Oscillatory behaviour and randomness of firing of chemoreceptor fibres in the cat.
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An isolated preparation of the lips, cerebral ganglia and buccal ganglia of the terrestrial slug, Limax maximus, can display one-trial associative learning. The lip-brain preparation can learn to suppress feeding motor program responses to lip stimulation with a standard food extract after a single pairing of food extract and quinidine stimulation to the isolated lips. Learning can occur with training stimuli applied to one lip and testing stimuli applied to the opposite, "naive' lip. Learning can also occur if the food extract and quinidine are applied during training to opposite lips. These results indicate that the synaptic alteration due to learning occurs in the CNS, not at the sensory periphery.
In this study we investigated the effects of intracellular pH (pHi) and extracellular pH (pHe) on whole-cell currents in cultured glomus cells of the rat carotid body and small, intensely fluorescent (SIF) cells of sympathetic ganglia. The use of the perforated-patch recording technique along with established methods of cytoplasmic acidification allowed us to carry out this study without greatly disturbing the cell's endogenous pH regulatory mechanisms. A reversible decrease in the outward K+ current (20-30%) was observed during acid loading of glomus (and SIF cells) using the K+/H+ ionophore nigericin (3 microM) and acetate (20 mM). A reversible decrease in the inward Na+ current was also observed in both cell types during nigericin application. Application of amiloride (0.1 mM) to the bathing solution inhibited recovery of the K+ current from an acid load implicating the Na+/H+ antiporter as a mechanism involved in pH homeostasis in glomus cells. A reversible decrease in K+ and Na+ currents was also observed during changes in pHe from 7.4 to 6.5. The effects of pHi on membrane currents, Ca2+ levels, and neurotransmitter release are discussed in the context of the role of glomus cells as primary transducers of chemosensory stimuli in arterial blood.
The effects of dopamine (DA) were studied on type I cells of the rat carotid body. DA (0.35 to 8.4 x 10(-4) M) elicited a long-lasting depolarization and decreased input resistance (Ro) in 75% of the cells, in a dose-dependent manner. Hyperpolarization and increased Ro were observed in 8% of cells. Membrane potential (Em) and Ro changes were highly correlated (-0.62, P < 0.001). The reversal potential (Erev) of the DA effect was +2.16 +/- 4.75 (mV +/- S.E.M.).
The presence and coexistence of tyrosine hydroxylase (TH), vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), substance P (SP) and galanin (GAL) were studied in the petrosal and jugular neurons innervating the carotid body and carotid sinus of the rat. The retrograde labeling of the carotid sinus nerve with Fluoro-gold (FG) demonstrated that most (94.5%) FG-labeled ganglionic neurons were observed in the petrosal ganglion. Fewer (5.2%) FG-labeled neurons were seen in the jugular ganglion and very few (0.3%) were observed in the nodose ganglion. Immunohistochemistry revealed that subpopulations of TH-, VIP-, CGRP-, SP- and GAL-immunoreactive (-ir) neurons in the petrosal ganglion projected to the carotid sinus nerve. Approximately 4% of FG-labeled neurons contained TH-ir and were predominantly found in the caudal portion of the petrosal ganglion. Nearly 90% of total TH-ir neurons in the petrosal ganglion were labeled with FG. Less than 1% of FG-labeled neurons were immunoreactive for VIP in this ganglion. In the petrosal ganglion, 25% of FG-labeled neurons contained CGRP-ir, and 16.7% of FG-labeled neurons contained SP-ir. 30% of CGRP-ir or SP-ir neurons in the petrosal ganglion were labeled with FG. In the jugular ganglion, no TH- or VIP-ir neurons projected to the carotid sinus nerve and only small populations of CGRP- or SP-ir neurons projected to the carotid sinus nerve. Many FG-labeled and GAL-ir neurons were observed in the petrosal and jugular ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)
High carbon monoxide (CO) gas tensions (> 500 Torr) at normoxic PO2 (125-140 Torr) stimulates carotid chemosensory discharge in the perfused carotid body (CB) in the absence but not in the presence of light. According to a metabolic hypothesis of O2 chemoreception, the increased chemosensory discharge should correspond to a photoreversible decrease of O2 consumption, unlike a non-respiratory hypothesis. We tested the respiratory vs. non-respiratory hypotheses of O2 chemoreception in the cat CB by measuring the effect of high CO. Experiments were conducted using CBs perfused and superfused in vitro with high CO in normoxic, normocapnic cell-free CO2-HCO3- buffer solution at 37 degrees C. Simultaneous measurements of the rate of O2 disappearance with recessed PO2 microelectrodes and chemosensory discharge were made after flow interruption with and without CO in the perfusate. The control O2 disappearance rate without CO was -3.66 +/- 0.43 (S.E.) Torr/s (100 measurements in 12 cat CBs). In the dark, high CO reduced the O2 disappearance rate to -2.35 +/- 0.33 Torr/s, or 64.2 +/- 9.0% of control (P < 0.005, 34 measurements). High CO was excitatory in the dark, with an increase in baseline neural discharge from 129.2 +/- 47.0 to 399.3 +/- 49.1 impulses per s (P < 0.0001), and maximum discharge rate of 659 +/- 76 impulses/s (N.S. compared to control) during flow interruption. During perfusion with high CO in the light, there were no significant differences in baseline neural discharge or in the maximum neural discharge after flow interruption, and little effect on O2 metabolism (88.8 +/- 11.5% of control, N.S., 29 measurements).(ABSTRACT TRUNCATED AT 250 WORDS)
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In this study we investigated the site and nature of the signal responsible for the generation of the gastrocolonic response at the rectosigmoid region. Sixteen healthy subjects participated in this study. Motor activities were recorded with pressure transducers placed in the rectosigmoid colon. Balloon distention of the stomach with 100, 200, or 300 ml of water caused a volume-dependent increase in rectosigmoid motility that was abolished by atropine. To investigate the intestinal phase of the gastrocolonic response, we infused into the duodenum isocaloric (178 kcal) solutions of normal saline, lipid, glucose, or essential amino acids at 1.5 ml/min for 30 min in random order on separate days. Only lipid infusion caused an increase in rectosigmoid pressure and this was accompanied by an elevation of plasma cholecystokinin from 1.2 +/- 0.1 to 4.3 +/- 1.0 fmol/ml. The increase in motility associated with lipid infusion was antagonized (58% +/- 7%) by atropine. To further investigate the possible role of cholecystokinin as a mediator of the gastrocolonic response, we infused cholecystokinin-octapeptide intravenously at doses of 5, 10, and 20 ng/kg.h. A significant increase in rectosigmoid motility was observed only at 20 ng/kg.h and this was accompanied by an increase in plasma cholecystokinin levels to 12 +/- 2 fmol/ml, a value threefold greater than that produced by lipid infusion. These studies demonstrate that gastric distention and intestinal lipid are potent stimuli for the generation of the gastrocolonic response involving the rectosigmoid region. The gastric phase can be generated by mechanoreceptors utilizing the cholinergic pathways, whereas the intestinal phase is nutrient-specific, partially atropine-sensitive, and independent of cholecystokinin.
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