Up-regulation of NaV1.7 sodium channels expression by tumor necrosis factor-α in cultured bovine adrenal chromaffin cells and rat dorsal root ganglion neurons.

Background: Tumor necrosis factor-α (TNF-α) is not only a key regulator of inflammatory response but also an important pain modulator. TNF-α enhances both tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant Na channel currents in dorsal root ganglion (DRG) neurons. However, it remains unknown whether TNF-α affects the function and expression of the TTX-S NaV1.

Clinical dose of lidocaine destroys the cell membrane and induces both necrosis and apoptosis in an identified Lymnaea neuron.

Purpose: Although lidocaine-induced cell toxicity has been reported, its mechanism is unclear. Cell size, morphological change, and membrane resistance are related to homeostasis and damage to the cell membrane; however, the effects of lidocaine on these factors are unclear. Using an identified LPeD1 neuron from Lymnaea stagnalis, we sought to determine how lidocaine affects these factors and how lidocaine is related to damage of the cell membrane.

Lidocaine treatment during synapse reformation periods permanently inhibits NGF-induced excitation in an identified reconstructed synapse of Lymnaea stagnalis.

Purpose: Nerve growth factor (NGF) has been reported to affect synaptic transmission and cause neuropathic pain. In contrast, lidocaine has been used to reduce neuropathic pain; however, the effect of NGF and lidocaine on spontaneous transmitter release and synapse excitation has not been fully defined. Therefore, the effect of NGF and lidocaine on nerve regeneration, synapse reformation, and subsequent spontaneous transmitter release was investigated.

Lidocaine depolarizes the mitochondrial membrane potential by intracellular alkalization in rat dorsal root ganglion neurons.

Purpose: The mitochondrial membrane potential (ΔΨm) is an important factor for apoptosis, and it is produced by the proton electrochemical gradient (ΔµH(+)). Therefore, the intracellular proton concentration (pH(in)) is an important factor for modifying the ΔΨm. However, the effects of lidocaine on pH(in) are unclear.

Capsaicin indirectly suppresses voltage-gated Na+ currents through TRPV1 in rat dorsal root ganglion neurons.

Background: Capsaicin is used to treat a variety of types of chronic pain, including arthritis and trigeminal neuralgia. Although the cellular effects of capsaicin have been widely studied, little is known about the effects of capsaicin on intracellular sodium ([Na(+)]i) concentrations and voltage-gated Na(+) currents (INa(+)) in nociceptive afferent neurons. Therefore, in this study we sought to characterize the effect of capsaicin on tetrodotoxin-sensitive (TTX-s) and resistant (TTX-r) INa(+).

Effects of orexin-A on propofol anesthesia in rats.

Purpose: An active sleep homeostatic process is present during propofol anesthesia. Activation of the orexin system induces wakefulness, and inhibition of the orexin system causes narcolepsy. We hypothesized that orexin would affect propofol anesthesia.

Local anesthetics depolarize mitochondrial membrane potential by intracellular alkalization in rat dorsal root ganglion neurons.

Background: Although it has been reported that local anesthetics, especially lidocaine, are cytotoxic, the mechanism is unclear. Depolarization of the mitochondrial membrane potential (DeltaPsim), one of the markers of mitochondrial failure, is regulated by the proton electrochemical gradient (Delta H(+)). Therefore, intracellular pH ([pH]in) and mitochondrial pH ([pH]m) are important factors for modifying DeltaPsim.

The effect of lidocaine on cholinergic neurotransmission in an identified reconstructed synapse.

Background: The presynaptic effect of lidocaine on cholinergic synaptic transmission is unclear because of the difficulty in identifying presynaptic neurons and the complexity of the central nervous system in vivo. To clarify the effect of lidocaine on cholinergic synapse, we reconstructed a cultured soma-soma chemical synapse model consisting of two identified visceral dorsal 4 (VD4) and left pedal e-1 (LPeD1) neurons from the snail, Lymnaea stagnalis, in vitro, and used it to determine how lidocaine affects cholinergic synaptic transmission.

Methods: The response to acetylcholine and excitatory postsynaptic potential (EPSP) amplitude was recorded in the reconstructed chemical synaptic transmission model composed of VD4 and LPeD1 neurons.

Lidocaine increases intracellular sodium concentration through a Na+-H+ exchanger in an identified Lymnaea neuron.

Background: The intracellular sodium concentration ([Na(+)]in) is related to neuron excitability. For [Na(+)]in, a Na(+)-H(+) exchanger plays an important role, which is affected by intracellular pH ([pH]in). However, the effect of lidocaine on [pH]in and a Na(+)-H(+) exchanger is unclear.

