Neuroscience
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Changes in chemical sensitivity of peripheral nociceptors following injury or inflammation have been studied in in vitro preparation of the saphenous nerve-hind paw skin from adult rats. Heat hyperalgesia in the hind paw was induced by a prior ultraviolet irradiation and the skin from these animals was investigated five days later. Polymodal nociceptors were quiescent in normal skin but were spontaneously active in the majority of fibres after ultraviolet exposure. ⋯ These data show that polymodal nociceptors change their activity and sensitivity to exogenous chemicals following the induction of peripheral hyperalgesia by ultraviolet irradiation. Specifically, evidence is provided for the expression of opioid sensitivity and inhibition of polymodal nociceptor activity through mu- and kappa-opioid receptors. These observations may account for peripheral antinociceptive actions of opioids during specific states of peripheral hyperalgesia.
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The anterograde and retrograde transport of wheat germ agglutinin-horseradish peroxidase was used to study the trigeminoperibrachial pathway in the muskrat after injections of tracer into either the medullary dorsal horn or the dorsolateral pons. After injections into the medullary dorsal horn, labeled fibers ascended into the ipsilateral dorsolateral pons via the spinal trigeminal tract, within the neuropil of the trigeminal sensory complex and within the reticular formation adjacent to the spinal trigeminal nucleus. At caudal levels of the ipsilateral peribrachial area, dense terminal-like label distributed in the Kölliker-Fuse nucleus continued into the lateral parabrachial nucleus. ⋯ In the medullary dorsal horn, they were found almost exclusively in laminae I and V. Labeled neurons in lamina I were especially prominent in rostral ventral levels of the medullary dorsal horn. Labeled cells in lamina I were continuous with others found in the displaced band of substantia gelatinosa at the interface of the subnucleus caudalis and subnucleus interpolaris, as well as with those found in the ventral and dorsal paratrigeminal nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)
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Neurogenesis, migration and maturation of ganglion cells in the posterior pole of chick retina have been studied using embryonic incorporation of [3H]thymidine, immunocytochemistry and retrograde labeling. Unlike previous studies, we have examined the neurogenesis of independently identified ganglion cells that have survived the period of naturally occurring cell death (embryonic days 11-16). Embryos were labeled with [3H]thymidine at different embryonic ages (embryonic days 3, 5 and 7). ⋯ Using immunocytochemistry with an antibody against neuron-specific beta-tubulin and retrograde labeling with the carbocyanine dye DiI we show that ganglion cells begin to differentiate before the completion of their migration to the presumptive ganglion cell layer. These results suggest the following developmental sequence. (1) Ganglion cells of the posterior pole undergo their final mitosis near the ventricular margin between embryonic days 2 and 8. (2) They maintain contacts with both retinal surfaces and their nuclei move toward the ganglion cell layer. At this time they start to differentiate, expressing a form of neuron-specific tubulin and growing axons that can reach the optic chiasm. (3) Once migration is completed dendritic development commences.
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Benzodiazepine receptors are expressed very early in the brain during embryonic life, suggesting that endogenous ligands for these receptors may play an important role during ontogenesis in the central nervous system. In the present study, the distribution and characterization of diazepam-binding inhibitor-related peptides (endozepines) in the rat brain was investigated during embryonic and postnatal development using an antibody raised against the biologically active region of the precursor molecule. Immunohistochemical labelling showed that, in newborn rats, endozepine-like immunoreactivity was present in ependymal cells of the hypothalamus. ⋯ In the telencephalon two major species were resolved, with apparent molecular weights of 10,000 and 8800, and a minor one of 6500 mol. wt. In conclusion, the present study shows that endozepines are expressed in the rat brain as early as embryonic day 18 and the amount of endozepine-like material increases rapidly during the two days preceding birth. The results also indicate that diazepam-binding inhibitor is processed to different molecular forms depending on the brain region.(ABSTRACT TRUNCATED AT 400 WORDS)
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Intracellular recordings were performed on hippocampal CA3 neurons in vitro to investigate the inhibitory tonus generated by endogenously produced adenosine in this brain region. Bath application of the highly selective adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine at concentrations up to 100 nM induced both spontaneous and stimulus-evoked epileptiform burst discharges. Once induced, the 1,3-dipropyl-8-cyclopentylxanthine-evoked epileptiform activity was apparently irreversible even after prolonged superfusion with drug-free solution. ⋯ Furthermore, even high concentrations of the selective phosphodiesterase inhibitor rolipram (10 microM), which displays no affinity to adenosine receptors, did not mimic the electrophysiological actions of 1,3-dipropyl-8-cyclopentylxanthine, thus excluding the possibility that the effects of the A1 receptor antagonist on neuronal discharge behavior can be ascribed to an inhibition of phosphodiesterases. The present data demonstrate that endogenously released adenosine exerts a vigorous control on the excitability of hippocampal CA3 neurons on both the pre- and postsynaptic sites. The long-lasting disinhibition following a transient suppression of adenosinergic inhibition strongly suggests that, besides its well-known short-term effects on neuronal activity, adenosine might also contribute to the long-term control of hippocampal excitability.