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At least 235 records · Page 13Linked to original sources
PubMed2006

High-frequency percussive ventilation improves oxygenation in trauma patients with acute respiratory distress syndrome: a retrospective review.

BACKGROUND: High-frequency percussive ventilation (HFPV), a hybrid of conventional mechanical ventilation and high-frequency oscillatory ventilation, has been used to salvage patients with persistent hypoxemia on conventional mechanical ventilation. We hypothesized that oxygenation would improve in injured patients with severe hypoxemia who were converted to HFPV after initial management with conventional ventilation. METHODS: Chart review identified patients with acute respiratory distress syndrome (ARDS) managed with HFPV. Oxygenation parameters (oxygenation index, OI; Pao(2)/Fio(2) ratio, P/F) and mean airway pressures (mPaw) were recorded at baseline and at 1 to 4, 8 to 12, and 12 to 24 hours after initiation of HFPV. Values at baseline and each time point after conversion to HFPV were compared by using analysis of variance or Kruskal-Wallis tests. RESULTS: Twelve patients, over 24 months, were reviewed. Baseline measurements were OI: 42.2 +/- 33, P/F: 70 +/- 31, (median +/- interquartile range), and mPaw: 29 +/- 8 (mean +/- standard deviation) cm H(2)O. After initiation of HFPV, mPaw did not differ from baseline. There was an improvement in OI (P = .01) from baseline at 12 to 24 hours after initiation of HFPV and in P/F at 12 to 24 hours (P = .002) and 8 to 12 hours (P = .001) after initiation of HFPV. CONCLUSIONS: HFPV may improve oxygenation in patients with ARDS without a concomitant increase in mPaw. A randomized trial of HFPV versus conventional ventilation in trauma patients is needed.

Adult↗
PubMed2006

Lateral fluid percussion injury in the developing rat causes an acute, mild behavioral dysfunction in the absence of significant cell death.

Lateral fluid percussion injury (LFP), a model of mild-moderate concussion, leads to the temporary loss of the capacity for experience-dependent plasticity in developing rats. To determine if this injury-induced loss in capacity for plasticity is due to cell death, we conducted stereological measurements within the cerebral cortex and CA3 of the hippocampus 2 weeks following mild, moderate or severe LFP in the post-natal day 19 (P19) rat. Results indicated that there was no significant change in the absolute number of neurons, regardless of injury severity, in either the ipsilateral cortex (sham = 10.6 +/- 1.7, mild = 11.5 +/- 2.1, moderate = 10.0 +/- 1.0, severe = 10.9 +/- 1.3 million neurons) or CA3 region of the hippocampus (sham = 251 +/- 38, mild = 289 +/- 2, moderate = 245 +/- 48, severe = 255 +/- 62 thousand neurons). Even though there was no evidence of a significant degree of injury-induced cell death, animals exhibited cognitive deficits as revealed in a Morris water maze task (MWM). The MWM results indicated that regardless of injury severity, P19-injured rats exhibited a significant increase in escape latency compared to age-matched shams (injury by day; P < 0.001) and a significant increase in the number of trials needed to reach criterion (P < 0.05). Analysis of a probe trial one week post-MWM training, however, indicated that there was no deficit in storage or recall of the learned behavior as analyzed by platform hits (sham = 2.9 +/- 0.37, mild = 2.0 +/- 0.40, moderate = 1 +/- 0, severe = 2.8 +/- 0.62) or percent time spent in, or immediately surrounding, the platform area (sham = 13.5 +/- 1.71, mild = 10.8 +/- 2.32, moderate = 12.7 +/- 0, severe = 13.5 +/- 1.69). Taken together, these results indicate that while LFP in P19-injured animals does not lead to significant cell death, it does generate acute, mild deficits in MWM performance.

Age Factors↗
PubMed2004

Neuroprotection in the rat lateral fluid percussion model of traumatic brain injury by SNX-185, an N-type voltage-gated calcium channel blocker.