[Burst spikes induced by lidocaine in the ganglion of Lymnaea stagnalis].

Background: To investigate the burst spikes (BS) induced by lidocaine in the ganglion of Lymnaea stagnalis, we used a multielectrode dish for extracellular recording in many points simultaneously.

Methods: Ganglion of Lymnaea stagnalis was placed in the multielectrode dish that has 64 planar microelectrodes. After the basal electrophysiological recordings of neuronal activity in the ganglion, the lidocaine concentrations were increased from 1 to 1,000 microg x ml(-1).

Increase in intracellular Ca2+ concentration is not the only cause of lidocaine-induced cell damage in the cultured neurons of Lymnaea stagnalis.

Purpose: To determine whether the increase in intracellular Ca2+ concentration induced by lidocaine produces neurotoxicity, we compared morphological changes and Ca2+ concentrations, using fura-2 imaging, in the cultured neurons of Lymnaea stagnalis.

Methods: We used BAPTA-AM, a Ca2+ chelator, to prevent the increase in the intracellular Ca2+ concentration, and Calcimycin A23187, a Ca2+ ionophore, to identify the relationship between increased intracellular Ca(2+) concentrations and neuronal damage without lidocaine. Morphological changes were confirmed using trypan blue to stain the cells.

Sevoflurane blocks cholinergic synaptic transmission postsynaptically but does not affect short-term potentiation.

Background: As compared with their effects on both inhibitory and excitatory synapses, little is known about the mechanisms by which general anesthetics affect synaptic plasticity that forms the basis for learning and memory at the cellular level. To test whether clinically relevant concentrations of sevoflurane affect short-term potentiation involving cholinergic synaptic transmission, the soma-soma synapses between identified, postsynaptic neurons were used.

Methods: Uniquely identifiable neurons visceral dorsal 4 (presynaptic) and left pedal dorsal 1 (postsynaptic) of the mollusk Lymnaea stagnalis were isolated from the intact ganglion and paired overnight in a soma-soma configuration.

Long-term exposure to local but not inhalation anesthetics affects neurite regeneration and synapse formation between identified lymnaea neurons.

Background: General and local anesthetics are used in various combinations during surgical procedures to repair damaged tissues and organs, which in almost all instances involve nervous system functions. Because synaptic transmission recovers rapidly from various inhalation anesthetics, it is generally assumed that their effects on nerve regeneration and synapse formation that precede injury or surgery may not be as detrimental as that of their local counterparts. However, a direct comparison of most commonly used inhalation (sevoflurane, isoflurane) and local anesthetics (lidocaine, bupivacaine), vis-a-vis their effects on synapse transmission, neurite regeneration, and synapse formation has not yet been performed.

Lidocaine excites both pre- and postsynaptic neurons of reconstructed respiratory pattern generator in Lymnaea stagnalis.

Lidocaine causes both inhibition and excitation in the central nervous system, including the respiratory pattern. The excitation induced by an excessive dose of local anesthetic is thought to be the result of an initial blockade of an inhibitory pathway in the cerebral cortex. To clarify the effect of lidocaine on the pre- and postsynaptic neurons of an inhibitory synapse, a cultured soma-soma respiratory pattern generator model consisting of two neurons from the snail Lymnaea stagnalis were reconstructed in vitro.

Lidocaine increases intracellular sodium concentration through voltage-dependent sodium channels in an identified lymnaea neuron.

Background: The local anesthetic lidocaine affects neuronal excitability in the central nervous system; however, the mechanisms of such action remain unclear. The intracellular sodium concentration ([Na]i) and sodium currents (INa) are related to membrane potential and excitability. Using an identifiable respiratory pacemaker neuron from Lymnaea stagnalis, the authors sought to determine whether lidocaine changes [Na]i and membrane potential and whether INa is related to these changes.

Procaine and mepivacaine have less toxicity in vitro than other clinically used local anesthetics.

Unlabelled: The neurotoxicity of local anesthetics can be demonstrated in vitro by the collapse of growth cones and neurites in cultured neurons. We compared the neurotoxicity of procaine, mepivacaine, ropivacaine, bupivacaine, lidocaine, tetracaine, and dibucaine by using cultured neurons from the freshwater snail Lymnaea stagnalis. A solution of local anesthetics was added to the culture dish to make final concentrations ranging from 1 x 10(-6) to 2 x 10(-2) M.