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Biomedical subjects

L S Leung

Publications and source records attributed to L S Leung.

At least 19 recordsLinked to original sources
PubMed2006

Surgical treatment of penile curvature.

OBJECTIVE: To review long-term efficacy and complications of surgical treatment of penile curvature in a Chinese population. DESIGN: Retrospective review. SETTING: Regional hospital, Hong Kong. PATIENTS. Patients who underwent surgical treatment of penile curvature between January 1997 and March 2005 inclusive. INTERVENTION: Penile curvature corrective surgery. MAIN OUTCOME MEASURES: Penile curvature recurrence, early and late complications. RESULTS: Of 22 patients who underwent surgical treatment of penile curvatures, 19 had congenital and three had acquired diseases. The mean angle of deformity was 52.5 (range, 20-90) degrees. Ten patients had Nesbit procedures, ten had modified Nesbit procedures, and two underwent vein grafting. Twenty patients had residual or recurrent penile curvatures at a mean follow-up of 50.9 months. Fifteen patients had less than 30 degrees curvature and five had 30 to 60 degrees curvature. Early complications included wound infection (n=3), penile skin necrosis (n=1) treated by skin graft, and urethral injury (n=1). Three patients had erectile dysfunction; four complained of glans paraesthesia. Penile shortening (mean, 1.4 cm) and palpable knots were common late complications. A total of 19 patients were satisfied with the final outcomes. CONCLUSIONS: Surgical treatment of penile curvature produces long-term patient satisfaction. Preoperative counselling on potential recurrence and common minor complications is crucial to produce favourable outcomes.

Adult↗
PubMed2004

Altered neurotrophin receptor function in the developing prefrontal cortex leads to adult-onset dopaminergic hyperresponsivity and impaired prepulse inhibition of acoustic startle.

BACKGROUND: Survival and differentiation of neurons and the formation and maintenance of synapses in the cerebral cortex may be affected in schizophrenia. Since neurotrophins play an important role in these events, behavioral effects relevant to schizophrenia were investigated in rats that had compromised neurotrophin function during prefrontal cortical development. METHODS: Neonatal rat pups were injected into the developing prefrontal cortex with a depot preparation of p75 receptor antibody conjugated to saporin. Animals were tested for dopaminergic hyperresponsivity and prepulse inhibition of acoustic startle at 5 or 10 weeks. Neonatal and adult brain sections were examined for morphologic abnormality. RESULTS: Animals that received neonatal injections of p75 antibody conjugated to saporin showed significantly increased amphetamine-induced locomotion and rearing and impairment of prepulse inhibition of acoustic startle at 10 weeks of age but not at 5 weeks. Examination of adult brain sections revealed apparently normal structure, whereas neonatal brain sections showed apoptotic cells in the developing prefrontal cortex in pups that received p75 antibody conjugated to saporin. CONCLUSIONS: Compromised p75 neurotrophin receptor function in the developing prefrontal cortex may be associated with the manifestation of adult-onset dopaminergic hyperresponsivity and impaired prepulse inhibition and therefore may be involved in the pathogenesis of schizophrenia.

Acoustic Stimulation↗
PubMed2003

Increased dendritic excitability in hippocampal ca1 in vivo in the kainic acid model of temporal lobe epilepsy: a study using current source density analysis.

We used kainic acid in rats as an animal model of temporal lobe epilepsy, and studied the synaptic transmission in hippocampal subfield CA1 of urethane-anesthetized rats in vivo. Dendritic currents were revealed by field potential mapping, using a single micropipette or a 16-channel silicon probe, followed by current source density analysis. We found that the population excitatory postsynaptic potentials in the basal dendrites and distal apical dendrites of CA1 were increased in kainate-treated as compared with control rats following paired-pulse, but not single-pulse, stimulation of CA3b or medial perforant path. In contrast, the trisynaptic midapical dendritic response in CA1 following medial perforant path stimulation was decreased in kainate-treated as compared with control rats. Increased coupling between excitatory postsynaptic potential and the population spike in CA1 was found after kainate seizures. Short-latency, presumably monosynaptic CA1 population spikes following medial perforant path stimulation was found in kainate-treated but not control rats. An enhancement of dendritic excitability was evidenced by population spikes that invaded into or originated from the distal apical dendrites of CA1 in kainate-treated but not control rats. Reverberation of hippocampo-entorhinal activity was evidenced by recurrent excitation of CA1 following CA3b stimulation in kainate-treated but not control rats. Blockade of inhibition by intraventricularly administered bicuculline induced excitatory potentials in CA1 that were stronger and more prolonged in kainate-treated than control rats. The bicuculline-induced excitation was mainly blocked by non-N-methyl-D-aspartate receptor antagonists. We conclude that kainate seizures induced disinhibition in CA1 that unveiled excitation at the basal and distal apical dendrites, resulting in enhancement of the direct entorhinal cortex to CA1 input and reverberations via the hippocampo-entorhinal loop. These changes in the output of the hippocampus from CA1 are likely detrimental to the behavioral functions of the hippocampus and they may contribute to increased seizure susceptibility after kainate seizures.