Overload of intracellular calcium ([Ca(2+)](i)) following traumatic brain injury (TBI) has been implicated in the pathogenesis of neuronal injury and death. Voltage-gated calcium channels (VGCCs) provide one of the major sources of Ca(2+) entry into cells. Therefore, the potential neuroprotective activity of SNX-185, a specific N-type VGCC blocker, was tested in rats using the lateral fluid percussion (LFP) model of TBI. SNX-185 (50, 100, or 200 pmol) or vehicle was injected 5 min after injury into the CA2-3 subregion of the hippocampus ipsilateral to TBI. Acute neuronal degeneration was visualized in brain sections 24 h postinjury using the histofluorescent marker Fluoro-Jade (FJ), and the number of surviving neurons in the CA2-3 subregion of the hippocampus 42 days after injury was determined stereologically. Behavioral outcome after TBI and drug treatment was assessed in the beam walk test and Morris water maze. Direct injection of SNX-185 into the CA2-3 region of the hippocampus reduced neuronal injury 24 h after TBI and increased neuronal survival at 42 days at each of the three drug concentrations. Behavioral outcome in both the beam walk and Morris water maze were also improved by SNX-185, with 100 and 200 pmol, but not 50 pmol SNX-185 providing neuroprotection. These data support previous studies demonstrating substantial neuroprotection after TBI by treatment with N-type VGCC blockers.

Animals↗
PubMed2006

Heavy neurofilament accumulation and alpha-spectrin degradation accompany cerebellar white matter functional deficits following forebrain fluid percussion injury.

Evidence for diffuse traumatic axonal injury (TAI) in clinical cases and animal models of traumatic brain injury (TBI) indicate that pathophysiological mechanisms extend to regions remote from the injury epicenter. The potential for indirect cerebellar trauma contributing to TBI pathophysiology is of significance since impairment of motor function and coordination is a common consequence of TBI but is also a domain associated with cerebellar function. The relationship between cerebellar white matter structure and function following traumatic head injury has not been examined. Using the fluid percussion injury (FPI) device applied unilaterally in the forebrain, evoked compound action potential (CAP) recordings from cerebellar white matter of Sprague-Dawley rats indicated a spatial and temporal pattern of electrophysiological deficits throughout the cerebellar vermis. The posterior and middle lobules of the cerebellum exhibited significant declines in evoked CAP amplitude compared to sham controls (p=0.004, p=0.005, respectively). Duration of the CAP decay also increased, suggesting that functional white matter deficits were a combination of axonal loss and compromised axonal integrity. Functional white matter deficits persisted at 14 days post-injury in the posterior and middle regions of the cerebellum. Evidence of heavy chain neurofilament (NF200) degradation was observed at 1 day post-injury by Western blot. Immunohistochemistry labeling for NF200 indicated the presence of highly immunoreactive NF200 axonal swellings consistent with morphological features of TAI. alpha-Spectrin degradation was also observed between 1 and 14 days post-injury. This study demonstrates the electrophysiological consequences of cerebellar white matter injury and a temporal profile of NF200 and spectrin degradation following forebrain FPI.

Action Potentials↗
PubMed2004

Injury-induced alterations in N-methyl-D-aspartate receptor subunit composition contribute to prolonged 45calcium accumulation following lateral fluid percussion.

Cells that survive traumatic brain injury are exposed to changes in their neurochemical environment. One of these changes is a prolonged (48 h) uptake of calcium which, by itself, is not lethal. The N-methyl-D-aspartate receptor (NMDAR) is responsible for the acute membrane flux of calcium following trauma; however, it is unclear if it is involved in a flux lasting 2 days. We proposed that traumatic brain injury induced a molecular change in the NMDAR by modifying the concentrations of its corresponding subunits (NR1 and NR2). Changing these subunits could result in a receptor being more sensitive to glutamate and prolong its opening, thereby exposing cells to a sustained flux of calcium. To test this hypothesis, adult rats were subjected to a lateral fluid percussion brain injury and the NR1, NR2A and NR2B subunits measured within different regions. Although little change was seen in NR1, both NR2 subunits decreased nearly 50% compared with controls, particularly within the ipsilateral cerebral cortex. This decrease was sustained for 4 days with levels returning to control values by 2 weeks. However, this decrease was not the same for both subunits, resulting in a decrease (over 30%) in the NR2A:NR2B ratio indicating that the NMDAR had temporarily become more sensitive to glutamate and would remain open longer once activated. Combining these regional and temporal findings with 45calcium autoradiographic studies revealed that the degree of change in the subunit ratio corresponded to the extent of calcium accumulation. Finally, utilizing a combination of NMDAR and NR2B-specific antagonists it was determined that as much at 85% of the long term NMDAR-mediated calcium flux occurs through receptors whose subunits favor the NR2B subunit. These data indicate that TBI induces molecular changes within the NMDAR, contributing to the cells' post-injury vulnerability to glutamatergic stimulation.

