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At least 469 records · Page 26Linked to original sources
PubMed2004

Eliminating surgical fires: a team approach.

The incidence of surgical fires is rising. One agency estimates that the frequency of surgical fires is comparable to that of wrong-site surgery with an incidence of 50 to 100 fires annually. Anesthetists must assist in the development and implementation of processes that eliminate the disfiguring or deadly results from surgical fires. Understanding the 3 components of fires--heat sources, fuels, and oxidizers--is essential to reduce or eliminate the risk of surgical fires. This AANA Journal course discusses the need for a clearly formulated plan, rehearsing a response to fires in or on the patient, and clearly designated prevention parameters. As part of the surgical team, the vigilance and dedication of nurse anesthetists can lead the efforts to prevent adverse outcomes from surgical fires.

Equipment Safety↗
PubMed2005

[Forest fire spread modeling and 3D visualization in virtual forest landscape].

The traditional method for simulating the behaviors of forest fire is to use a single ellipse to represent all of the fire points in fire scene, which has many disadvantages, e.g., the simulated result is quite different to the real situation, and it is mainly based on 2D. As a result, the represented information is limited. In this paper, the most widely used Rothermel fire spreading model and the principal of Huygen were adopted to simulate the behaviors of forest fire in different position and wind direction, and the results were shown by pseudo-particle system in 3D, which could not only get the area of fire suffering, the direction of fire spreading and the size of fire, but also provide realistic simulation to observers. The method has been successfully applied to Zhangpu forest in Fujian Province.

China↗
PubMed1993

Accidental fires in clinical laboratories.

The National Fire Protection Association, Quincy, Mass, estimates that 169 fires have occurred annually in health care, medical, and chemical laboratories. On the average, there are 13 civilian injuries and $1.5 million per year in direct property damage. Most fires in which the cause or ignition source can be identified originate in malfunctioning electrical equipment (41.6%) or in the facility's electrical distribution system (14.7%). The prevalence of fire safety deficiencies was measured in the College of American Pathologists Laboratory Accreditation Program. Of the 1732 inspected laboratories, 5.5% lacked records of electrical receptacle polarity and ground checks in the preceding year. Of these inspected laboratories, 4.7% had no or incomplete documentation of electrical safety checks on laboratory instruments. There was no evidence of quarterly fire exit drills in 9% of the laboratories. Deficiencies were also found in precautionary labeling (6.8%), in periodic review of safe work practices (4.2%), in the use of safety cans (3.7%), and in venting of flammable liquid storage areas (2.8%). Fire preparedness would be improved if all clinical laboratories had smoke detectors and automatic fire-extinguishing systems. In-service training courses in fire safety should be targeted to the needs of specific service areas.

Fires↗
PubMed1996

Manipulation of pyramidal cell firing in the hippocampus of freely behaving rats by local application of K+ via microdialysis.

In this study, microdialysis was performed in the hippocampus of freely behaving rats, and the firing of pyramidal cells, including place cells, was recorded at the site of the microdialysis probe. For 10-min periods, the artificial cerebrospinal fluid (ACSF) in the microdialysis system was replaced with ACSF containing 50 mM K+ (high K+ solution). Complementary in vitro tests determined that microdialysis with such high K+ solution produced an outflow of 5% of the perfused K+ from the microdialysis probe. Application of K+ with this method into the CA1 region significantly increased the firing of the local pyramidal cells, including place cells, during both movement and sleep. On average, K+ exposures increased the firing rate of the neurons to 306% and 448% of the control firing rate during movement and sleep, respectively. After the termination of the K+ outflow, the cells continued to discharge for 5-30 min with a significantly higher frequency than before the K+ challenge. This phenomenon also occurred in both behavioral states. During the period of enhanced firing, the out-of-field firing rate of the recorded place cells was dramatically increased. It was also found that during the K+ applications, otherwise silent pyramidal cells often became electrically active. The K(+)-induced firing modifications were usually not accompanied by behavioral or EEG changes. The data raise the possibility that transient elevations in the extracellular K+ concentration contribute to the ionic/molecular processes which are responsible for plastic firing pattern modifications in hippocampus. Pharmacological manipulation of place cells with the described method offers a new strategy to understand the molecular bases of spatial memory.

Animals↗
PubMed1996

D1 dopamine receptor stimulation inhibits firing activity of midbrain dopamine neurons in reserpine treated rats: an effect eliminated after hemitransection of diencephalon.

