Mean Action Potential Amplitude Research Articles

Neurophysiological Characterization of Thalamic Nuclei in Epileptic Anaesthetized Patients.

Deep brain stimulation (DBS) requires precise localization, which is especially difficult at the thalamus, and even more difficult in anesthetized patients. We aimed to characterize the neurophysiological properties of the ventral intermediate (V.im), ventral caudal (V.c), and centromedian parvo (Ce.pc) and the magnocellular (Ce.mc) thalamic nuclei. We obtained microelectrode recordings from five patients with refractory epilepsy under general anesthesia. Somatosensory evoked potentials recorded by microelectrodes were used to identify the V.c nucleus. Trajectories were reconstructed off-line to identify the nucleus recorded, and the amplitude of the action potential (AP) and the tonic (i.e., mean frequency, density, probability of interspike interval) and phasic (i.e., burst index, pause index, and pause ratio) properties of the pattern discharges were analyzed. The Mahalanobis metric was used to evaluate the similarity of the patterns. The mean AP amplitude was higher for the V.im nucleus (172.7 ± 7.6 µV) than for the other nuclei, and the mean frequency was lower for the Ce.pc nucleus (7.2 ± 0.8 Hz) and higher for the V.c nucleus (11.9 ± 0.8 Hz) than for the other nuclei. The phasic properties showed a bursting pattern for the V.c nucleus and a tonic pattern for the centromedian and V.im nuclei. The Mahalanobis distance was the shortest for the V.im/V.c and Ce.mp/Ce.pc pairs. Therefore, the different properties of the thalamic nuclei, even for patients under general anesthesia, can be used to positively define the recorded structure, improving the exactness of electrode placement in DBS.

An electrophysiological analysis of deep cerebellar nuclei, with particular focus on Kv3 channels

Deep cerebellar nuclei (DCN) form three symmetrical, bilateral nuclei, deep within the white matter of the cerebellum and represent the sole output of the cerebellum to the central nervous system. Although innervated by spontaneously active inhibitory Purkinje cells, DCN neurons also fire action potentials spontaneously at a relatively high frequency, a property attributed to Kv3 channels. In the present study, an electrophysiological approach was carried out on DCN neurons, the purpose of which was to investigate the properties and elucidate the involvement of Kv3 channels. Using whole-cell patch clamp techniques, electrophysiological recordings from the dentate nucleus were obtained from coronal cerebellar slices of Wistar rats (P 12) in both current and voltage clamp modes. Kv3-mediated currents were investigated in the presence of tetrodotoxin (1 mM), by applying low concentration tetraethyl ammonium (TEA) (100 mM). Current-clamp recordings revealed a population of tonically firing neurons, exhibiting a maximum action potential firing frequency of 18.1+ 6.9 Hz and a steady firing frequency of 14.2+4.8 Hz (n 1⁄4 6). These neurons were also shown to exhibit a mean action potential amplitude of 48.7+ 9.5 mV, mean half-width of 2.9+ 1 ms and mean afterhyperpolarization amplitude of 19.6+ 7.5 mV. Depolarizing sag (indicative of the Ih current), followed by rebound depolarization, was observed in all neurons. Voltageclamped neurons revealed a voltage-dependent slowly inactivating outward current with a peak amplitude of 1538.5+1096.6 pA (n 1⁄4 10). Application of low concentration TEA (100 mM) reduced the current by a statistically significant 19.4+13.4% (P, 0.05; paired t-test) and this effect was reversible. Application of a Boltzmann function yielded a V1/2 value of 9.9 mV for the TEA-sensitive current. As Kv3 channels have been previously localized in DCN, the results suggest that the TEA-sensitive current ( 20% of the total outward current exhibited) is mediated by Kv3 channels.

Effects of serotonin 1A agonist on acute spinal cord injury.

We evaluated the effects of serotonin (5-HT) agonists on in vitro models of spinal cord compressive injury. Evoked potentials in injured rat spinal cords (n=24) were recorded during perfusion with 5-HT agonists. To evaluate the therapeutic effects of 5-HT agonists on the recovery of compound action potentials in injured spinal cords. Rat dorsal columns were isolated, placed in a chamber, and injured by extradural compression with a clip. Conducting action potentials were activated by supramaximal constant current electrical stimuli and recorded during perfusion with 5-HT agonists and antagonists. After inducing compression injuries, mean action potential amplitudes were reduced to 33.9+/-5.4% of the pre-injury level. After 120 min of perfusion with Ringer's solution, the mean amplitudes recovered to 62.8+/-8.4% of the pre-injury level. At a concentration of 100 micro M, perfusion with tandospirone (a 5-HT1A agonist) resulted in a significantly greater recovery of mean action potential amplitudes at 2 h after the injury (86.2+/-6.9% of pre-injury value) as compared with the control Ringer's solution (62.8+/-8.4% of pre-injury value, P<0.05). In contrast, quipazine (a 5-HT2A agonist) accelerated the decrease of amplitude (54.5+/-11.7% of pre-injury value). 5-HT1A and 5-HT2A agonist did not consistently alter latencies of the action potentials. The 5-HT1A receptor agonist was effective for the recovery of spinal action potential amplitudes in a rat spinal cord injury model.