Animals↗
PubMed2004

Effects of mechanical load on flow, volume and pressure delivered by high-frequency percussive ventilation.

High-frequency percussive ventilation (HFPV) has proved its unique efficacy in the treatment of acute respiratory distress, when conventional mechanical ventilation (CMV) has demonstrated a limited response. We analysed flow (V(dot)), volume (V) and airway pressure (Paw) during ventilation of a single-compartment mechanical lung simulator, in which resistance (R) and elastance (E) values were modified, while maintaining the selected ventilatory settings of the HFPV device. These signals reveal the physical effect of the imposed loads on the output of the ventilatory device, secondary to constant (millisecond by millisecond) alterations in pulmonary dynamics. V(dot), V and Paw values depended fundamentally on the value of R, but their shapes were modified by R and E. Although peak Paw increased 70.3% in relation to control value, mean Paw augmented solely 36.5% under the same circumstances (maximum of 9.4 cm H2O). Finally, a mechanism for washing gas out of the lung was suggested.

Airway Resistance↗
PubMed2006

Mechanical loads modulate tidal volume and lung washout during high-frequency percussive ventilation.

High-frequency percussive ventilation (HFPV) has been proved useful in patients with acute respiratory distress syndrome. However, its physiological mechanisms are still poorly understood. The aim of this work is to evaluate the effects of mechanical loading on the tidal volume and lung washout during HFPV. For this purpose a single-compartment mechanical lung simulator, which allows the combination of three elastic and four resistive loads (E and R, respectively), underwent HFPV with constant ventilator settings. With increasing E and decreasing R the tidal volume/cumulative oscillated gas volume ratio fell, while the duration of end-inspiratory plateau/inspiratory time increased. Indeed, an inverse linear relationship was found between these two ratios. Peak and mean pressure in the model decreased linearly with increasing pulsatile volume, the latter to a lesser extent. In conclusion, elastic or resistive loading modulates the mechanical characteristics of the HFPV device but in such a way that washout volume and time allowed for diffusive ventilation vary agonistically.

Airway Resistance↗
PubMed2006

Physiological response to intrapulmonary percussive ventilation in stable COPD patients.

Intrapulmonary percussive ventilation (IPV) is a ventilatory technique that delivers bursts of high-flow respiratory gas into the lung at high rates, intended for treating acute respiratory failure and for mobilization of secretions. We performed a study, aimed at assessing the physiological response to IPV, on patients' breathing pattern, inspiratory effort, lung mechanics and tolerance to ventilation. Ten COPD patients underwent randomized trials of IPV through a face mask at different pressure/frequency combinations (1.2 bar/250 cycles/min; 1.8/250; 1.2/350; 1.8/350), separated by return to baseline (SB), using the IMP2 ventilator. In 5 patients we have also compared the physiological changes of IPV with those obtained during pressure support ventilation (PSV). Minute ventilation did not vary among the trials, but tidal volumes (VT) were significantly greater during 1.2/250, 1.2/350 and 1.8/350 compared to SB. The pressure time product of the diaphragm per minute (PTPdi/min) estimate of the diaphragm oxygen expenditure was also significantly reduced during 1.2/250 and 1.8/250 (209 cmH2O x s/min for SB vs. 143 and 125 for 1.2/250 and 1.8/250, respectively P < 0.05), as well as dynamic intrinsic end-expiratory pressure (PEEPi,dyn). Similar reduction in PTPdi/min were obtained also during PSV. Tolerance to ventilation and oxygen saturation were satisfactory and did not change during the different trials. In 5 normal subjects a prolonged apnea trial lasting > 2 min was also performed, without any significant decrease in SaO2 or subjective discomfort. In conclusion, IPV was able to guarantee an adequate ventilation, while inducing a significant unloading of the diaphragm during the "low-frequency" trials.

Adult↗
PubMed2000

Chronic failure in the maintenance of long-term potentiation following fluid percussion injury in the rat.