Action Potentials↗
PubMed2003

Temporal lobe seizures alter the amplitude and timing of rat behavioral rhythms.

Daily rhythms of spontaneous locomotor activity (SLA) in rats were studied before and after an episode of pilocarpine-induced convulsive status epilepticus (SE). A pronounced increase in activity levels during both the light and dark phases was found 1 week after SE as compared with baseline SLA and controls administered saline. Rats with bilateral lesions of the nucleus accumbens (shell) did not exhibit any significant change in SLA 1 week after SE compared with controls. We suggest that during the first week after SE the increase in SLA was induced by abnormal neuronal activity in the hippocampus driving a descending limbic-motor pathway via the nucleus accumbens. EEG recordings revealed high-amplitude interictal spikes in hippocampal CA1. During subsequent weeks, SLA rhythms of nonlesioned chronic epileptic rats remained elevated but progressively normalized over a period of 12 weeks. Although both chronic epileptic and control groups displayed near-24-hour activity patterns under light-dark conditions, significant delays (>4 hour) in acrophase were observed after spontaneous seizures had developed. The phase delay was positively correlated with seizure history and likely the result of postictal hyperactivity associated with seizures during the normal rest period. Despite these changes, cell density in the suprachiasmatic nucleus (SCN) and intergeniculate leaflet (IGL) did not differ significantly between epileptic and control groups. In the absence of damage to brain areas directly involved with the regulation of behavioral rhythms, chronic seizure activity presumably alters the timing of activity patterns through a nonphotic mechanism, perhaps involving activation of the SCN or IGL during limbic seizures.

Animals↗
PubMed2001

Enhanced but fragile inhibition in the dentate gyrus in vivo in the kainic acid model of temporal lobe epilepsy: a study using current source density analysis.

Temporal lobe epilepsy is related to many structural and physiological changes in the brain. We used kainic acid in rats as an animal model of temporal lobe epilepsy, and studied the neural interactions of the dentate gyrus in urethane-anesthetized rats in vivo. Our initial hypothesis was that sprouting of mossy fibers, the axons of the granule cells, increases proximal dendritic excitatory currents in the inner molecular layer of the dentate gyrus. Extracellular currents were detected in vivo using current source density analysis. Backfiring the mossy fibers in CA3 or orthodromic excitation of the granule cells through the medial perforant path induced a current sink at the inner molecular layer. However, the sink or inferred excitation at the inner molecular layer was not increased in kainic acid-treated rats and the sink actually correlated negatively with the degree of mossy fiber sprouting. It is inferred that the latter sink was mediated mainly by association fibers and not by recurrent mossy fibers. After kainic acid treatment, paired-pulse inhibition of the population spikes in the dentate gyrus was increased. In contrast, reverberant activity that involved looping around an entorhinal-hippocampal circuit was increased in kainic acid-treated rats, compared to control rats. The increase of inhibition in kainic acid-treated rats was readily blocked by a small dose of GABA(A) receptor antagonist bicuculline. The latter dose of bicuculline induced paroxsymal spike bursts in kainic acid-treated but not control rats, demonstrating that the increased inhibition in dentate gyrus was fragile. In conclusion, after kainic acid induced seizures, the dentate gyrus in vivo showed an increase in inhibition that appeared to be fragile. The hypothesized increase in proximal dendritic excitation due to mossy fiber sprouting was not detected. However, the fragile inhibition could explain the seizure susceptibility in patients with temporal lobe epilepsy.

Animals↗
PubMed2001

Diurnal variation in pilocarpine-induced generalized tonic-clonic seizure activity.

