Canadian journal of physiology and pharmacology
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Can. J. Physiol. Pharmacol. · Sep 1979
The development of central nervous system control of the gill withdrawal reflex evoked by siphon stimulation in Aplysia.
In older Aplysia, the central nervous system (CNS) (abdominal ganglion) exerts suppressive and facilitatory control over the peripheral nervous system (PNS) which initially mediates the gill withdrawal reflex and its subsequent habituation evoked by tactile stimulation of the siphon. In young animals, both the suppressive and facilitatory CNS control were found to be absent. In older animals, removal of branchial nerve (Br) input to the gill resulted in a significantly reduced reflex latency and, with ctenidial (Ct) and siphon (Sn) nerves intact, a significantly increased reflex amplitude and an inability of the reflex to habituate with repeated siphon stimulation. ⋯ The lack of CNS control in young animals was found to be due to incompletely developed neural processes within the abdominal ganglion and not the PNS. The lack of CNS control in young Aplysia results in gill reflex behaviours being less adaptive in light of changing stimulus conditions, but may be of positive survival value in that the young will not habituate as easily. The fact that CNS control is present in older animals strengthens the idea that in any analysis of the underlying neural mechanisms of habituation the entire integrated CNS-PNS must be taken into account.
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Can. J. Physiol. Pharmacol. · Dec 1978
Picrotoxin prevents habituation of the gill withdrawal reflex in Aplysia.
The gill withdrawal reflex evoked by tactile stimulation of the siphon in Aplysia habituates with repeated presentation of the stimulus. This adaptive behaviour is mediated by the integrated activity of the central (CNS) and peripheral (PNS) nervous systems. The PNS mediates the basic reflex and its habituation while the CNS exerts both suppressive and facilitatory control over the PNS. ⋯ Thus the reflex amplitude was increased, the reflex latency decreased, and repeated stimulation did not result in habituation. This effect of picrotoxin was completely reversible. It is thus proposed that gamma-aminobutyric acid, a putative neurotransmitter, plays an important role in the mediation of the CNS's suppressive influence.
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Can. J. Physiol. Pharmacol. · Dec 1977
CNS control of the PNS-mediated gill withdrawal reflex and its habituation.
Removal of the branchial (Br) nerve input to the gill significantly reduced the latency and increased the amplitude of the gill withdrawal reflex evoked by siphon stimulation. Further, after Br removal repeated siphon stimulation which previously resulted in habituation now resulted in facilitation of the flex. However, the synaptic input to gill motor neurons in the abdominal ganglion continued to decrement as before. ⋯ Thus, changes in synaptic efficacy to gill motor neurons in the abdominal ganglion are not the ultimate cause of gill reflex habituation. Habituation is the result of adaptive neural processes which occur together in the abdominal ganglion, the PNS, and the peripheral terminations of the central motor pathways to the gill. Therefore, in any analysis of the underlying neural mechanisms of habituation all these loci must be included and taken into account.
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Can. J. Physiol. Pharmacol. · Feb 1977
Effect of subacute dosing and phenobarbital and 3-methylcholanthrene pretreatment on the metabolism of acetaminophen in rats.
The metabolism of 14C-ring-labelled acetaminophen was studied in male Wistar rats. Pretreatment with phenobarbital increased the initial rate of elimination of 14C from the blood and increased the amount of acetaminophen glucuronide excreted in the urine. ⋯ Subacute dosing with acetaminophen had a diuretic effect but this did not correlate with the increased excretion of the drug. It is concluded that acetaminophen elimination is increased by phenobarbital pretreatment and by subacute dosing with acetaminophen, but by different mechanisms.
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Can. J. Physiol. Pharmacol. · Oct 1976
Differences in the altered energy metabolism of hemorrhagic shock and hypoxemia.
The effect of hemorrhagic shock, hypoxemia, and anoxia on the levels of adenine and pyridine nucleotides of liver and kidney was assessed. ATP levels in liver and kidney of animals in shock or animals subjected to 7 min of anoxia decreased by 85 and 73%, respectively. ⋯ Thus, shock produced greater alterations in adenine and pyridine nucleotides than did hypoxemia alone, indicating that stagnant hypoxemia due to shock is more deleterious to energy metabolism than is severe hypoxemia with an otherwise normal circulation. The results also suggest that if an anterial PO2 OF 18 MMHg represents the initial stages of tissue hypoxia, then tissue ATP levels are a more sensitive indicator of this than NAD levels.