Traumatic brain injury (TBI) can produce chronic cognitive learning/memory deficits that are thought to be mediated, in part, by impaired hippocampal function. Experimentally induced TBI is associated with deficits in hippocampal synaptic plasticity (long-term potentiation, or LTP) at acute post-injury intervals but plasticity has not been examined at long-term survival periods. The present study was conducted to assess the temporal profile of LTP after injury and to evaluate the effects of injury severity on plasticity. Separate groups of rats were subjected to mild (1.1-1.4 atm), moderate (1.8-2.1 atm), or severe (2.2-2.7 atm) fluid percussion (FP) injury (or sham surgery) and processed for hippocampal electrophysiology in the first or eighth week after injury. LTP was defined as a lasting increase in field excitatory post-synaptic potential (fEPSP) slope in area CA1 following tetanic stimulation of the Schaffer collaterals. The fEPSP slope was measured for 60 min after tetanus. Assessment of LTP at the acute interval (6 days) revealed modest peak slope potentiation values (129-139%), which declined in each group (including sham) over the hour-long recording session and did not differ between groups. Eight weeks following injury, slices from all groups exhibited robust maximal potentiation (134-147%). Levels of potentiation among groups were similar at the 5-min test interval but differed significantly at the 30- and 60-min test intervals. Whereas sham slices showed stable potentiation for the entire 60-min assessment period, slices in all of the injury groups exhibited a significant decline in potentiation over this period. These experiments reveal a previously unknown effect of TBI whereby experimentally induced injury results in a chronic inability of the CA1 hippocampus to maintain synaptic plasticity. They also provide evidence that sham surgical procedures can significantly influence hippocampal physiology at the acute post-TBI intervals. The results have implications for the mechanisms underlying the impaired synaptic plasticity following TBI.

Animals↗
PubMed2001

Behavioral, electrophysiological, and histopathological consequences of mild fluid-percussion injury in the rat.

Metabolic dysfunction in the relay nuclei of the rat vibrissa circuit follows traumatic brain injury (TBI). This study examined the effects of mild (1.4-1.5 atm) parasagittal fluid-percussion injury on the electrophysiology of this circuit. TBI caused significant reductions in slope and increases in latency of vibrissa-evoked field potentials 3 days after injury. Assessment of open-field swimming revealed an increase in thigmotaxis 2 days after injury. TBI caused mild selective cortical damage and limited axonal swelling at the injury site. Thus mild injury disrupts somatosensory electrophysiology and exploratory behavior.

Afferent Pathways↗
PubMed1997

Hippocampally dependent and independent chronic spatial navigational deficits following parasagittal fluid percussion brain injury in the rat.

Previous reports have documented spatial navigational deficits following experimental traumatic brain injury (TBI), although the majority of the work to date has involved assessment at acute intervals following TBI, and has focused on tasks sensitive to hippocampal dysfunction. The present experiments were designed to investigate the chronic consequences of TBI, and the possible contribution of extrahippocampal dysfunction to TBI-induced spatial navigational deficits, in a moderate parasagittal fluid percussion TBI model. In Experiment 1, animals were pre-trained in a water maze, subjected to TBI or sham procedures, and re-evaluated in the water maze 48 h following the insult. Six to 8 weeks following TBI, the same animals were required to navigate to a different platform location. TBI animals exhibited significant deficits in retention of previously learned spatial information at the 48 h interval, and marginally impaired acquisition of a novel platform location during the chronic test sessions. In Experiment 2, animals were required to navigate to novel spatial locations using cued (to evaluate extrahippocampal function) as well as non-cued variants of the water maze task during the 8 week period following the insult. Injured animals exhibited deficits in both tasks which gradually diminished over the course of testing. The results of these experiments indicate that moderate TBI is accompanied by both retention and acquisition deficits, and that some of the navigational deficits observed in the water maze can be attributed to extrahippocampal damage. The possible recovery of spatial navigational ability following parasagittal TBI at moderate intensities is also discussed.

Acute Disease↗
PubMed1998

Selective loss of hippocampal long-term potentiation, but not depression, following fluid percussion injury.