It has been reported that systemic administration of the D1 dopamine (DA) receptor agonist SKF 38393 inhibits the firing rate of substantia nigra pars compacta (SNC, A9) DA neurons after repeated reserpine treatment in locally anesthetized rats, although SKF 38393 induces little effect on the firing of midbrain DA neurons in normal rats. The present study found that local pressure microejection of SKF 38393 (10(-2) M, 20-100 nl) to SNC or substantia nigra pars reticulata (SNR) failed to influence the firing of SNC DA neurons in reserpinized rats (reserpine 1 mg/kg x 6 days, s.c.); subsequent intravenous (i.v.) injection of SKF 38393 (4 mg/kg), however, inhibited their firing and the inhibition was reversed by the D1 receptor antagonist SCH 23390. Similarly, systemic administration of SKF 38393 (4 mg/kg, i.v.) inhibited the firing of ventral tegmental area (VTA, A10) DA cells in reserpinized rats, while local microejection of SKF 38393 (10(-2) M, 30-60 nl) did not affect their firing. Furthermore, the inhibitory effect of systemic SKF 38393 on firing rate of either SNC or VTA DA neurons in reserpinized rats was eliminated after hemitransection of diencephalon. These results suggest that repeated reserpine treatment renders midbrain DA neurons responsive to D1 receptor stimulation and that D1 receptor agonist-induced inhibition of midbrain DA cell firing in reserpinized rats may require the involvement of long-loop feedback pathways.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1999

GABA(A) and GABA(B) antagonists differentially affect the firing pattern of substantia nigra dopaminergic neurons in vivo.

The effects of local pressure application of the selective GABA(A) antagonists, bicuculline, gabazine, and picrotoxin, and the selective GABA(B) antagonists, 2-OH-saclofen and CGP-55845A, on the spontaneous activity of electrophysiologically identified substantia nigra dopaminergic neurons were recorded in vivo in urethane anesthetized rats. Blockade of GABA(A) inputs by bicuculline powerfully and reversibly induced burst firing in dopaminergic neurons along with a modest (25%) increase in firing rate, but the increase in burst firing was not correlated with the increase in firing rate. Picrotoxin and gabazine also produced an increase in burst firing without an increase in firing rate. In contrast, local application of GABA(B) antagonists did not produce bursting but rather caused a modest shift to a more regular firing pattern in 50% of the cases. These data demonstrate that dopaminergic neurons in vivo are under tonic GABAergic inhibition mediated by GABA(A) receptors and suggest that GABAergic afferents to substantia nigra comprise a major pathway by which the firing pattern of dopaminergic neurons is controlled in vivo.

Action Potentials↗
PubMed2002

Correlation between CGRP immunoreactivity and firing activity in cat abducens motoneurons.

A relationship between motoneuron activity and calcitonin gene-related peptide (CGRP) expression was previously suggested based on indirect inferences. We show here a positive correlation between CGRP immunoreactivity and firing activity in an experimental model that used tetanus neurotoxin (TeNT) to alter basal firing levels. A low dose (0.5 ng/kg) of TeNT injected in the lateral rectus muscle raised the basal firing rate of ipsilateral abducens motoneurons, estimated as the firing rate at straight-ahead gaze (F(0)); the firing rate returned to control values after 2 weeks. In contrast, a high dose (5 ng/kg) of TeNT decreased basal firing, which recovered slowly over a 7-week period. Expression of CGRP immunoreactivity by abducens motoneurons, preferentially related to betaCGRP gene expression, was analyzed during these periods of altered firing activity. The number of CGRP-immunofluorescent abducens motoneurons increased to approximately 120% by 7 days after low-dose TeNT, to include all available motoneurons in the nucleus. In addition, the average CGRP immunofluorescence optical density inside motoneurons almost doubled after 4 days and returned toward control values in the following 2 weeks. In contrast, a high-dose injection of TeNT reduced the number of CGRP-immunofluorescent motoneurons to 5.4% of control 7 days post injection, and the number returned to 77.6% after 42 days. CGRP immunofluorescence intensity inside motoneurons was also reduced. Regression analysis of F(0) values with either the number of CGRP-immunolabeled motoneurons, their average immunofluorescence intensity, or both factors combined resulted in positive correlations with regression coefficients of 0.87 or higher. Therefore, CGRP expression and firing activity in abducens motoneurons are positively correlated.