Postnatal changes in membrane properties of mice trigeminal ganglion neurons.

Intracellular recordings from neurons in the mouse trigeminal ganglion (TG) in vitro were used to characterize changes in membrane properties that take place from early postnatal stages (P0-P7) to adulthood (>P21). All neonatal TG neurons had uniformly slow conduction velocities, whereas adult neurons could be separated according to their conduction velocity into Adelta and C neurons. Based on the presence or absence of a marked inflection or hump in the repolarization phase of the action potential (AP), neonatal neurons were divided into S- (slow) and F-type (fast) neurons. Their passive and subthreshold properties (resting membrane potential, input resistance, membrane capacitance, and inward rectification) were nearly identical, but they showed marked differences in AP amplitude, AP overshoot, AP duration, rate of AP depolarization, rate of AP repolarization, and afterhyperpolarization (AHP) duration. Adult TG neurons also segregated into S- and F-type groups. Differences in their mean AP amplitude, AP overshoot, AP duration, rate of AP depolarization, rate of AP repolarization, and AHP duration were also prominent. In addition, axons of 90% of F-type neurons and 60% of S-type neurons became faster conducting in their central and peripheral branch, suggestive of axonal myelination. The proportion of S- and F-type neurons did not vary during postnatal development, suggesting that these phenotypes were established early in development. Membrane properties of both types of TG neurons evolved differently during postnatal development. The nature of many of these changes was linked to the process of myelination. Thus myelination was accompanied by a decrease in AP duration, input resistance (R(in)), and increase in membrane capacitance (C). These properties remained constant in unmyelinated neurons (both F- and S-type). In adult TG, all F-type neurons with inward rectification were also fast-conducting Adelta, suggesting that those F-type neurons showing inward rectification at birth will evolve to F-type Adelta neurons with age. The percentage of F-type neurons showing inward rectification also increased with age. Both F- and S-type neurons displayed changes in the sensitivity of the AP to reductions in extracellular Ca(2+) or substitution with Co(2+) during the process of maturation.

Differential L-glutamate responsiveness among superficial dorsal horn neurons

1. Intracellular recordings were made from 128 superficial dorsal horn (laminae I and II) neurons in slice preparations of the lumbosacral spinal cord obtained from young hamsters. Stimulation of the segmental dorsal root evoked postsynaptic potentials in all neurons. The average transmembrane resting potential was -61 +/- 1 mV (mean +/- SE; n = 123). The mean action potential amplitude was 75 +/- 1 mV (n = 105) with a duration at half peak of 1.1 +/- 0.1 ms (n = 102). The mean input resistance of these neurons was 72 +/- 4 M omega (n = 125). These values are comparable to those reported in other studies on neurons of this region using penetrating microelectrodes. 2. Bath application of N-methyl-D-aspartate (NMDA; 50 microM) depolarized 67 of 71 (94%) of the tested neurons. Superfusion with the non-NMDA amino acid agonists DL-alpha-amino-3-hydroxy-5-methyl-4- isoxazole propionic acid (AMPA; 20 microM) and kainate (KA; 50 microM) depolarized all tested neurons by > 10 mV. On the other hand, only 13 of 67 (19%) tested neurons were depolarized > 4 mV by superfusion solutions containing 3 mM L-glutamate (Glu). L-Aspartate at 3 mM depolarized three out of seven neurons by > 4 mV and appeared to be equally as effective as Glu. 3. The non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) substantially attenuated the AMPA- and KA-induced depolarizations and partially attenuated the NMDA-induced depolarizations. The NMDA antagonist 3 [(+/-)-2-carboxypiperazin-4-yl]-propyl-1-phosphonic acid (CPP; 50 microM) reversibly blocked the NMDA-induced depolarization in all tested neurons. Glu-induced depolarization was unaffected by CNQX but was attenuated by CPP in three of three tested neurons. These observations indicate that some of the Glu-induced depolarization was mediated by NMDA receptors. 4. CNQX reversibly attenuated excitatory postsynaptic potentials (EPSPs) produced by primary afferent activity in A delta- and C-fibers whereas CPP suppressed only the late EPSP components. Therefore in the neurons sampled, synaptic responses evoked from primary afferent fibers appear to be mediated by both non-NMDA and NMDA receptors. 5. The glutamate uptake inhibitors, L-trans-pyrrolidine-2,4-dicarboxylate (L-trans PDC; 50 microM; n = 6) and threo-3-hydroxy-D-aspartate (1 mM; n = 1) did not have a consistent effect upon Glu action background discharge, RN or Vm in Glu-unresponsive neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

