Journal of neurophysiology
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Microneurographic recordings were obtained in the peroneal nerve from 20 mechano-insensitive units (CMi) and six mechano-heat responsive C units (CMH) in healthy human subjects. Their innervation territories in the skin of the leg or foot were assessed by transcutaneous electrical stimulation with a pointed probe at intensities of 10 to 100 mA (0.2 ms) and, when applicable, by mechanical von Frey hair stimulation. Electro-receptive fields (eRFs) of CMH units had a median area of 1.95 cm(2) when mapped with 10 mA that coincided approximately with mechano-receptive fields (mRFs) as mapped with a 750-mN von Frey hair. ⋯ Responsiveness to these stimuli was inhomogeneous within the eRFs. It was concluded that innervation territories of CMi units in human skin exceed those of CMH units in size by a factor of approximately 3. The widely branched terminals underlying the large fields are consistent with a role of this nociceptor class in axon reflex flare and preclude a role in exact spatial discrimination of noxious stimuli.
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Comparative Study
Comparison of morphine and kainic acid microinjections into identical PAG sites on the activity of RVM neurons.
The rostral ventromedial medulla (RVM) modulates nociception through changes in the activity of two classes of neuron, ON- and OFF-cells. The activity of these neurons is regulated, in part, by input from the periaqueductal gray (PAG). The objective of this study was to determine whether PAG-mediated antinociception is associated with excitation of both ON- and OFF-cells in the RVM. ⋯ That is, ON-cells were inhibited and OFF-cells were activated. These data indicate that the excitatory connection between the PAG and RVM is directed at RVM OFF-cells specifically. In addition, these data suggest that direct activation of PAG output neurons, as occurs with kainic acid, is much more likely to produce antinociception than disinhibition of output neurons as occurs following morphine administration.
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The ability of oscillating networks to synchronize despite significant separation in space, and thus time, is of biological significance, given that human gamma activity can synchronize over distances of several millimeters to centimeters during perceptual and learning tasks. We use computer simulations of networks consisting of excitatory pyramidal cells (e-cells) and inhibitory interneurons (i-cells), modeling two tonically driven assemblies separated by large (>or=8 ms) conduction delays. The results are as follows. 1) Two assemblies separated by large conduction delays can fire synchronously at beta frequency (with i-cells firing at gamma frequency) under two timing conditions: e-cells of (say) assembly 2 are still inhibited "delay + spike generation milliseconds" after the e-cell beat of assembly 1; this means that the e-cell inhibitory postsynaptic potential (IPSP) cannot be significantly shorter than the delay (2-site effect). ⋯ They can also synchronize without pyramidal cell --> pyramidal cell connections being present. The presence of pyramidal cell --> pyramidal cell connections allows, however, for synchronization if other parameters are at inappropriate values for synchronization to occur. 5) Synchronization of two assemblies separated by large conduction delays with the help of interneuron plasticity is not simply due to slowing down of the oscillation frequency. It is reached with the help of a "synchronizing-weak-beat," which induces sudden changes in the oscillation period length of the two assemblies.
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Nicotine regulates respiratory pattern by modulating excitatory neurotransmission affecting inspiratory neurons within the preBötzinger Complex (preBötC). The nicotinic acetylcholine receptor (nAChR) subtypes mediating these effects are unknown. Using a medullary slice preparation from neonatal rat, we recorded spontaneous respiratory-related rhythm from the hypoglossal nerve (XIIn) and patch-clamped inspiratory neurons in the preBötC simultaneously. ⋯ We do not exclude the possibility that co-assembly of alpha4beta2 with other subunits or other nAChR subtypes are also expressed in preBötC neurons. The parallel changes in the cellular and systems level responses induced by different nicotinic agonists and antagonists support the idea that modulation of excitatory neurotransmission affecting preBötC inspiratory neurons is a mechanism underlying the cholinergic regulation of respiratory pattern (). This study provides a useful model system for evaluating potential therapeutic cholinergic agents for their respiratory effects and side effects.