Abducens Nerve↗
PubMed2003

Fire exit is a potential four transmembrane protein expressed in developing Drosophila glia.

Glia from many diverse organisms play a number of important roles during the development of the nervous system. Therefore, knowing the molecules that control glial cell function will further our understanding of the mechanisms that control nervous system development. We have isolated a novel gene in Drosophila melanogaster that is expressed in a subset of the peripheral glia. We call this gene "Fire exit" (Fie), as the glia that express this gene do so during a time when they mark the entry and exit point of axons at the CNS/PNS boundary. This subset of peripheral glia act as intermediate targets during pathfinding and migration of the sensory axons in particular. Fire exit has been cloned and found to encode a novel transmembrane protein. Fire exit belongs to a group of proteins identified in the Drosophila melanogaster and Anopheles gambiae databases which contain four predicted transmembrane domains and a shared intracellular motif. Mutations that remove the fire exit protein have no obvious disruption to glial function. On the other hand, glia expressing the Fire exit gene bridge the transition zone between CNS and PNS and play a role in sensory axon guidance. Therefore, it appears that, while the glia that express this protein mediate axon guidance, Fire exit itself plays a nonessential part in this function. A role for Fire exit in glial development may be suggested by its evolutionary relationship to a family of lysosome-associated proteins called LAPTMs and suggests that Fire exit may function in intracellular transport during glial development.

Amino Acid Sequence↗
PubMed2001

Serotonin (1A) receptor ligands act on norepinephrine neuron firing through excitatory amino acid and GABA(A) receptors: a microiontophoretic study in the rat locus coeruleus.

It was previously shown that the excitatory effect of the 5-HT(1A) agonist 8-OH-DPAT on firing activity of locus coeruleus (LC) norepinephrine (NE) neurons and the inhibitory action of the 5-HT(1A) antagonist WAY 100,635 are dependent on the presence of 5-HT neurons, whereas the inhibitory action of the 5-HT(2) agonist DOI is not. Using in vivo extracellular unitary recordings performed in anesthetized rats, iontophoretic applications of the excitatory amino acid antagonist kynurenate attenuated the enhancement in firing produced by glutamate and kainate. In contrast, GABA applications decreased the firing activity of NE neurons which was attenuated by the enhancement produced by glutamate and kainate. In contrast, GABA applications decreased the firing activity of NE neurons which was attenuated by the GABA(A) receptor antagonist bicuculline. 8-OH-DPAT (10-60 microg kg(-1), i.v.) produced a dose-dependent enhancement in the firing activity of NE neurons that was abolished in the presence of kynurenate application. The selective 5-HT(1A) receptor antagonist WAY 100,635 (100 microg kg(-1), i.v.) suppressed NE firing which was reversed by the selective 5-HT(2A) antagonist MDL 100,907 (200 microg kg(-1), i.v.). In the presence of bicuculline, the inhibitory effect of WAY 100,635 was blunted. These results suggest that WAY 100,635 mainly attenuates NE neuron firing by blocking inhibitory 5-HT(1A) receptors on glutamatergic neurons, thereby enhancing glutamate release and activating excitatory amino acid receptors, possibly of the kainate subtype, on 5-HT terminals. The ensuing increased 5-HT release would then act on excitatory 5-HT(2A) receptors on GABA neurons that would ultimately mediate the inhibition of NE neurons. The prevention of the excitatory action of 8-OH-DPAT on NE neuron firing by kynurenate is also consistent with this neurocircuitry.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2006

Effects of COX-1 and COX-2 inhibitors on the firing of rat midbrain dopaminergic neurons--possible involvement of endogenous kynurenic acid.