We investigated the early effects of in vivo fluid percussion injury (FPI) on hippocampal synaptic potentials and excitability. In vitro field potential recordings and immunocytochemistry were performed in the CA1 region in slices from naïve, post-FPI, or sham-operated rats. The following electrophysiological and morphological parameters were affected following FPI: (1) threshold for population spike generation was increased suggesting that post-FPI neurons were hypoexcitable; (2) long-term potentiation (LTP) could not be induced in injured hippocampi; (3) GFAP and inducible NO synthase (iNOS) immunoreactivity were enhanced post-FPI; and (4) following injury, synaptophysin immunoreactivity was enhanced in CA1 stratum radiatum. The effects of FPI on synaptic plasticity were LTP-specific, since long-term depression (LTD) could be equally induced and maintained in post-FPI, sham-operated and control slices. Sham-operated slices were characterized by synaptic excitability indistinguishable from naïve controls, but displayed decreased ability for LTP production and expressed high levels of iNOS. We conclude that FPI causes a selective loss of LTP, possibly due to a previous potentiation induced by trauma as reflected by the increased expression of synaptic proteins. Sham surgical procedures were, however, not without effects on long-term potentiation itself; the latter effects appear to be mediated by an increased production of NO. Our study demonstrates for the first time that hippocampal slices can be used to investigate the correlates of in vivo FPI. Furthermore, we describe LTP-specific deficits in post-traumatic brain injury, suggesting that FPI can selectively erase one of the two main NMDA-dependent forms of synaptic plasticity in the hippocampus.

Animals↗
PubMed1998

Amphetamine administration improves neurochemical outcome of lateral fluid percussion brain injury in the rat.

This study examined the effects of the administration of D-amphetamine on the regional accumulation of lactate and free fatty acids (FFAs) after lateral fluid percussion (FP) brain injury in the rat. Rats were subjected to either FP brain injury of moderate severity (1.9 to 2.0 atm) or sham operation. At 5 min after injury, rats were treated with either d-amphetamine (4 mg/kg, i.p.) or saline. At 30 min and 60 min after brain injury, brains were frozen in situ, and cortices and hippocampi were excised at 0 degrees C. In the saline-treated brain injured rats, levels of lactate were increased in the ipsilateral left cortex and hippocampus at 30 min and 60 min after injury. These increases were attenuated by the administration of D-amphetamine at 5 min after lateral FP brain injury. At 30 and 60 min after FP brain injury, increases in the levels of all individual FFAs (palmitic, stearic, oleic and arachidonic acids) and of total FFAs were also observed in the ipsilateral cortex of the saline-treated injured rats. These increases in the ipsilateral cortex and hippocampus were also attenuated by the administration of d-amphetamine. Neither levels of lactate nor levels of FFAs were increased in the contralateral cortex in the saline-treated injured rats at 30 min or 60 min after FP brain injury. The levels of lactate and FFAs in the contralateral cortex were also unaffected by the administration of D-amphetamine. These results suggest that the attenuation of increases in the levels of lactate and FFAs in the ipsilateral cortex and hippocampus may be involved in the amphetamine-induced improvement in behavioral outcome after lateral FP brain injury.

Animals↗
PubMed2003

Neuroprotection by aminoguanidine after lateral fluid-percussive brain injury in rats: a combined magnetic resonance imaging, histopathologic and functional study.

The present study examined the effects of a selective inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG), on neuronal cell survival and post-traumatic recovery in rats following a lateral fluid percussive brain injury. Daily treatment of AG at the dosage of 100 mg/kg or normal saline was given intraperitoneally into rats starting 2 h before or 30 min after brain injury. Treatment with AG significantly reduced lesion volumes in the brains of rats after injury, as evaluated by high-resolution magnetic resonance imaging (MRI). Immunohistochemical analysis showed a marked induction of iNOS expression in brain macrophages ipsilateral to the injury. Apoptotic neurons were observed in the ipsilateral cerebral cortex by in situ terminal transferase d-UTP nick-end labelling (TUNEL) and caspase-3 immunohistochemistry. In rats receiving prophylactic or post-injury treatment of AG, the number of degenerating neurons was markedly reduced in the cerebrum compared to those receiving saline injection. The location and extent of these pathologic changes correlated with MRI findings. Neurobehavioral studies showed that rotametric performance, grip-strength score, total and ambulatory locomotor responses and acoustic startle response were reduced in rats subjected to the injury but were significantly improved in AG-treated rats. It is suggested that inhibition of iNOS by AG may represent a potential therapeutic strategy for the treatment of traumatic brain injury.

Animals↗
PubMed2000

Development of an air bubble curtain to reduce underwater noise of percussive piling.

