Abnormality in re-programing of preparatory muscle activity for landing following unpredictable events in patients with anterior cruciate ligament injury.

BACKGROUND: Anterior cruciate ligament deficiency (ACL-D) causes dysfunction in the quadriceps femoris muscle, and this dysfunction hampers a safe return to sports. However, how the dysfunctional quadriceps femoris muscle affects instantaneous re-programming of motor command in response to unpredictable events remains unknown. This study aimed to examine the effects of ACL-D on re-programming of preparatory muscle activity during an unpredictable landing task. METHODS: Eighteen patients with ACL-D and 20 healthy participants (controls) performed normal landing and surprise landing tasks. In the surprise landing task, a false floor, designed to dislodge easily under load, was positioned in the middle of the descent path. This setup causes participants to unpredictably fall through the false floor onto the actual landing surface. Electromyography data collected during the period after passing through the false floor until landing was segmented into two equal halves. The average electromyography amplitude for each muscle in each period was compared between patients and controls. RESULTS: In the vastus medialis and rectus femoris during the surprise landing task, the average electromyography amplitude during only the second half period in patients with ACL-D was significantly smaller than that in controls (p = 0.011 and 0.004, respectively). CONCLUSIONS: Abnormalities were detected in the re-programming of preparatory muscle activation during an unpredictable landing task in the vastus medialis and rectus femoris of patients with ACL-D. The surprise landing task used in the present study has the potential to become a diagnostic tool to evaluate readiness for safely returning to sports.

Primate retina trades single-photon detection for high-fidelity contrast encoding.

How the spike output of the retina enables human visual perception is not fully understood. Here, we address this at the sensitivity limit of vision by correlating human visual perception with the spike outputs of primate ON and OFF parasol (magnocellular) retinal ganglion cells in tightly matching stimulus conditions. We show that human vision at its ultimate sensitivity limit depends on the spike output of the ON but not the OFF retinal pathway. Consequently, nonlinear signal processing in the retinal ON pathway precludes perceptual detection of single photons in darkness but enables quantal-resolution discrimination of differences in light intensity.

Tactile stimulation restores inhibited stretch reflex attributable to attenuation of Ia afferents during surprise landing.

Arthrogenic muscle inhibition (AMI) is induced by pathological knee conditions. The present study aimed to investigate the effect of tactile stimulation on reflex changes induced by simulated AMI during unpredictable landing performances. Twenty participants performed six unilateral landing tasks: 15 cm normal landing (15NL), 30 cm normal landing (30NL), surprise landing (SL), 30 cm normal landing following vibration (30NLV), SL following vibration (SLV), and SL following vibration with Kinesiology tape (SLK). For SL, the solid landing platform (15 cm) was removed and replaced by a false floor. Since the false floor dislodged easily under load, participants unpredictably fell through the platform to the actual landing surface 15 cm below. After completing 15NL, 30NL, and SL, vibration was applied to participants' knees to induce neurological changes similar to AMI. After vibration, participants performed 30NLV, SLV, and SLK in a random order. EMG signals in the post-landing short latency (31-60 ms) and medium latency (61-90 ms) periods were examined. EMG signals from the vastus lateralis (VL), vastus medialis (VM), and biceps femoris (BF) were recorded and compared between tasks. EMG signals of all muscles in SL were significantly enhanced in the medium latency period as compared with 30NL. Enhanced EMG signals in SL were suppressed by vibration stimulation in the VL, but the suppressed EMG signals were restored after cutaneous stimulation with Kinesiology tape (p < 0.01). Our findings suggest that AMI could alter motor control patterns during unpredictable landing and that tactile stimulation could restore the altered motor control to a normal state.

Long-term wheel-running prevents reduction of grip strength in type 2 diabetic rats.

Diabetic skeletal muscles show reduced contractile force and increased fatigability. Hands are a target for several diabetes-induced complications. Therefore, reduced handgrip strength often occurs as a consequence of diabetes. The aim of this study was to examine whether long-term exercise can prevent reduction of grip strength in type 2 diabetes mellitus (T2DM) model OLETF rats, and to explore the mechanisms underlying diabetes-induced grip strength reduction. Ten 5-week-old OLETF rats were used as experimental animals, and five non-diabetic LETO rats as controls of OLETF rats. Half OLETF rats performed daily voluntary wheel-running for 17 months (OLETF + EXE), and the rest of OLETF and LETO rats were sedentary. Grip strength was higher in OLETF + EXE and LETO groups than in OLETF group. OLETF group with hyperglycemia showed an increase in HbA1c, serum TNF-α, and muscle SERCA activity, but a decrease in circulating insulin. Each fiber area, total fiber area, and % total fiber area in type IIb fibers of extensor digitorum longus muscles were larger in OLETF + EXE and LETO groups than in OLETF group. There was a positive correlation between grip strength and the above three parameters concerning type IIb fiber area. Therefore, type IIb fiber atrophy may be the major direct cause of grip strength reduction in OLETF group, although there seems multiple etiological mechanisms. Long-term wheel-running may have blocked the diabetes-induced reduction of grip strength by preventing type IIb fiber atrophy. Regular exercise may be a potent modality for preventing not only the progression of diabetes but muscle dysfunction in T2DM patients.