Kynurenic acid (KYNA) is an endogenous glutamate-receptor antagonist with a preferential action at the glycine-site of the NMDA-receptor. In the present in vivo study, the importance of brain KYNA to modulate the activity of dopamine (DA) neurons in the ventral tegmental area (VTA) was analyzed by utilizing the decrease in brain KYNA formation induced by the cyclooxygenase (COX)-2 inhibitor parecoxib. A reduction in brain KYNA concentration (39-44%) by parecoxib (25 mg/kg, i.v., 1 h or, i.p., 3.5 h) was associated with a decreased firing rate and burst firing activity. In concordance, an increase in brain KYNA concentration (150-300%), induced by the COX-1 inhibitor indomethacin (50 mg/kg, i.v., 1 h or, i.p., 3.5 h), produced opposite effects, that is, increased firing rate and burst firing activity. The decrease and increase in neuronal firing of VTA DA neurons by the COX-inhibitors was reversed by L-701,324 (antagonist at the NMDA-glycine site; 0.06-2 mg/kg, i.v.) and by D-cycloserine (partial agonist at the NMDA-glycine site; 2-32 mg/kg, i.v.), respectively. In addition, the parecoxib-induced decrease in firing rate and burst firing activity was effectively blocked by pretreatment with kynurenine (5 mg/kg, i.p., 30 min), the immediate precursor of KYNA. Present results suggest that the action of COX-inhibitors on the firing of VTA DA neurons are linked to their effects on KYNA formation and that endogenous KYNA is tonically modulating the neuronal activity of VTA DA neurons. Such a modulatory action of KYNA should be of importance for the functioning of mesocorticolimbic DA pathway.

Action Potentials↗
PubMed1996

Acute toxicity of fire control chemicals to Daphnia magna (Straus) and Selenastrum capricornutum (Printz).

Acute toxicity tests were conducted exposing Daphnia magna Straus (daphnid) in soft and hard reconstituted waters (hardness 42 and 162 mg/liter as CaCO3, respectively), and Selenastrum capricornutum Printz (algae) in ASTM algal assay medium (hardness 15 mg/liter as CaCO3) to fire retardants Fire-Trol GTS-R, Fire-Trol LCG-R, and Phos-Chek D75-F, and foam suppressants Phos-Check WD-881 and Silv-Ex. The chemicals were slightly toxic to practically harmless to daphnids and moderately toxic to algae. Water quality did not consistently alter the toxicity of the test chemicals to daphnids. The most toxic chemical to daphnids was Silv-Ex (48-hr EC50 7 mg/liter in soft and hard waters), whereas the least toxic chemical to daphnids was Fire-Trol LCG-R (48-hr EC50 848 mg/liter in soft water, 813 mg/liter in hard water). The most toxic chemical to algae was Fire-Trol LCG-R (96-hr IC50 10 mg/liter), and the least toxic chemical was Phos-Chek D75-F (96-hr IC50 79 mg/liter). Un-ionized ammonia concentrations near the EC50 or IC50 value in tests with the Fire-Trol compounds were frequently equal to or above reported LC50 un-ionized ammonia concentrations. Un-ionized ammonia concentrations in tests with Phos-Chek D75-F were low, thus other toxic components present in the compounds probably contributed to the toxicity. When compared to the daphnids tested in ASTM soft water, the Fire-Trol compounds were most toxic to algae, whereas Phos-Chek D75-F and the foam suppressants were most toxic to daphnids. The results of these tests are comparable to those obtained from research conducted in other laboratories with the same species and similar chemicals. Accidental entry of fire-fighting chemicals into aquatic environments could adversely affect algae and aquatic invertebrates, thus disrupting ecosystem function.

Ammonia↗
PubMed1990

Firing relations of lateral septal neurons to the hippocampal theta rhythm in urethane anesthetized rats.

The firing of lateral septal neurons was examined in relation to the hippocampal theta rhythm in urethane anesthetized rats. In general, the firing rates of these cells were low during both theta and non-theta EEG states. There was no significant change in firing rate between the two states (theta: 8.5 +/- 9.9 spks/sec; non-theta: 6.0 +/- 5.3). Sixty-four of 68 cells fired simple spikes and 4 cells were found to fire bursts of action potentials (complex-spikes). Approximately 30% (21/65) of the cells showed a significant phase relation to the hippocampal theta rhythm. The preferred phases of firing of these 21 cells were broadly distributed. The possibility that the phase-locked firing of LSN cells is due to the phase-locked firing of hippocampal projection cells is discussed.

Action Potentials↗
PubMed1989

An early outward conductance modulates the firing latency and frequency of neostriatal neurons of the rat brain.

