Neuroscience
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Electrical stimuli were applied to tooth-pulp in cats and the thresholds of the jaw-opening reflex and of neurons in the trigeminal sensory nuclei were determined. The effects of the method of preparation of the animal for stereotaxic recording were determined by making observations on animals set up in one of three ways: acutely in the usual manner; chronically, three to five days before recording; and acutely with precautions to minimize nociceptive input to the central nervous system. The threshold of the jaw-opening reflex increased progressively during the setting up of the normal, acute preparations and at the time brainstem recording began was significantly higher in these than in either the chronic or low-trauma acute preparations. ⋯ In the chronic and in low-trauma acute preparations, there was no significant difference between the thresholds of the units in the main sensory trigeminal nucleus and spinal subnucleus oralis compared with those in subnucleus caudalis. Thus the preparation of an animal for stereotaxic recording can cause a severe and long-lasting depression in the excitability of neurons in the trigeminal sensory nuclei and an increase in the threshold of the jaw-opening reflex. This effect will have influenced the results of previous studies on the responses evoked in central neurons by stimulation of tooth-pulp, and may have similarly affected recordings from other regions.
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The effects of elevated CO2 (i.e. hypercapnia) on neurons in the nucleus tractus solitarii were studied using extracellular (n = 82) and intracellular (n = 33) recording techniques in transverse brain slices prepared from rat. Synaptic connections from putative chemosensitive neurons in the ventrolateral medulla were removed by bisecting each transverse slice and discarding the ventral half. In addition, the response to hypercapnia in 20 neurons was studied during high magnesium-low calcium synaptic blockade. ⋯ These neurons were not driven synaptically by putative chemosensitive neurons of the ventrolateral medulla since this region was removed from the slice. Furthermore, because chemosensitivity persisted in most neurons tested during synaptic blockade, we conclude that some neurons in the nucleus tractus solitarii are inherently CO2-chemosensitive. Although the function of dorsal medullary chemosensitive neurons cannot be determined in vitro, their location and their inherent chemosensitivity suggest a role in cardiorespiratory central chemoreception.
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Intracellular recordings from the intermediolateral cell nucleus of the neonate rat thoracolumbar spinal cord slice preparation revealed a population of neurons which displayed three types of spontaneous rhythmic activity: burst firing, tonic beating and membrane oscillations. Most neurons displayed more than one of these types of activity. Neurons had mean resting potentials of -59 mV and input resistances ranging from 10 to 48 m omega. ⋯ Burst firing was abolished by cobalt and membrane hyperpolarization but not by barium, low calcium or tetraethylammonium chloride. The switch from tonic beating to burst firing may, in part, involve activation of a voltage- and calcium-dependent afterdepolarization potential. We conclude that a population of neurons in the lateral horn of the spinal cord are capable of rhythmic activity with underlying spontaneous pacemaker-like oscillations.
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Electrical stimulus intensity, capsaicin, excitatory amino acid antagonists and the substance P antagonist, spantide, have been used to investigate the roles of primary afferent C fibres and excitatory amino acid receptors in the generation of long duration (half time 9.1 s +/- 1.1 S. E. M., N = 24) contralateral reflexes recorded in ventral roots of immature rat spinal cords in vitro. ⋯ The depressant effect of spantide, unlike that of (+/-)-2-amino-5-phosphonopentanoic acid, was associated with a long lasting excitatory action. In the presence of tetrodotoxin (0.1 microM), spantide (33 microM) failed to antagonize substance P-induced depolarizations. It is suggested that long duration of the dorsal root-evoked contralateral ventral root potential is a consequence of the activation of the N-methyl-D-aspartate receptor operated ion channels by excitatory amino acid transmitters.
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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.