Neuroscience
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Comparative Study
In vivo and in vitro effects of peripheral galanin on nociceptive transmission in naive and neuropathic states.
Galanin is widely distributed in the nervous system and is consistently upregulated in both dorsal root ganglion and spinal neurones by peripheral nerve injury. This study investigates the peripheral effects of galanin on nociceptive neurones using in vitro and in vivo electrophysiological techniques in naive and neuropathic rats. Using an in vitro skin-nerve preparation recording from single nociceptive fibres, galanin (1 microM) significantly inhibited firing induced by noxious heat in 65% of fibres examined. ⋯ Injection of galanin (0.1-10 microg) into hindpaw receptive fields inhibited responses to innocuous mechanical, noxious mechanical and noxious heat stimuli in a proportion of neurones in each animal group and facilitated the remaining neurones. However, a higher proportion of neurones (80-90%) was inhibited by peripheral galanin administration in SNL rats compared with naive (45-55%) and sham (70-80%) rats. These results show that galanin can have both excitatory and inhibitory effects on peripheral sensory neurones, perhaps reflecting differential receptor activation, and that the proportion of these receptors may change following peripheral neuropathy.
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It is known that the level of activity in nociceptive primary afferent nerve fibers increases in neuropathic conditions that produce pain, but changes in the temporal patterning of action potentials have not been analyzed in any detail. Because the patterning of action potentials in sensory nerve fibers might play a role in the development of pathological pain states, we studied patterning of mechanical stimulus-evoked action potential trains in nociceptive primary afferents in a rat model of vincristine-induced painful peripheral neuropathy. Systemic administration of vincristine (100 microg/kg) caused approximately half the C-fiber nociceptors to become markedly hyperresponsive to mechanical stimulation. ⋯ Variability in the temporal pattern of action potential firing was quantified by determining the coefficient of variability (CV2) for adjacent interspike intervals. This analysis revealed that vincristine altered the pattern of action-potential timing, so that combinations of higher firing frequency and higher variability occurred that were not observed in control fibers. The abnormal temporal structure of nociceptor responses induced by vincristine in some C-fiber nociceptors could contribute to the pathogenesis of chemotherapy-induced neuropathic pain, perhaps by inducing activity-dependent post-synaptic effects in sensory pathways.
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Electroencephalographic activity at the transition from wakefulness to sleep is characterized by the appearance of spindles (12-15 Hz) and slow wave rhythms including delta activity (1-4 Hz) and slow oscillations (0.2-1 Hz). While these rhythms originate within neocortico-thalamic circuitry, their emergence during the passage into slow wave sleep (SWS) critically depends on the activity of neuromodulatory systems. Here, we examined the temporal relationships between these electroencephalogram rhythms and the direct current (DC) potential recorded from the scalp in healthy men (n=10) using cross-correlation analyses. ⋯ Data indicate close links between increasing spindle, delta and slow oscillatory activity and the occurrence of a steep surface negative cortical DC potential shift during the transition from wake to SWS. Likewise, a DC potential shift toward surface positivity accompanies the disappearance of these oscillatory phenomena at the end of the non-REM sleep period. The DC potential shifts may reflect gradual changes in extracellular ionic (Ca2+) concentration resulting from the generation of spindle and slow wave rhythms, or influences of neuromodulating systems on cortical excitability thereby controlling the emergence of cortical spindle and slow wave rhythms at SWS transitions.
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Comparative Study
Low-threshold heat receptor in chick sensory neurons is upregulated independently of nerve growth factor after nerve injury.
In mammals, the cloned low-threshold heat receptor, vanilloid receptor subtype 1 (VR1), is involved in the genesis of thermal hyperalgesia after inflammation. However, there is evidence that VR1 is not involved in the thermal hyperalgesia that occurs after nerve injury. In search for other heat receptors which might be involved in this phenomenon, we previously demonstrated that chick dorsal root ganglion neurons, which are insensitive to capsaicin, respond to low-threshold heat. ⋯ On the molecular level, there was an increase of chick VR1 mRNA level in dorsal root ganglion cells cultured for 3 days in medium lacking NGF. In rat dorsal root ganglion neurons cultured for 1-4 days without NGF, patch-clamp experiments revealed that after 1 day almost all neurons responding to heat also responded to capsaicin, whereas after 3-4 days, more than one-half of the heat-responsive neurons did not respond to capsaicin. These data suggest the existence of low-threshold heat receptors in chick dorsal root ganglion neurons, the expression of which is regulated independently of NGF.
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Comparative Study
Propagation pattern of entorhinal cortex subfields to the dentate gyrus in the guinea-pig: an electrophysiological study.
Anatomical studies demonstrated that neurons located in the superficial layers of the medial and lateral aspects of the rat entorhinal cortex (EC) project to temporal and septal portions of both the dentate gyrus (DG) and the CA1 region of the hippocampus, respectively. In the present study we investigated with electrophysiological techniques the propagation pattern of different EC subfields to the DG of the in vitro isolated brain of the guinea-pig. Laminar field potential profiles from different portions of the DG were recorded with multi-channel silicon probes following direct stimulation of the ipsilateral EC surface performed in different positions under direct visual control. ⋯ The EC-evoked monosynaptic DG potentials were followed by disynaptic responses coupled with sinks located in the inner molecular layer, proximal to the EC-induced sink, where intra-DG associative synapses were demonstrated by anatomical studies. The present detailed topographical study of the EC connections with the DG in the guinea-pig demonstrates with an electrophysiological approach a projection pattern similar, even if not identical, to that described with tracer techniques in the rat. This report is essential for future studies of the dynamic parahippocampal-hippocampal interactions in the guinea-pig, and in particular in the isolated guinea-pig brain preparation.