Neuroscience
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The study was designed to obtain information on the spinal processing of input from receptors in deep somatic tissues (muscle, tendon, joint). In anaesthetized rats, the impulse activity of single dorsal horn cells was recorded extracellularly. In a pilot series, the proportion of neurons responding to mechanical stimulation of deep tissues was determined: 46.7% had receptive fields in the skin only, 35.5% could only be driven from deep tissues (deep cells), and 17.7% possessed a convergent input from both skin and deep tissues (cutaneous-deep cells). ⋯ In these presumably nociceptive cells the descending inhibition had a differential action in that the input from deep tissues was more strongly affected than was the cutaneous input to the same neuron. The recording sites of the neurons with deep input were located in the superficial dorsal horn and in and around lamina V. The results suggest that in the rat a considerable proportion of dorsal horn cells receives input from deep nociceptors and that this input is controlled by descending pathways in a rather selective way.
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The intradermal injection of adenosine produces a dose-dependent decrease in mechanical nociceptive threshold in the hindpaw of the rat that is not attenuated by elimination of indirect pathways for the production of hyperalgesia. Adenosine-induced hyperalgesia is mimicked by the A2-agonists, 5'-(N-ethyl)-carboxamido-adenosine and 2-phenylaminoadenosine but not by the A1-agonist, N6-cyclopentyladenosine and antagonized by the adenosine A2-receptor antagonist, PD 081360-0002 but not by the A1-antagonist, 1,3-dipropyl-8-(2-amino-4-chlorophenyl)xanthine. ⋯ However, 1-acetyl-2-(8-chloro-10,11-dihydrodibenz[b,f]oxazepine-10-ca rbonyl) hydrazine, a prostaglandin-receptor antagonist, inhibits prostaglandin E2 (Taiwo and Levine, Brain Res. 458, 402-406, 1988) but not 2-phenylamino-adenosine hyperalgesia and PD 081360-0002, the adenosine receptor antagonist, inhibits 2-phenylamino-adenosine but not prostaglandin E2 hyperalgesia. These data suggest that adenosine is a directly acting agent that produces hyperalgesia by an action at the A2-receptor and that this hyperalgesia is mediated by the cAMP second messenger.
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Local treatment of rat peripheral nerves with capsaicin induces permanent impairment of afferent C-fiber functions and changes in the response properties of spinal dorsal horn neurons. In this study a new experimental approach, the "capsaicin gap" technique, has been utilized in an attempt to unravel pathomorphological alterations which commence in the domain of primary sensory neurons as a consequence of perineural treatment with capsaicin. The technique relies on the facts that peripheral nerves in the spinal dorsal horn are represented in a strict somatotopic manner, and on the observation that in the adult rat systemic injection of appropriate doses of capsaicin results in a selective degeneration of primary afferent fibers within Rexed's laminae I and II of the spinal cord. ⋯ It is concluded that the central terminals of capsaicin-sensitive sciatic afferents underwent transganglionic degeneration as a result of prior perineural treatment with capsaicin, and a subsequent systemic injection of this neurotoxin therefore failed to cause axon terminal degeneration in somatotopic areas served by the treated nerve. Comparative quantitative morphometric analysis of cell populations of dorsal root ganglia related to capsaicin- or vehicle-treated nerves disclosed (1) a marked reduction in the proportion of small-sized neurons, (2) a fall of about 80% in the percentage of neurons which undergo degeneration after the systemic injection of capsaicin, and (3) a marked decrease in the total number of neurons in ganglia ipsilateral to the capsaicin-treated nerves. Quantitative electron microscopic studies on saphenous nerves treated perineurally with capsaicin revealed a 32% reduction in the number of unmyelinated axons as compared with the controls, whereas the number of myelinated fibers was unchanged.(ABSTRACT TRUNCATED AT 400 WORDS)
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The distribution of acetylcholinesterase and of two neuropeptide (substance P and calcitonin gene-related peptide) immunoreactivities has been investigated in sensory neurons of lumbosacral dorsal root ganglia during chick embryo development, combining immunolocalization of neuropeptides with simultaneous histochemical detection of acetylcholinesterase, in order to study co-localization of the two peptides and their relations with acetylcholinesterase. Acetylcholinesterase at E7 of development appears in only a few neurons, usually the larger ones located in the lateroventral region of the ganglia. As development proceeds the number of neurons and intensity of staining increase. ⋯ Neuropeptide-positive cells are usually devoid of any acetylcholinesterase activity until E15. They become positive for the enzyme at later stages. The significance of acetylcholinesterase expression in sensory neurons and the possible relation of its appearance and neuron size is discussed.
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When adult dorsal root ganglion cells are dissociated and maintained in vitro, both the small dark and the large light neurons show increases in the growth-associated protein GAP-43, a membrane phosphoprotein associated with neuronal development and plasticity. Immunoreactivity for GAP-43 appears in the cytoplasm of the cell bodies as early as 3.5 h post axotomy and is present in neurites and growth cones as soon as they develop. At early stages of culture (4 h to eight days) satellite/Schwann cells are also immunoreactive for GAP-43. ⋯ Axotomy of primary sensory neurons or the interruption of axon transport in the periphery therefore acts to trigger GAP-43 production in the cell body. The GAP-43 is transported to both the peripheral and the central terminals of the afferents. In the CNS the elevated GAP-43 levels may contribute to an inappropriate synaptic reorganization of afferent terminals that could play a role in the sensory disorders that follow nerve injury.