An in vitro slice preparation was used to obtain intracellular recordings of neostriatal neurons. Indirect evidence for the presence of an early outward conductance in neostriatal neurons is presented. With near threshold stimulation neostriatal neurons fired very late during the pulse. The long firing latency was associated with a slow (ramp-like) depolarization. In the presence of TTX the slow depolarization was lost and outward-going rectification dominated the subthreshold response. This finding demonstrated that both, outward- and inward-going conductances play a role during the ramp-like depolarization. Outward-going rectification during depolarizing responses could be further augmented if the depolarizing stimulus was preceded by a conditioning hyperpolarization. A conditioning hyperpolarization prolonged the firing latency and slowed the firing frequency. A conditioning depolarization had opposite effects. After TTX treatment, the response showed a hyperpolarizing "sag" when depolarizing stimulation was preceded by conditioning hyperpolarization. 4-AP (0.5-2.5 mM) blocked the effects of the conditioning hyperpolarization on the firing latency and on the voltage trajectory. 4-AP also disclosed a slow depolarization which could produce neuronal firing very early during the pulse. This depolarization was TTX-sensitive and Co++-insensitive. In contrast to 4-AP, TEA (20 mM) did not produce a reduction in the firing latency but disclosed a membrane oscillatory behavior most probably produced by the interplay of these opposing conductances: the slow inward (probably Na+) and the transient outward (probably K+). Repetitive firing during 4-AP treatment was of the "phasic-tonic" type with an initial burst riding on the initial Co++-insensitive slow depolarization and a somehow irregular train of spikes during the remainder of the stimulation. Action potentials during 4-AP treatment were followed by an afterdepolarization which dominated the initial part of the interspike interval.

Action Potentials↗
PubMed1997

Inhibition of 5-HT cell firing in the DRN by non-selective 5-HT reuptake inhibitors: studies on the role of 5-HT1A autoreceptors and noradrenergic mechanisms.

Improved clinical antidepressant efficacy may result if the acute inhibition of 5-HT cell firing induced by antidepressants is prevented. Here we examined whether inhibition of 5-HT cell firing by non-selective 5-HT uptake inhibiting antidepressant drugs is reversed by a selective 5-HT1A receptor antagonist. In addition, we examined whether concomitant blockade of NA uptake offsets the inhibition of 5-HT cell firing resulting from 5-HT uptake blockade. Antidepressants which block 5-HT uptake (paroxetine, clomipramine, amitriptyline, venlafaxine), all caused dose-dependent and complete inhibition of 5-HT cell firing. Desipramine, a selective NA uptake blocker, caused a slight reduction in firing. The selective 5-HT1A receptor antagonist, WAY 100635, reversed the inhibition of 5-HT cell firing induced by clomipramine, amitriptyline, venlafaxine, and paroxetine, but not that induced by the alpha 1 adrenoceptor antagonist, prazosin. Desipramine, at a dose which increased extracellular NA in the DRN, reversed the effect of prazosin but did not alter the ability of paroxetine to inhibit 5-HT cell firing. Our data indicate that antidepressant drugs with 5-HT uptake blocking properties inhibit 5-HT cell firing via activation of 5-HT1A autoreceptors, and do so irrespective of their effects on NA uptake. These data are discussed in relation to the application of 5-HT1A receptor antagonists to enhance the clinical efficacy of antidepressant drugs.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2005

Firing rates of pallidal neurons are similar in Huntington's and Parkinson's disease patients.

According to the now classical basal ganglia-thalamocortical circuitry model, the chorea of Huntington's disease (HD) and the hypokinesia in Parkinson's disease (PD) are explained by a decrease in the inhibitory output (reduced firing rates) from the globus pallidus internus (GPi) in HD and increased output in PD. Differences between firing patterns might also be a factor contributing to the different symptoms, however. To test the predictions of the model we examined neuronal firing rates and patterns in two HD patients and 14 PD patients. Single-cell, microelectrode recordings were obtained from awake patients undergoing stereotactic surgery for implantation of deep brain stimulating (DBS) electrodes in the GPi. The mean neuronal firing rate in the GPi of HD patients was 81.8+/-4.3 Hz (mean+/-SEM), which was not significantly different from that in PD patients (89.9+/-3.0 Hz). Firing pattern analyses using measurements of burst index, coefficient of variation, and percentage participation of spikes in bursts revealed, however, that GPi neurons in HD patients fired in a more regular pattern (fewer "bursts") than in PD patients. These results suggest that the rate-based model does not adequately explain the motor abnormalities present in the two HD patients studied. Furthermore, the findings did reveal a difference between firing patterns in the HD and PD groups, thereby supporting the role of altered firing patterns in the pathophysiology of these diseases.

Action Potentials↗
PubMed2004

Afterhyperpolarization-firing rate relation of turtle spinal neurons.