The efficacy of the cholinergic agonist pilocarpine to evoke generalized seizures in rats was examined over the 24-h photocycle. Both seizure latency and severity during the 24-h period exhibited marked diurnal variation. Seizure activity generalized more rapidly throughout the dark phase and was often characterized by wild running clonus and tonic extensor convulsions. In contrast, electrographic seizures during the light phase were mainly associated with facial/forelimb clonus and rearing typical of pilocarpine-induced seizures. These data suggest that the sensitivity of the rodent brain to pilocarpine exhibits day-night variation and seizure activity induced during the dark phase may generalize via the brainstem.

Animals↗
PubMed2001

Apical and basal orthodromic population spikes in hippocampal CA1 in vivo show different origins and patterns of propagation.

There is controversy concerning whether orthodromic action potentials originate from the apical or basal dendrites of CA1 pyramidal cells in vivo. The participation of the dendrites in the initialization and propagation of population spikes in CA1 of urethan-anesthetized rats in vivo was studied using simultaneously recorded field potentials and current source density (CSD) analysis. CSD analysis revealed that the antidromic population spike, evoked by stimulation of the alveus, invaded in succession, the axon initial segment (stratum oriens), cell body and approximately 200 microm of the proximal apical dendrites. Excitation of the basal dendrites of CA1, following stimulation of CA3 stratum oriens, evoked an orthodromic spike that started near the cell body or initial segment and then propagated approximately 200 microm into the proximal apical dendrites. In contrast, the population spike that followed excitation of the apical dendrites of CA1 initiated at the proximal apical dendrites, 50-100 microm distal to the cell body layer, and then propagated centripetally to the cell body and the proximal basal dendrites. A late apical dendritic spike may arise in the mid-apical dendrites (250-300 microm from the cell layer) and propagated distally. The origin or the pattern of propagation of each population spike type was similar for near-threshold to supramaximal stimulus intensities. In summary, population spikes following apical dendritic and basal dendritic excitation in vivo appeared to originate from different locations. Apical dendritic excitation evoked a population spike that initiated in the proximal apical dendrites while basal dendritic excitation evoked a spike that started near the initial segment or cell body. An original finding of this study is the propagation of the population spike from basal to apical dendrites in vivo or vice versa. This backpropagation from one dendritic tree to the other may play an important role in the synaptic plasticity among a network of CA3 to CA1 neurons.

Action Potentials↗
PubMed2000

Relation between hippocampal gamma waves and behavioral disturbances induced by phencyclidine and methamphetamine.

The relationship between hippocampal electrical activity and behavioral hyperactivity induced by either phencyclidine (PCP) or methamphetamine (MAP) was examined in freely behaving rats. The EEGs at the hippocampal CA1 region were simultaneously recorded with the animal's behavior for 2 h after administration of either PCP or MAP. PCP (10 mg/kg, intraperitoneal (i.p.)) significantly increased locomotor activity including rearing, walking, head-weaving and circling. Spectral analysis of the EEG showed that hippocampal gamma waves (30-70 Hz), but not other frequency bands, were significantly increased from 5 to 120 min after systemic injection of PCP. Inactivation of the medial septum with muscimol, a gamma-aminobutyric acid receptor A agonist, 15 min prior to injection of PCP, suppressed both hippocampal gamma waves and locomotor activity. MAP (1.5 mg/kg, i.p.) also increased locomotor activity for longer than 2 h. During the behavioral hyperactivity induced by MAP, hippocampal EEG showed θ and gamma rhythms that were not significantly different from those during walking before MAP. However, MAP-induced behavioral activity was suppressed by pre-injection of muscimol in the medial septum, which also decreased hippocampal gamma activity. It is suggested that the medial septum plays a role in mediating behavioral disturbances induced by both PCP and MAP through control of the hippocampal electrical activity, and that hippocampal gamma waves may play a permissible role in the expression of behaviors.

Animals↗
PubMed2000

Excitability of rat dentate gyrus granule cells in vivo is controlled by tonic and evoked GABA(B) receptor-mediated inhibition.