Parasympathetic nervous activity is associated with oxytocin in multiparous, but not primiparous, women during the perinatal period.

Oxytocin (OXT) is thought to have antidepressant/anxiolytic effects in postpartum women. Primiparous women tend toward an attenuated lactation compared with multiparous women. However, so far, little is known about the relationship between OXT and autonomic nervous activity (ANA) in perinatal women and whether it may be different in primiparous and multiparous women. Therefore, the objective of this study was to answer this question by determining both ANA and salivary OXT levels in primiparous and multiparous perinatal women. In 18 primiparous and 18 multiparous women, who underwent a physical and physiological examination, ANA measurement by heart rate variability and saliva sampling were performed during the perinatal period. Saliva OXT concentration was determined by a highly sensitive ELISA. OXT release into saliva was obtained from multiplying saliva OXT concentration by saliva flow rate. In the postpartum period, multiparous women had higher parasympathetic nervous activity (PNA) and lower physical stress index (PSI) compared with primiparous women. Furthermore, multiparous postpartal women had higher OXT compared with primiparous or multiparous prepartal women. In addition, in multiparous perinatal women, OXT correlated positively with PNA, but negatively with PSI. These results suggest that after parturition, multiparous mothers may switch over to the "feed and breed" system more quickly due to increased OXT compared with primiparous mothers. Our findings support antidepressant/anxiolytic and anti-stress effects of OXT. In postpartal women exposed to synthetic OXT, ANA measurement may provide a clue to clarify the effects of exogenous OXT on postpartum psychiatric disorders.

Paradoxical Rules of Spike Train Decoding Revealed at the Sensitivity Limit of Vision.

All sensory information is encoded in neural spike trains. It is unknown how the brain utilizes this neural code to drive behavior. Here, we unravel the decoding rules of the brain at the most elementary level by linking behavioral decisions to retinal output signals in a single-photon detection task. A transgenic mouse line allowed us to separate the two primary retinal outputs, ON and OFF pathways, carrying information about photon absorptions as increases and decreases in spiking, respectively. We measured the sensitivity limit of rods and the most sensitive ON and OFF ganglion cells and correlated these results with visually guided behavior using markerless head and eye tracking. We show that behavior relies only on the ON pathway even when the OFF pathway would allow higher sensitivity. Paradoxically, behavior does not rely on the spike code with maximal information but instead relies on a decoding strategy based on increases in spiking.

Left ventricular mechanoenergetics in excised, cross-circulated rat hearts under hypo-, normo-, and hyperthermic conditions.

We investigated the effects of altering cardiac temperature on left ventricular (LV) myocardial mechanical work and energetics using the excised, cross-circulated rat heart model. We analyzed the LV end-systolic pressure-volume relationship (ESPVR) and linear relationship between myocardial oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA; total mechanical energy per beat) in isovolumically contracting rat hearts during hypo- (32 °C), normo- (37 °C), and hyperthermia (42 °C) under a 300-beats per minute pacing. LV ESPVR shifted downward with increasing cardiac temperature. The VO2-PVA relationship was superimposable in these different thermal conditions; however, each data point of VO2-PVA shifted left-downward during increasing cardiac temperature on the superimposable VO2-PVA relationship line. VO2 for Ca2+ handling in excitation-contraction coupling decreased, which was associated with increasing cardiac temperature, during which sarcoplasmic reticulum Ca2+-ATPase (SERCA) activity was suppressed, due to phospholamban phosphorylation inhibition, and instead, O2 consumption for basal metabolism was increased. The O2 cost of LV contractility for Ca2+ also increased with increasing cardiac temperature. Logistic time constants evaluating LV relaxation time were significantly shortened with increasing cardiac temperature related to the acceleration of the detachment in cross-bridge (CB) cycling, indicating increased myosin ATPase activity. The results suggested that increasing cardiac temperature induced a negative inotropic action related to SERCA activity suppression in Ca2+ handling and increased myosin ATPase activity in CB cycling. We concluded that thermal intervention could modulate cardiac inotropism by changing CB cycling, Ca2+ handling, and basal metabolism in rat hearts.

Processing of single-photon responses in the mammalian On and Off retinal pathways at the sensitivity limit of vision.

