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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 12 (1971), S. 132-149 
    ISSN: 1432-1106
    Keywords: Cerebral cortex ; Spreading Depression ; Glutamic acid ; Excitation ; Depression ; Cat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Variations in the excitability of individual cortical neurones during the invasion of spreading depression (SD) have been monitored by observing the alterations of spontaneous and L-glutamate-induced firing. Invasion of many neurones during SD is marked by a brief burst of firing which occurs concurrently with the onset of the negative slow extracellular potential. Other neurones do not fire, although the microelectrode records a negative slow wave. Depression of glutamate-induced and spontaneous firing follows and may last for several minutes. The initial loss of excitability of those neurones that discharge during SD invasion may be due to excessive depolarization. This phase is rapidly succeeded by a period of depressed excitability, during which the neurones can be invaded by an antidromic spike or excited by increased amounts of L-glutamate. These findings indicate that SD propagation initially involves the release of an excitant substance, possibly glutamic acid. The continuing effects of SD are due to the reduction in cell excitability. As many neurones are depressed without undergoing an initial excitation, it appears that a depressant substance is also involved. This may be gamma-aminobutyric acid.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Morphine ; Habituation ; Precipitated Abstinence Syndrome ; ACh Release ; Push-Pull Cannulae ; Cerebral Cortex ; Lateral Ventricle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The rate of release of central acetylcholine (ACh) was determined in unanaesthetized cats by perfusing the sensorimotor cortex or the lateral ventricles with a neostigmine-containing solution by means of push-pull cannulae. Cats were made physically dependent on morphine over a 10-day schedule of daily increasing doses of the narcotic. No difference in both cortical and ventricular ACh release was noted between these morphine-dependent animals (determined following the last dose of morphine-20 mg/kg i.p.) and the same animals prior to the injection of any morphine. When the abstinence syndrome was precipitated in these habituated animals (0.2 mg/kg of naloxone, i.p.), both cortical and ventricular ACh release was enhanced, coincident with behavioural agitation of the animal. While the behavioural symptoms of the abstinence syndrome persisted, this increased release of ACh was only of short duration. In non-dependent cats, a 1-h localized perfusion of the sensorimotor cortex with a morphine-containing solution (10−4 or 5×10−4 g/ml) had no effect on either cortical ACh release or the behaviour of the animal. These results raise questions concerning the hypothesis that a cholinergic mechanism governs the occurrence of the morphine abstinence syndrome in cats.
    Type of Medium: Electronic Resource
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