Tonic or evoked gamma-aminobutyric acid(B) (GABA(B)) receptor-mediated modulation of dentate gyrus excitability was evaluated in vivo in urethane-anesthetized rats. Two stimuli at an interpulse interval (IPI) of 10-9000 ms were given to the medial perforant path. Population excitatory postsynaptic potentials (pEPSPs) and population spikes (PSs) were recorded in the dentate gyrus using a glass micropipette or a multichannel silicon probe. The GABA(B) receptor antagonist CGP35348, delivered intracerebroventricularly (i.c.v.) or locally, caused a significant increase in the PS amplitude evoked by the first pulse (PS1) without an increase in either the slope or current sink of the population EPSP evoked by the first pulse (pEPSP1). The average spontaneous firing rate of putative granule cells was also increased following i. c.v. CGP35348. The PS evoked by the second pulse (PS2) relative to PS1 (PS2/PS1) was consistently suppressed at IPIs from 30 to 70 ms, even when PS1 was matched before and after CGP35348. CGP35348 increased PS1 mainly by blocking tonic postsynaptic GABA(B) receptors and decreased PS2 at 30-70 ms IPI by blocking presynaptic GABA(B) autoreceptors. These data suggest that GABA(B) receptors are tonically active in the dentate gyrus in vivo.

Action Potentials↗
PubMed2000

Behaviors induced or disrupted by complex partial seizures.

We reviewed the neural mechanisms underlying some postictal behaviors that are induced or disrupted by temporal lobe seizures in humans and animals. It is proposed that the psychomotor behaviors and automatisms induced by temporal lobe seizures are mediated by the nucleus accumbens. A non-convulsive hippocampal afterdischarge in rats induced an increase in locomotor activity, which was suppressed by the injection of dopamine D(2) receptor antagonist in the nucleus accumbens, and blocked by inactivation of the medial septum. In contrast, a convulsive hippocampal or amygdala seizure induced behavioral hypoactivity, perhaps by the spread of the seizure into the frontal cortex and opiate-mediated postictal depression. Mechanisms underlying postictal psychosis, memory disruption and other long-term behavioral alterations after temporal lobe seizures, are discussed. In conclusion, many of the changes of postictal behaviors observed after temporal lobe seizures in humans may be found in animals, and the basis of the behavioral change may be explained as a change in neural processing in the temporal lobe and the connecting subcortical structures.

Animals↗
PubMed2000

Effects of propofol on hippocampal synaptic transmission in behaving rats.

BACKGROUND: The action of propofol has been studied in vitro and in vivo, but the effects of intravenously administered propofol on synaptic transmission in freely behaving rats have not been studied before. METHODS: Rats were implanted with recording electrodes in the dentate gyrus and with stimulation electrodes in the medial perforant path (MPP). Paired pulses at different interpulse intervals (IPIs) were delivered to the MPP, and average evoked potentials were recorded in the dentate gyrus before and after a bolus of propofol (10 or 20 mg/kg administered intravenously) or control vehicle was injected via femoral vein cannula. Because of the layered structure of the hippocampus, population excitatory postsynaptic potentials and population spikes could be distinguished and analyzed. RESULTS: Propofol has no significant effect on the population excitatory postsynaptic potentials or population spike evoked by a single MPP stimulus pulse. However, paired-pulse inhibition of the dentate population spikes was increased at IPI of 20 and 30 ms. Paired-pulse inhibition of the population spike was most prominent when tail pinch response was lost (deep and moderate anesthesia), but it persisted during light anesthesia. At 200 ms IPI, paired-pulse facilitation of population spikes was observed during moderate anesthesia in most rats. CONCLUSIONS: In freely behaving rats, intravenous propofol enhanced paired-pulse inhibition at < 50 ms IPI, likely by enhancing gamma-aminobutyric acid A receptor-mediated inhibition. Propofol also increased paired-pulse facilitation at 200 ms IPI through an unknown mechanism, which may contribute to the neuroexcitatory effect of propofol.

Anesthesia, Intravenous↗
PubMed2000

Physiology of the entorhinal and perirhinal projections to the hippocampus studied by current source density analysis.

Evoked field potentials and current-source-density analysis were used to study the olfactory, entorhinal, and perirhinal projections to the hippocampus. In urethane-anesthetized rats, various structures were electrically stimulated, and evoked potentials were mapped using glass micropipettes or multichannel silicon probes. Stimulation of the olfactory bulb, lateral olfactory tract, piriform cortex, amygdala-entorhinal transition, lateral entorhinal cortex, or lateral perforant path (LPP) evoked an outer molecular layer sink (inferred distal dendritic excitation) in the dentate gyrus, with progressively decreasing onset latency. Medial perforant path (MPP) stimulation evoked a middle molecular layer sink (mid-dendritic excitation) in the dentate gyrus. LPP and MPP were also inferred to monosynaptically excite the distal dendrites of CA3, often resulting in a population spike in CA3. CA3 spiking, in turn, was often followed by excitation at the inner molecular layer of the dentate gyrus. LPP and MPP evoked distal dendritic sinks but no population spikes in CA1. Stimulation of the perirhinal cortex activated a sink in the subiculum/CA1 border without activating the dentate gyrus. In addition, reverberatory activity through a hippocampal-entorhinal-hippocampal pathway may be activated by MPP or CA3 stimulation. It is suggested that the parallel projections of the entorhinal and perirhinal inputs to the distal dendrites of hippocampal principal neurons enhance local and distributed processing as characterized by CA3 to dentate gyrus feedback, and hippocampal-entorhinal reverberation.

