records · Page 8Linked to original sources
PubMed1982

Adjacent laminar terminations of two centrifugal afferent pathways to the accessory olfactory bulb in the mouse.

Anterograde and retrograde axonal tracing methods have been combined with transection of the stria terminalis to investigate the centrifugal afferent connections of the accessory olfactory bulb in the mouse. Injection of tritiated proline into the postero-medial cortical amygdaloid nucleus (C3) gives rise to anterograde autoradiographic labelling of a pathway terminating in the internal granular layer of the accessory olfactory bulb (AOB). Transection of the ipsilateral stria terminalis completely abolishes labelling of this pathway. Injections further rostral, in the bed nucleus of the accessory olfactory tract (bnAOT) and medial amygdaloid nucleus (M), give rise to labelling of a second ipsilateral afferent pathway to the AOB which terminates in the internal plexiform layer (IPL) and is unaffected by strial transection. Injections of wheat germ lectin-HRP conjugate into the AOB confirm that it receives afferents from the ipsilateral bnAOT, M and C3, and from a few cells in the contralateral C3. Transection of the ipsilateral stria terminalis prevents retrograde labelling of any cells in the ipsilateral C3, but does not affect labelling of cells in M or bnAOT (or contralateral C3). The conjugate is also transported anterogradely in this system, labelling the efferent projections of the AOB to bnAOT, M and C3. It is concluded that the AOB receives at least two sets of ipsilateral afferents: one set from C3, via the stria terminalis, terminating in the internal granular layer, and a second set from M and/or bnAOT terminating in the IPL and probably running in the accessory olfactory tract.

Amygdala↗
PubMed1992

Evidence for two different afferent pathways carrying stress-related information (noxious and amygdala stimulation) to the bed nucleus of the stria terminalis.

The bed nucleus of the stria terminalis (BNST) is an important nucleus involved in mediating amygdala-regulated endocrine effects. Since the amygdala is important in mediating the endocrine response to noxious somatosensory stimuli and olfactory stimulation, this experiment studies whether noxious input (tail pinch, TP) and stress-related input (amygdala stimulation, AmygS) will modulate BNST neuronal activity. One hundred and fifty-eight BNST neurons were studied following AmygS, TP and cutaneous stroke. AmygS was effective in 66% of BNST neurons and produced one of the following five responses: oligosynaptic excitation (43%), polysynaptic excitation (5%), time-locked inhibition (4%), generalized increase in firing rate (8%), or generalized decrease in firing rate (6%). TP produced an increase in firing rate in 27% of BNST neurons tested. Analysis of a contingency table constructed to determine the degree of correspondence between neurons responsive to AmygS and neurons responsive to TP showed that the distributions of reactivity to these stimuli in BNST neurons are independent of each other. This suggests that although AmygS and TP are both capable of altering the firing rate of BNST neurons, the pathways by which they reach BNST differ.

Afferent Pathways↗
PubMed1993

Duodenal lipid inhibits gastric acid secretion by vagal, capsaicin-sensitive afferent pathways in rats.

Neural and endocrine pathways mediate the inhibitory effects of intestinal fat on gastric acid secretion. To study whether vagal and/or spinal afferent nerves contribute to the neural component of the enterogastric reflex, the sensory neurotoxin capsaicin was applied topically either to the vagus nerves bilaterally or to the celiac-superior mesenteric ganglia in rats with chronic gastric and duodenal fistulas. In lightly restrained, awake rats acid secretion was stimulated for 2 h by continuous intragastric perfusion with 8% peptone and was measured by extragastric titration to pH 5.5. Duodenal lipid perfusion (0-20%) during the 2nd h caused inhibition of peptone-stimulated acid output. Acid output was inhibited by 81% during 5% lipid perfusion of the duodenum and was restored after capsaicin treatment of the vagus nerves. In contrast, capsaicin treatment of the celiac ganglion did not alter the acid inhibitory response to any dose of intestinal lipid. Basal and maximum acid outputs were not significantly different among rats treated by either method with capsaicin. The neural component of the enterogastric reflex in awake rats is mediated in part by a capsaicin-sensitive, vagal-afferent neural reflex.

Afferent Pathways↗
PubMed1998

Afferent pathways of pyrogen signaling.

We and others recently showed that fever induced by intravenously or intraperitoneally injected lipopolysaccharide (LPS) may involve brain signaling via hepatic vagal afferents. This suggests that LPS fever may be initiated by mediators released mainly by cells in the liver, presumably macrophages (Kupffer cells, Kc). To verify this possibility, we disabled the Kc of conscious guinea pigs with gadolinium chloride and monitored their core temperature and associated preoptic prostaglandin E2 (PGE2) responses to i.v. LPS. Gadolinium chloride pretreatment significantly attenuated both the febrile and PGE2 rises, thus supporting the hypothesis. Additionally, fluorescein-labeled LPS was detected in Kc 15 minutes after its i.v. administration. Paradoxically, however, the label was also present in gadolinium chloride-pretreated guinea pigs. Thus, either Kc are not the primary source of pyrogenic mediators or LPS does not provide the stimulus for their production. Because the i.v. injection of LPS elicits virtually immediately the production of complement fragments, and Kc express their receptors and produce various mediators on their activation, we hypocomplemented guinea pigs with cobra venom factor. The core temperature rises produced by i.v. LPS were reduced by complement depletions > 60%. LPS i.v. per se decreased complement, that is, complement was consumed by 12% within 10 minutes. Thus, the onset of LPS fever may involve complement system and Kc activation, but their precise roles await clarification.

Afferent Pathways↗
PubMed1987

Tracing of afferent pathways from the femoral-saphenous vein to the dorsal root ganglia using transport of horseradish peroxidase.

The retrograde transport of horseradish peroxidase (HRP) was used to trace afferents from the femoral-saphenous vein to the dorsal root ganglia in the cat. Afferents arising along the entire length of the vein projected to very localized spinal levels; 63% of the labeled cells counted were located in the L6 dorsal root ganglion, 37% were located in the L5 ganglion and less than 1% were located at other levels. Most of the cell bodies labeled by the application of HRP to the femoral-saphenous vein were small in size (diameter less than 35 microns). However, some large cell bodies (diameter greater than 50 microns) were also noted. It was estimated that over two-thirds of the femoral-saphenous venous afferents were C fibers; at least 15% were estimated to be A fibers. The largest venous afferents were predicted to conduct action potentials at approximately 60 m/s.

Afferent Pathways↗
PubMed1983

Vasoactive intestinal polypeptide in visceral afferent pathways to the sacral spinal cord of the cat.

Immunohistochemical studies revealed that vasoactive intestinal polypeptide (VIP) is localized primarily to sacral segments of the cat's spinal cord. VIP is most prominent in afferent axons and terminals in Lissauer's tract and in lateral laminae I and V of the dorsal horn. The distribution of VIP terminals is very similar to that of visceral afferent projections identified by horseradish peroxidase. Dye-tracing experiments combined with immunohistochemistry demonstrated that VIP is located in visceral afferent perikarya in the sacral dorsal root ganglia and also in terminals in the sacral autonomic nucleus. These observations suggest that VIP is a neurotransmitter in afferent projections from the pelvic viscera.

Afferent Pathways↗