C mechanical nociceptive neurons in the crotaline trigeminal ganglia

Using 32 Crotaline snakes, Trimeresurus flavoviridis, intrasomal recordings were made from 44 neurons of the trigeminal ganglia in vivo. They were 10 C neurons from 9 snakes and 34 A-delta mechanical nociceptive neurons from 23 snakes. 5 of the 10 C neurons were identified as mechanical nociceptive neurons. The neurons were labeled with iontophoretically injected HRP. Each of the 5 C nociceptive neurons had one receptive field, on which 1 spike was elicited by pricking the skin or mucosa with a pin. They were sensitized after repeated stimulation. The fields were insensitive to thermal stimulation. No background discharge was observed. Average conduction velocity was 0.95 m/s (± 0.4 S.D., n = 5). Mean resting potential was −62.5 mV (± 6.0 S.D., n = 4), and mean action potential amplitude was 88.0 mV (± 10.9 S.D., n = 4). Two somata were successfully visualized with HRP (22 μm × 20 μm, 20 μm × 18 μm). Total lengths of labeled axons were 1260 and 1480 μm peripherally to the edge of the section, and 1810 and 770 μm centrally. Neither of the neurons had branching of the peripheral or central axons in the ganglion.

Excitatory and inhibitory effects of serotonin on spinal axons

We studied the effects of serotonin on compound action potentials in dorsal columns isolated from young (nine to 13 days old) rats. Conducting action potentials were activated by submaximal (50%) and supramaximal constant current electrical stimuli and recorded with glass micropipettes. At 10 μM and 100 μM concentrations, serotonin significantly increased mean action potential amplitudes by9.6 ± 6.5% (± S.D., P <0.05) and16.6 ± 12.2% (± S.D., P < 0.005), respectively. Likewise, 10μM and 100μM of quipazine (a serotonhin 2A agonist) increased the amplitudes by9.6 ± 2.5% (± S.D., P < 0.0005) and37.7 ± 8.7% (± S.D., P < 0.0005), respectively. In contrast, 10 μM and 100 μM concentrations of 8-hydroxy-dipropylaminotetralin-hydrobromide (a serotonin 1A agonist) reduced axonal excitability by−9.4 ± 5.5% (±S.D., P <0.05) and−32.9 ± 10.6% (±S.D., P < 0.0005), respectively. At 50 μM concentration, mianserin (a serotonin 2A and serotonin 2C antagonist) eliminated the excitatory effects of 100 μM quipazine dimaleate. The combination of 50 μM mianserin and 100 μM serotonin reduced action potential amplitudes by−5.6 ± 4.9% (±S.D., P < 0.05). These results suggest that serotonin 1A and serotonin 2A receptor subtypes are present on spinal dorsal column axons. These two receptor subtypes have opposing effects on axonal excitability. The ratios and sensitivies of these two axonal receptor subtypes may modulate axonal excitability in rat dorsal column axons and have important implications for both development and injury of axons.

Effects of internal mammary artery dissection on phrenic nerve perfusion and function

The effects of left internal mammary artery (LIMA) dissection and distal division on phrenic nerve perfusion and function were examined in an adult swine model. Phrenic nerve perfusion was determined by left atrial injection of radioactively labeled microspheres. Phrenic nerve function was determined by measuring nerve and diaphragm potentials evoked by bilateral phrenic nerve stimulation. In the first group of animals (n = 9), the LIMA was dissected with ligation of all its branches. Left phrenic nerve perfusion and function decreased after LIMA dissection in every animal studied, whereas only minimal changes were observed on the right. Sixty minutes after LIMA dissection, left phrenic nerve mean perfusion decreased 71%. Left phrenic nerve and left diaphragm mean action potential amplitudes decreased 54% and 80%, respectively. In the second group of animals (n = 4), the LIMA dissection was performed without division of the pericardiacophrenic artery, a small proximal branch of the internal mammary artery that supplies the phrenic nerve. Sixty minutes after LIMA dissection, left phrenic nerve perfusion had decreased by 21% from control values, with a corresponding decrease in left phrenic nerve and diaphragm mean action potential amplitudes of 19% and 23%, respectively. These results indicate that LIMA dissection with division of all its branches in this model is associated with a significant impairment in left phrenic nerve perfusion and function and suggests a causal relationship. These results may also explain the apparent increased phrenic nerve cold sensitivity and increased incidence of phrenic nerve dysfunction associated with LIMA grafting. Compared with the universally advocated method of complete LIMA dissection, sparing the pericardiacophrenic artery during the LIMA dissection significantly improves left phrenic nerve perfusion and function.

Altered invertebrate nerve function after chronic exposure to low concentrations of alcohol.

Previous studies of direct alcohol toxicity on nerve tissue have been carried out using acute, extremely high doses of alcohol. Chronic administration of 20 mM ethanol to the mollusc Aplysia californica was achieved by adding ethanol to surrounding seawater. Although the animals appeared healthy, isolated ganglion cells from treated animals had significantly decreased mean action potential amplitudes and prolonged mean action potential durations compared to controls. These findings suggest that chronic exposure to a low concentration of ethanol comparable to that producing drunkeness in humans may have a direct toxic effect on invertebrate nerve tissue.