This study addressed the afterhyperploarization-firing rate relationship of unanesthetized turtle spinal motoneurons and interneurons. The afterhyperploarization of their solitary action potential at rheobase was compared to that during the cells' minimum and maximum firing rates. Like previous mammalian findings, afterhyperpolarization duration and area at rheobase were 32 and 19% less for high- versus low-threshold motoneurons. Contrariwise, maximum firing rate was two times less for the high-threshold group. Other new findings were that for high- versus low-threshold interneurons, afterhyperpolarization duration and area were 25 and 95% less, and maximum firing rate 21% higher for the high-threshold group. For combined motoneurons versus interneurons, there were no differences in afterhyperpolarization duration and area at rheobase, whereas maximum firing rate was 265% higher for the interneurons. For high-threshold motoneurons alone, there were significant associations between minimum firing rate and afterhyperpolarization duration and area measured at rheobase. In summary, this study showed that (1) the afterhyperploarization values of both turtle spinal motoneurons and interneurons at rheobase provided little indication of their corresponding values at the cells' minimum and maximum firing states, and (2) the evolution of afterhyperploarization from rheobase to maximum firing state differed both qualitatively and quantitatively for motoneurons versus interneurons.

Action Potentials↗
PubMed2003

Voluntary drive-dependent changes in vastus lateralis motor unit firing rates during a sustained isometric contraction at 50% of maximum knee extension force.

The purpose of the present study was to relate the expected inter-subject variability in voluntary drive of the knee extensor muscles during a sustained isometric contraction to the changes in firing rates of single motor units. Voluntary activation, as established with superimposed electrical stimulation was high (range: 91-99%, n=8) during a short maximal contraction, but was lower (range: 69-100%) in most subjects at the point of force failure during a sustained (49.1+/-10.1 s) fatiguing contraction at 50% of maximum force. On a different experimental day the firing behaviour of 27 single motor units was recorded with wire electrodes in the vastus lateralis muscle, 24 of which could be monitored from the time of recruitment to the point of force failure (53.6+/-9.8 s). Motor unit firing behaviour differed considerably among subjects. During the second half of the sustained, fatiguing contraction the changes in firing rate firing rate variability of early recruited units ranged from -10% to +100% and from -50% to +160% respectively among subjects. There were significant positive linear relations between voluntary activation, on the one hand, and rectified surface electromyogram (rsEMG, r=0.82), the changes in motor unit firing rate ( r=0.49) and firing rate variability ( r=0.50) towards the point of force failure on the other. The present data suggest that differences in voluntary drive that appear among subjects during fatigue may be an important determinant of motor unit firing behaviour.

Action Potentials↗
PubMed1999

Spontaneous Na+ and Ca2+ spike firing of cerebellar Purkinje neurons at high pressure.

The effects of high pressure (up to 10.1 MPa) on the spontaneous firing of Purkinje neurons in guinea-pig cerebellar slices were studied using the macropatch clamp technique. Pressure did not significantly alter the single somatic Na+ spike parameters or the frequency of regular Na+ spike firing. When Na+ currents were blocked by 0.5-1 microM tetrodotoxin (TTX), a pressure of 10.1 MPa slightly reduced the dendritic Ca2+ spike amplitude to 90.2+/-3.1% of its control value, and slowed its kinetics. The effects of pressure on the single Ca2+ spike were even less prominent when K+ currents were blocked by 5 mM 4-aminopyridine (4-AP). Pressure prolonged the active period of Ca2+ spike firing to 152.2+/-10.4% of the control value. Within the active period pressure increased the inter-spike interval to 164.9+/-8.7% and suppressed the typical firing of doublets. The latter changes were reversed by a high extracellular potassium concentration ([K+]o) and 1 microM 4-AP, whereas in the presence of 5 mM 4-AP the pattern was insensitive to pressure. A high [Ca2+]o reduced the firing frequency and suppressed doublet firing in a manner reminiscent of the pressure effect, but these changes could not be reversed by 4-AP. A low [Ca2+]o slightly increased the firing of doublets. These results show that the single somatic Na+ spike is insensitive and the dendritic Ca2+ spike is only mildly sensitive to pressure. However, alterations in Ca2+ spike firing pattern suggest that modulation of dendritic K+ currents induce depression of dendritic excitability at pressure.

4-Aminopyridine↗