Journal of neurophysiology
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Cisplatin causes both acute and chronic forms of tinnitus as well as increases in spontaneous neural activity (hyperactivity) in the dorsal cochlear nucleus (DCN) of hamsters. It has been hypothesized that the induction of hyperactivity in the DCN may be a consequence of cisplatin's effects on cochlear outer hair cells (OHCs); however, systematic studies testing this hypothesis have yet to appear in the literature. In the present investigation, the relationship between hyperactivity and OHC loss, induced by cisplatin, was examined in detail. ⋯ In several of the animals with severe OHC loss and hyperactivity, there was no significant damage to IHC stereocilia nor any observable irregularities of the reticular lamina that might have interfered with normal IHC function. Hyperactivity was also observed in the DCN of animals showing severe losses of OHCs accompanied by damage to IHCs, although the degree of hyperactivity in these animals was less than in animals with severe OHC loss but intact IHCs. These results support the view that loss of OHC function may be a trigger of tinnitus-related hyperactivity in the DCN and suggest that this hyperactivity may be somewhat offset by damage to IHCs.
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Comparative Study
Differentiating noxious- and innocuous-related activation of human somatosensory cortices using temporal analysis of fMRI.
The role of the somatosensory cortices (SI and SII) in pain perception has long been in dispute. Human imaging studies demonstrate activation of SI and SII associated with painful stimuli, but results have been variable, and the functional relevance of any such activation is uncertain. The present study addresses this issue by testing whether the time course of somatosensory activation, evoked by painful heat and nonpainful tactile stimuli, is sufficient to discriminate temporal differences that characterize the perception of these stimulus modalities. ⋯ This prolonged period of activation paralleled the perception of increasing pain intensity that persists even after stimulus offset. On the other hand, the temporal profile of the initial minor peak in pain-related activation closely matched that of the brush-evoked activity, suggesting a possible relationship to tactile components of the thermal stimulation procedure. These data indicate that both SI and SII cortices are involved in the processing of nociceptive information and are consistent with a role for these structures in the perception of temporal aspects of pain intensity.
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We recorded spontaneous and evoked synaptic currents in pyramidal neurons of layer V in chronically injured, epileptogenic neocortex to assess changes in the efficacy of excitatory and inhibitory neurotransmission that might promote cortical hyperexcitability. Partial sensory-motor neocortical isolations with intact blood supply ("undercuts") were made in 20 rats on postnatal day 21-25 and examined 2-6 wk later in standard brain slice preparations using whole cell patch-clamp techniques. Age-matched, uninjured naive rats (n = 20) were used as controls. ⋯ In contrast, the N-methyl-D-aspartate receptor-mediated component of evoked EPSCs was not significantly different in neurons of injured versus control cortex, suggesting that the increased AMPA/KA component was due to postsynaptic alterations. Results support the conclusion that layer V pyramidal neurons receive increased AMPA/KA receptor-mediated excitatory synaptic drive and decreased GABA(A) receptor-mediated inhibition in this chronically injured, epileptogenic cortex. This shift in the balance of excitatory and inhibitory synaptic activation of layer V pyramidal cells toward excitation might be maladaptive and play a critical role in epileptogenesis.
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Comparative Study
Constraints on the source of short-term motion adaptation in macaque area MT. I. the role of input and intrinsic mechanisms.
Neurons in area MT, a motion-sensitive area of extrastriate cortex, respond to a step of target velocity with a transient-sustained firing pattern. The transition from a high initial firing rate to a lower sustained rate occurs over a time course of 20-80 ms and is considered a form of short-term adaptation. The present paper asks whether adaptation is due to input-specific mechanisms such as short-term synaptic depression or if it results from intrinsic cellular mechanisms such as spike-rate adaptation. ⋯ Further, the transient was suppressed or extinguished, not delayed, in trials in which the neuron emitted zero spikes during the interval that showed a transient in average firing rate. We conclude that the transition from transient to sustained firing in neurons in area MT is caused by mechanisms that are neither input-specific nor controlled by the spiking of the adapting neuron. We propose that the short-term adaptation observed in area MT emerges from the intracortical circuit within MT.
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Diabetic neuropathic pain is often considered to be caused by peripheral neuropathy. The involvement of the CNS in this pathological condition has not been well documented. Development of hypersensitivity of spinal dorsal horn neurons is involved in neuropathic pain induced by traumatic nerve injury. ⋯ However, such an inhibitory effect of morphine on the evoked response of STT neurons was diminished in 14 diabetic animals. This electrophysiological study provides new information that development of hypersensitivity of spinal dorsal horn projection neurons may be closely related to neuropathic pain symptoms caused by diabetes. Furthermore, the attenuated inhibitory effects of morphine on evoked responses of STT neurons in diabetes likely accounts for its reduced analgesic efficacy in this clinical form of neuropathic pain.