Afferent Pathways↗
PubMed1999

N-methyl-D-aspartate receptor antagonists are less effective in blocking long-term potentiation at apical than basal dendrites in hippocampal CA1 of awake rats.

Long-term potentiation (LTP) of field excitatory postsynaptic potentials (fEPSPs) at the apical or basal dendrites of CA1 pyramidal cells was induced by stimulation with a 1-s train of 200-Hz pulses in awake rats, with or without the presence of various doses of an N-methyl-D-aspartate (NMDA) receptor antagonist. Apical LTP was blocked by an intracerebroventricular (i.c.v.) dose of 40 microg D-2-amino-5-phosphonopentanoic acid (D-AP5) or 20 mg/kg i.p. D-2-amino-4-methyl-5-phosphono-3-pentanoic acid (CGP-40116), whereas basal LTP was blocked by half the dose of D-AP5 or CGP-40116. The noncompetitive antagonist MK-801 (< or =1 mg/kg i.p.) had no significant effect on apical LTP. Apical LTP was not blocked by i.c.v. nifedipine. The effect of an NMDA receptor antagonist alone on apical and basal fEPSPs was also evaluated, to assess the net effect of the NMDA receptor antagonist in blocking LTP. MK-801 (0.5-1 mg/kg i.p.) or CGP-40116 (10-20 mg/kg i.p.) but not D-AP5 suppressed apical fEPSPs for several hours and confounded the expression of apical LTP during this time. We concluded that hippocampal LTP at different synapses has different sensitivity to NMDA receptor antagonists and that a general blockade of hippocampal NMDA receptor functions cannot be inferred by a single hippocampal LTP measure.

2-Amino-5-phosphonovalerate↗
PubMed1998

Monosynaptic activation of CA3 by the medial perforant path.

The functional projection of the medial perforant path (MPP) to different CA3 subfields was studied in urethan-anesthetized rats using current source density analysis. MPP stimulation resulted in an early-latency (presumed monosynaptic) sink with onset of 2-3 ms at the distal apical dendritic layer of CA3 (stratum lacunosum molecule) and a long-latency (presumed disynaptic, >7 ms) sink at stratum lucidum and radiatum of CA3. The population spike (onset 5. 3-6.1 ms), a sink at CA3 pyramidal cell layer, was observed 67% of the time (12 of 18 rats) in CA3a, 44% (8 of 18) in CA3b and 58% (7 of 12 rats) in CA3c following MPP stimulation. Population spike was not observed during presumed disynaptic excitation of CA3. Both early-latency sink (excitatory postsynaptic potential) and population spike in CA3 revealed robust paired-pulse facilitation (PPF). In contrast, little PPF was found for the MPP-evoked excitatory sink at the middle molecular layer of the dentate gyrus. The data suggested that the entorhinal cortex provides a strong monosynaptic excitation of different subfields of CA3. A direct entorhinal to CA3 input bypasses the dentate gyrus and may play a role in normal hippocampal signal processing and neural plasticity.

Action Potentials↗
PubMed1998

Functional interconnections between CA3 and the dentate gyrus revealed by current source density analysis.

