Medullary pathways for adrenocorticotropic hormone and vasopressin secretion in rabbits
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We determined, in urethan-anesthetized rabbits, whether pharmacological alteration of neuronal function in the ventrolateral medulla oblongata, including the A1 area, and in the nucleus tractus solitarii (NTS), alters plasma adrenocorticotropic hormone (ACTH) and vasopressin and whether inhibition of neuronal function in the ventrolateral medulla impairs the secretion of ACTH normally observed in response to hemorrhage or constriction of the inferior vena cava. We also tested whether the increase in plasma ACTH and vasopressin after pharmacological inhibition of neuronal function in the NTS is dependent on a pathway that synapses in the A1 area of the ventrolateral medulla. Activation of the A1 area with bicuculline increased both ACTH and vasopressin. Inhibition of the NTS with muscimol increased levels of both hormones, as did hemorrhage and constriction of the inferior vena cava. Inhibition of neuronal function within the A1 area with muscimol eliminated the secretion of vasopressin but did not significantly alter the secretion of ACTH, obtained by injecting muscimol into the NTS. Injection of muscimol into the A1 area eliminated the secretion of both ACTH and vasopressin in response to constriction of the inferior vena cava and, in the case of vasopressin, in response to hemorrhage. Although hemorrhage-initiated secretion of ACTH was significantly reduced by injection of muscimol into the A1 area, it was not completely eliminated by these injections or by injections of muscimol into a more rostrocaudally extensive region of the medulla oblongata. We conclude that the net output from the NTS tonically inhibits secretion of both ACTH and vasopressin, reflecting tonic baroreceptor tone. For vasopressin, the pathway from the NTS to the hypothalamus is dependent on a synapse in the A1 area. For ACTH, there are pathways to the hypothalamus that do not synapse in the A1 area, but neurons in this region do have an excitatory effect on secretion of ACTH.Keywords:
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GABA receptor
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The central mechanism controlling food intake in response to the change in environmental temperature has been little examined. The GABA agonist, muscimol, was injected into the lateral ventricle of rats which were acclimated to temperate (26 degrees C) and hot (33 degrees C) environments. Muscimol obviously stimulated the feeding behavior of rats in both environments. However, when muscimol was administered at doses of 100 and 250 ng, the food intake at 26 degrees C was greater than that at 33 degrees C. In addition, the stimulating effect of muscimol (250 ng) on food intake at 26 degrees C lasted longer than that at 33 degrees C. These findings suggested that there might be a difference in muscimol metabolism at the two temperatures.
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There were extensive efferent and afferent projections in the ventrolateral medulla.The ventrolateral medulla play a key role in the modulation of blood pressure,respiration,pain and so on.The study summarized the results got in the research of the functions and neural pathway of the ventrolateral medulla in last years.
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Rostral ventrolateral medulla
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By the use of combined radioreceptor binding and autoradiographic techniques, the pharmacological characteristics of (3H)-muscimol binding and the localization of the label were studied. (3H)-Muscimol was bound by sections of rat kidney in a manner consistent with the existence of specific γ-aminobutyric acid 'A' (GABAA) receptors with Kd and Bmax values of 23.7 nmol/l and 1.15 pmol/mg tissue, respectively. (3H)-Muscimol was bound by convoluted tubules of the renal cortex and by the collecting tubules. Our findings demonstrating the existence of recognition sites for the GABAA receptor agonist muscimol in the kidney suggest that GABA has a role in renal function.
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Muscimol infusions into the entorhinal cortex (ERC) have previously been reported to impair the retention of passive avoidance learning, but only when infusions were delayed until 90 min after training. In the present study, three experiments were carried out to examine further the effects of muscimol infusions into the ERC prior to training. In Experiment 1, muscimol infusions prior to training had no effect on retention, confirming earlier findings, but blocked the amnestic effect of a second muscimol infusion 90 min post-training. In Experiment 2, muscimol infusions prior to training blocked the improvement of retention normally seen following a second training trial 2 h after the first. In Experiment 3, the technique of summation of performance across training trials was used to confirm that the direct effects of muscimol infusions lasted less than 2 h. The results indicate that the GABA-ergic mechanism in the ERC is normally involved in the formation of memory for passive avoidance, but if the ERC is inactivated at the time of training, memory formation is diverted to other structures, which appear less capable of integrating consecutive memories across time.
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Gamma-aminobutyric acid (GABA) is a candidate as a neurotransmitter in the vertebrate retina. The GABA analogue muscimol has been used to probe the properties of GABA receptors in other parts of the vertebrate central nervous system (CNS). We thus used 3H-muscimol to investigate potential GABA receptors in the retinas of goldfish and chick by means of biochemical assay techniques and light microscopic autoradiography. In both animals 3H-muscimol shows specific and saturable binding with a dissociation constant (KD) of about 10 nM. GABA effectively inhibits 3H-muscimol binding at 50% inhibitory concentration (IC50) of 10(-6) M. The labeling pattern of 7 x 10(-7) M 3H-muscimol shows common features for both species in that amacrine cell bodies are intensely labeled, horizontal cells are much less so, and there is a laminar pattern throughout the inner plexiform layer (IPL). A 1 mM concentration of GABA abolishes 3H-muscimol labeling in the chick retina and throughout much of the goldfish retina except for some label over amacrine cells and the distal two thirds of the IPL. The intense somatic labeling suggests neuronal uptake of 3H-muscimol, and indeed, virtually all 3H-muscimol labeling is abolished with the addition of 0.4 mM ouabain. The uptake pattern of 3H-GABA differs from that of 3H-muscimol and is largely unaffected by the addition of 1 mM muscimol. We conclude that 3H-muscimol binding in retinas can be adequately demonstrated biochemically but that only 3H-muscimol uptake is observed with autoradiography from tissue conventionally processed through Epon. The fact that GABA can inhibit 3H-muscimol uptake whereas the reverse is not the case shows that the transport carriers for muscimol and GABA are different. Finally, the strong degree of 3H-muscimol uptake by retinal neurons raises serious questions about the use of 3H-muscimol as a probe for GABA synaptic receptors in the retina with autoradiography.
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