Journal of neurophysiology
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Touch and pain are intimately related modalities. Despite a substantial overlap in their cortical representations interactions between both modalities are largely unknown at the cortical level. We therefore used magnetoencephalography and selective nociceptive cutaneous laser stimulation to investigate the effects of brief painful stimuli on cortical processing of touch. ⋯ Control experiments show that pain-induced facilitation of tactile processing is not restricted to the site of the painful conditioning stimulus, whereas auditory conditioning does not yield a comparable facilitation. Apart from a lack of spatial specificity, the facilitating effect of pain closely resembles attentional effects on cortical processing of tactile stimuli. Thus these findings may represent a physiological correlate of an alerting function of pain as a change in the internal state to prepare for processing signals of particular relevance.
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Anesthetics appear to produce neurodepression by altering synaptic transmission and/or intrinsic neuronal excitability. Propofol, a widely used anesthetic, has proposed effects on many targets, ranging from sodium channels to GABA(A) inhibition. We examined effects of propofol on the intrinsic excitability of hippocampal CA1 neurons (primarily interneurons) recorded from adult rat brain slices. ⋯ Similar results were found in both interneurons and pyramidal cells and with the chemically unrelated anesthetic thiopental. These results suggest that suppression of CA1 neuron intrinsic excitability, by these anesthetics, is largely due to activation of tonic GABA(A) conductances; although other sites of action may play important roles in affecting synaptic transmission, which also can produce strong neurodepression. We propose that for some anesthetics, suppression of intrinsic excitability, mediated by tonic GABA(A) conductances, operates in conjunction with effects on synaptic transmission, mediated by other mechanisms, to depress hippocampal function during anesthesia.
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Cultures of neurons from rat neocortex exhibit spontaneous, temporally patterned, network activity. Such a distributed activity in vitro constitutes a possible framework for combining theoretical and experimental approaches, linking the single-neuron discharge properties to network phenomena. In this work, we addressed the issue of closing the loop, from the identification of the single-cell discharge properties to the prediction of collective network phenomena. ⋯ Such a network reproduced a collective activity, matching the spontaneous irregular population bursting, observed in cultured networks. We finally interpret such a collective activity and its link with model details by the mean-field theory. We conclude that the IF model is an adequate minimal description of synaptic integration and neuronal excitability, when collective network activities are considered in vitro.
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Mitral cells, the principal cells of the olfactory bulb, respond to sensory stimulation with precisely timed patterns of action potentials. By contrast, the same neurons generate intermittent spike clusters with variable timing in response to simple step depolarizations. We made whole cell recordings from mitral cells in rat olfactory bulb slices to examine the mechanisms by which normal sensory stimuli could generate precisely timed spike clusters. ⋯ The amplitude of the first simulated EPSP in a train gated the generation of spikes on subsequent EPSPs. 4-aminopyridine (4-AP)-sensitive K(+) channels are critical to the generation of spike clusters and reproducible spike timing in response to phasic stimuli. Based on these results, we propose that spike clustering is a process that depends on the interaction between a 4-AP-sensitive K(+) current and a subthreshold TTX-sensitive Na(+) current; interactions between these currents may allow mitral cells to respond selectively to stimuli in the theta frequency range. These intrinsic properties of mitral cells may be important for precisely timing spikes evoked by phasic stimuli that occur in response to odor presentation in vivo.
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Although a major output of the hippocampal formation is from the subiculum to the deep layers of the entorhinal cortex, the parasubiculum projects to the superficial layers of the entorhinal cortex and may therefore modulate how the entorhinal cortex responds to sensory inputs from other cortical regions. Recordings at multiple depths in the entorhinal cortex were first used to characterize field potentials evoked by stimulation of the parasubiculum in urethan-anesthetized rats. Current source density analysis showed that a prominent surface-negative field potential component is generated by synaptic activation in layer II. ⋯ Paired-pulse tests were then used to assess the effect of parasubicular stimulation on responses to piriform cortex stimulation. Responses of the entorhinal cortex to piriform cortex inputs were inhibited when the parasubiculum was stimulated 5 ms earlier and were enhanced when the parasubiculum was stimulated 20-150 ms earlier. These results indicate that excitatory inputs to the entorhinal cortex from the parasubiculum may enhance the propagation of neuronal activation patterns into the hippocampal circuit by increasing the responsiveness of the entorhinal cortex to appropriately timed inputs.