Underwater bubbles can inhibit sound transmission through water due to density mismatch and concomitant reflection and absorption of sound waves. For the present study, a perforated rubber hose was used to produce a bubble curtain, or screen, around pile-driving activity in 6-8-m depth waters of western Hong Kong. The percussive hammer blow sounds of the pile driver were measured on 2 days at distances of 250, 500, and 1000 m; broadband pulse levels were reduced by 3-5 dB by the bubble curtain. Sound intensities were measured from 100 Hz to 25.6 kHz, and greatest sound reduction by the bubble curtain was evident from 400 to 6400 Hz. Indo-Pacific hump-backed dolphins (Sousa chinensis) occurred in the immediate area of the industrial activity before and during pile driving, but with a lower abundance immediately after it. While hump-backed dolphins generally showed no overt behavioral changes with and without pile driving, their speeds of travel increased during pile driving, indicating that bubble screening did not eliminate all behavioral responses to the loud noise. Because the bubble curtain effectively lowered sound levels within 1 km of the activity, the experiment and its application during construction represented a success, and this measure should be considered for other appropriate areas with high industrial noises and resident or migrating sound-sensitive animals.

Air↗
PubMed2003

The effects of combined fluid percussion traumatic brain injury and unilateral entorhinal deafferentation on the juvenile rat brain.

The current study was designed to address the effects of traumatic brain injury (TBI) on plasticity and reorganization in the juvenile brain. Given that two of the major pathological sequelae of TBI involve a generalized neuroexcitation insult and diffuse axonal injury, we have employed models of these pathologies, delivered either independently or in combination, to examine their effects on injury-induced synaptic reorganization of the dentate gyrus in the developing rat. Postnatal day 28 rats received either sham, central fluid percussion traumatic brain injury (TBI), unilateral entorhinal cortical lesion (UEC), or TBI+UEC (TUEC) injury. Cognitive performance was assessed in the Morris water maze (MWM) between 11 and 15 days post-injury and the brains were processed for synaptophysin immunohistochemistry and routine electron microscopy. The MWM results revealed that TBI or UEC lesions delivered independently do not produce significant morbidity in P28 rats. However, when these injuries are combined, they reveal significant deficits in the MWM, accompanied by measurable changes in the distribution of presynaptic synaptophysin immunoreactivity over the deafferented dentate molecular layer. These observations are further supported by qualitative ultrastructural alterations in synaptic architecture in the same subregions of the dentate neuropil. The present findings show that the resilience of the immature brain following TBI is reduced when neuroexcitatory insult is combined with deafferentation. Moreover, when deafferented tissue is assessed morphologically, evidence exists for aberrant plasticity and abnormal synaptic reorganization in the juvenile brain.

Animals↗
PubMed2000

Local neutrophil influx following lateral fluid-percussion brain injury in rats is associated with accumulation of complement activation fragments of the third component (C3) of the complement system.

Traumatic brain injury can lead to locally destructive secondary events mediated by several inflammatory components. Following lateral fluid-percussion (FP) brain injury in rats, we examined cortical and hippocampal sections for neutrophil infiltration and accumulation of complement component C3. Neutrophil influx into the brain after injury was detected by an improved myeloperoxidase (MPO) microassay and manual cell counting, while C3 accumulation was detected using immunocytochemistry. MPO levels were elevated in the injured cortical tissue, whereas C3 immunoreactivity was increased in both injured cortical and ipsilateral hippocampal sections. These results show that the FP model of head injury leads to an intense local inflammatory reaction and subsequent tissue destruction.

Animals↗
PubMed2002

Hyperexcitability of hippocampal CA1 neurons after fluid percussion injury of the rat cerebral cortex.

Effects of fluid percussion injury (FPI) of the parietal cerebral cortex on the neuronal activity in the temporal region of the rat hippocampal CA1 area were investigated by using optical and extracellular recording techniques. Application of moderate impact (1.5-2.0 atm) to the parietal cerebral cortex enhanced the optical signal of the neuronal activity in the ipsilateral hippocampal CA1 area. The field potential evoked by the Schaffer collaterals had multiple population spikes in the ipsilateral hippocampal CA1 pyramidal cell layer. Bicuculline (15 microM) increased the amplitude and the number of population spikes of the field potential even after the brain injury. These results suggest that FPI produces hyperexcitability of hippocampal CA1 neurons, probably by increasing the activity of the Schaffer collaterals of hippocampal CA3 neurons.

Action Potentials↗