Reassessment of central neural pathways necessary for adrenaal catecholamine output in response to hypoglycemia.
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In addition to its sympathetic innervation, a mammalian pineal gland also receives a distinct central pinealopetal innervation. Earlier studies in rat have established that the photic signals originating in the retina pass via the retinohypothalamic tract to the suprachiasmatic nucleus, to the tuberal hypothalamus, over medial forebrain bundle, reticular formation, and upper thoracic interomediolateral cell column to the superior cervical ganglion, whose postganglionic sympathetic fibers, traveling along the tentorium cerebelli, enter the pineal gland via the conarian nerve. Recent electron microscopic analyses of the pineal gland of several mammalian species have revealed intrapineal nerve terminals different from the sympathetic ones. In addition, lesion experiments performed in the habenular nuclei or the posterior commissure support the central origin of these terminals. The intact sympathetic innervation, the functional beta-adrenergic receptors, and the appropriate level of norepinephrine are all essential prerequisites for the circadian pattern of melatonin synthesis. However, other receptors such as alpha-adrenergic, D2-dopaminergic, GABAergic, benzodiazepinergic, and glutamatergic receptors and their agonists are also able to modulate the synthesis of melatonin, and this function depicts dramatic species variation. The impact of pinealopetal projections and intrapineal neurons on the physiological and biochemical aspects of pineal functions awaits clarification.
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Intracardiac nerves of the frog isolated heart were cut and the central or the peripheral end was stimulated. The atrioventricular (a-v) conduction was measured. The data showed that the intracardiac parasympathetic nervous system could induce both acceleration and deceleration of the a-v conduction, depending on the parameters of stimulation. Atropine blocked both the positive and the negative dromotropic effects whereas beta-adrenoblocking agent inderal was ineffective. The possible mechanism of the dromotropic effects observed are discussed.
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Peptide YY (PYY) is a powerful inhibitor of intestinal secretion mediated by cAMP agonists such as vasoactive intestinal peptide and prostaglandin E2. We hypothesized that PYY would attenuate the secretory diarrhea in piglet cryptosporidiosis, which is mediated by prostaglandins E2 and I2. Control and infected ileal tissues from piglets were studied in Ussing chambers. The addition of PYY to the serosal bathing solution abolished net Cl- secretion in infected tissue. The inhibitory effect of PYY was eliminated with the prostaglandin synthesis inhibitor indomethacin and with the nerve conduction blocker tetrodotoxin. PYY completely blocked the antiabsorptive and secretory effects of the prostaglandin I2 analog carbacyclin, which has previously been shown to operate through enteric nerve pathways in this tissue. In contrast, PYY had no inhibitory effect on the secretory responses induced by prostaglandin E2 or vasoactive intestinal peptide. Results suggest that the antisecretory effects of PYY are mediated by inhibition of prostaglandin I2 induction of enteric nerves. Thus, PYY may play an important role in moderating the secretory diarrhea in cryptosporidiosis.
We have studied the role of afferent renal nerve fibres in anaesthetized cats in mediating the decrease in sodium and water excretion from the contralateral kidney caused by unilateral renal denervation. Transient denervation of one kidney obtained by cooling of the left renal nerves increases contralateral efferent renal nerve activity and decreased sodium and water excretion from the opposite kidney. The results observed in animals with intact neural pathways were compared with those obtained after the left kidney had been selectively deafferentated by cutting the dorsal roots from T9 to L4. Bilateral section of dorsal roots did not affect the increase in sodium and water excretion from the transiently denervated left kidney, but entirely abolished the decrease in sodium and water excretion from the contralateral kidney. Neither the left nor the right dorsal root section alone, affected the response of the contralateral right kidney. Our data demonstrate that afferent renal nerve fibres project bilaterally to the spinal cord and form the afferent branch of the reno-renal reflex by which one kidney can control the function of the opposite one.
In this paper, we consider a neural field model comprised of two distinct populations of neurons, excitatory and inhibitory, for which both the velocities of action potential propagation and the time courses of synaptic processing are different. Using recently-developed techniques, we construct the Evans function characterising the stability of both stationary and travelling wave solutions, under the assumption that the firing rate function is the Heaviside step. We find that these differences in timing for the two populations can cause instabilities of these solutions, leading to, for example, stationary breathers. We also analyse "anti-pulses", a novel type of pattern for which all but a small interval of the domain (in moving coordinates) is active. These results extend previous work on neural fields with space-dependent delays, and demonstrate the importance of considering the effects of the different time-courses of excitatory and inhibitory neural activity.
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At early neural tube stages, individual stem cells can generate neural crest cells as well as dorsal or ventral spinal cord cells. To determine whether this pluripotency is lost as development proceeds, we back-transplanted quail spinal cells from different developmental stages and different spinal locations into the crest migratory pathways of st 16-20 chicken host embryos. The transplanted spinal cells from st 27 dorsal cord and st 18 ventral cord differentiated within the new crest environment into sensory and sympathetic neurons, satellite and Schwann cells, and melanocytes. St 27 ventral cells still generated several crest derivatives but not sensory or sympathetic neurons. This loss in ability to produce neurons correlates with the end of neurogenesis in ventral cord. The end of neurogenesis in the cord, therefore, results from an intrinsic change in the potential of spinal neuroepithelial cells to generate neurons.