The physiological interactions between the dentate gyrus (DG) and CA3 were studied in urethane-anesthetized rats by using field potential recording and current source density (CSD) analysis. Stimulation of CA3b resulted in a short-latency (<2.5-ms onset latency) antidromic population spike in both the DG and CA3c. An excitation (current sink) at the middle molecular layer (MML) was observed at 3-ms latency, possibly mediated by the backfiring of perforant path fibers that projected to both DG and CA3. CA3 stimulation also resulted in a sink at the dendritic layers of CA3c, which was likely mediated by excitatory CA3 recurrent collaterals. It was inferred that the DG was excited at the inner molecular layer (IML) after stimulation near the CA3b/CA3c border. This IML excitation (sink) probably resulted from orthodromic CA3 or hilar projections to the IML and not from mossy fiber backfiring. The IML and the CA3c dendritic sinks were blocked by an intracerebroventricular injection of a non-N-methyl-D-aspartate receptor antagonist, 6-cyano-7-nitroquinoxaline-2, 3-dione, but not by a gamma-aminobutyric acid type A (GABA(A)) receptor antagonist, bicuculline. CA3b stimulation evoked population spike bursts (3-7-ms latency) in both DG and CA3c when GABA(A) inhibition was suppressed by bicuculline, thus confirming that the excitatory afferents project from CA3b to DG and CA3c. A CA3 conditioning stimulus pulse given 30-200 ms before a perforant-path test pulse increased the amplitude of the perforant-path-evoked DG population spike (as compared with the test response without conditioning). After a moderate-intensity stimulation of CA3, a late (<20-ms latency) excitation of the MML of the DG was found. The late DG excitation was blocked by procaine injection at the medial perforant path, suggesting its origin from the medial entorhinal cortex. In conclusion, rich interactions between CA3 and other hippocampal structures were studied quantitatively by CSD analysis in vivo. We infer that CA3 provides an early excitatory feedback path to DG through recurrent collaterals or hilar interneurons and a late feedback through the medial entorhinal cortex.

Animals↗
PubMed1998

Generation of theta and gamma rhythms in the hippocampus.

In the behaving rat, theta rhythm was dominant during walking and rapid-eye-movement sleep, while irregular slow activity predominated during immobility and slow-wave sleep. Oscillatory evoked potentials of 20-50 Hz and spontaneous fast (gamma) waves were more prominent during theta compared with non-theta behaviors. The oscillations were simulated by a systems model with recurrent inhibition. The model also predicts a behaviorally dependent inhibition, which was confirmed experimentally using paired-pulse responses. Paired-pulse facilitation (PPF) of the population spikes in CA1 was larger during walking than immobility, mostly mediated by a cholinergic input. Spike responses in vitro were characterized by a relative lack of inhibition or disinhibition compared with the behaving rat. The two-input, two-dipole model of the theta rhythm in CA1 is reviewed. Afferents to the CA1 pyramidal cells are assumed to be rhythmic and consist of atropine-sensitive and atropine-resistant inputs driving the somata and distal dendrites, respectively. The atropine-sensitive theta rhythm was mainly caused by a series of Cl- mediated inhibitory postsynaptic potentials (IPSPs) on pyramidal cells. It is suggested that previous claims of the participation of excitatory postsynaptic potentials (EPSPs) and not IPSPs in the intracellular recordings in vivo were flawed. Single cell recordings in vitro suggested that intrinsic voltage-dependent membrane potential oscillations modulate the response to a theta-frequency driving. Membrane potentials of pyramidal cells in vitro showed resonance in the theta frequency range.

Animals↗
PubMed1998

Theta-frequency resonance in hippocampal CA1 neurons in vitro demonstrated by sinusoidal current injection.

Sinusoidal currents of various frequencies were injected into hippocampal CA1 neurons in vitro, and the membrane potential responses were analyzed by cross power spectral analysis. Sinusoidal currents induced a maximal (resonant) response at a theta frequency (3-10 Hz) in slightly depolarized neurons. As predicted by linear systems theory, the resonant frequency was about the same as the natural (spontaneous) oscillation frequency. However, in some cases, the resonant frequency was higher than the spontaneous oscillation frequency, or resonance was found in the absence of spontaneous oscillations. The sharpness of the resonance (Q), measured by the peak frequency divided by the half-peak power bandwidth, increased from a mean of 0.44 at rest to 0.83 during a mean depolarization of 6.5 mV. The phase of the driven oscillations changed most rapidly near the resonant frequency, and it shifted about 90 degrees over the half-peak bandwidth of 8.4 Hz. Similar results were found using a sinusoidal function of slowly changing frequency as the input. Sinusoidal currents of peak-to-peak intensity of >100 pA may evoke nonlinear responses characterized by second and higher harmonics. The theta-frequency resonance in hippocampal neurons in vitro suggests that the same voltage-dependent phenomenon may be important in enhancing a theta-frequency response when hippocampal neurons are driven by medial septal or other inputs in vivo.

Action Potentials↗