Visually guided behaviour at its sensitivity limit relies on single-photon responses originating in a small number of rod photoreceptors. For decades, researchers have debated the neural mechanisms and noise sources that underlie this striking sensitivity. To address this question, we need to understand the constraints arising from the retinal output signals provided by distinct retinal ganglion cell types. It has recently been shown in the primate retina that On and Off parasol ganglion cells, the cell types likely to underlie light detection at the absolute visual threshold, differ fundamentally not only in response polarity, but also in the way they handle single-photon responses originating in rods. The On pathway provides the brain with a thresholded, low-noise readout and the Off pathway with a noisy, linear readout. We outline the mechanistic basis of these different coding strategies and analyse their implications for detecting the weakest light signals. We show that high-fidelity, nonlinear signal processing in the On pathway comes with costs: more single-photon responses are lost and their propagation is delayed compared with the Off pathway. On the other hand, the responses of On ganglion cells allow better intensity discrimination compared with the Off ganglion cell responses near visual threshold.This article is part of the themed issue 'Vision in dim light'.

Saccharin Taste Conditions Flavor Preference in Weanling Rats.

Innate and learned taste/flavor preferences to chemical stimuli in weanling rats are not fully understood. Our previous study showed that weanling rats could establish conditioned flavor preferences when low, but not high, concentrations of sucrose solutions were used as associative rewarding stimuli. Here, we examined whether 3-week-old rats could acquire flavor learning when the rewarding stimulus was saccharin, a non-nutritive artificial sweetener. In the acquisition session, they consumed water with a flavor (cherry or grape) and 0.1% sodium saccharin with another flavor (grape or cherry) for 15 min daily on alternative days over 6 consecutive days. The subsequent test session revealed significant preferences for the flavor previously associated with saccharin. However, they failed to retain the preference when retested in adulthood at the age of 20 weeks. These behavioral results were similar to those previously demonstrated when 2% sucrose was used as an associative sweetener. Although these 2 solutions were equally preferred, the taste quality may not be the same because the weanling rats showed neophobia to 0.1% saccharin and a larger chorda tympani response than 2% sucrose. The present study showed that a conditioned flavor preference was established to saccharin in weanling rats on the basis of flavor-taste association.

Nonlinear spatial integration in the receptive field surround of retinal ganglion cells.

Throughout different sensory systems, individual neurons integrate incoming signals over their receptive fields. The characteristics of this signal integration are crucial determinants for the neurons' functions. For ganglion cells in the vertebrate retina, receptive fields are characterized by the well-known center-surround structure and, although several studies have addressed spatial integration in the receptive field center, little is known about how visual signals are integrated in the surround. Therefore, we set out here to characterize signal integration and to identify relevant nonlinearities in the receptive field surround of ganglion cells in the isolated salamander retina by recording spiking activity with extracellular electrodes under visual stimulation of the center and surround. To quantify nonlinearities of spatial integration independently of subsequent nonlinearities of spike generation, we applied the technique of iso-response measurements as follows: using closed-loop experiments, we searched for different stimulus patterns in the surround that all reduced the center-evoked spiking activity by the same amount. The identified iso-response stimuli revealed strongly nonlinear spatial integration in the receptive field surrounds of all recorded cells. Furthermore, cell types that had been shown previously to have different nonlinearities in receptive field centers showed similar surround nonlinearities but differed systematically in the adaptive characteristics of the surround. Finally, we found that there is an optimal spatial scale of surround suppression; suppression was most effective when surround stimulation was organized into subregions of several hundred micrometers in diameter, indicating that the surround is composed of subunits that have strong center-surround organization themselves.

Left ventricular mechanical and energetic changes in long-term isoproterenol-induced hypertrophied hearts of SERCA2a transgenic rats.

Overexpression of cardiac sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) has been suggested as a strategic intervention for cardiac failure. However, its benefit in wild-type (WT) rats with normal SERCA2a levels seems to be small. To investigate whether it would be beneficial in a cardiac failure model with down-regulated SERCA2a levels, we made a cardiac hypertrophy model using isoproterenol infusion (1.2mgkg(-1)day(-1) for 1 or 4weeks; TG-ISO1w and TG-ISO4w, respectively) in SERCA2a transgenic (TG) rats and compared these rats with littermate WT rats that underwent the same treatments (WT-ISO1w and WT-ISO4w). We analyzed the left ventricular (LV) mechanoenergetics in the excised heart using our original cross-circulation system. The downward shift of curvilinear LV end-systolic pressure-volume relations (ESPVRs) observed in WT-ISO4w rats was abolished in TG-ISO4w rats. The slope and VO2 intercept of the VO2 (myocardial oxygen consumption per beat)-PVA (systolic pressure-volume area: total mechanical energy per beat) linear relation did not differ in any of the groups. The most important finding was a significantly smaller O2 cost of LV contractility in the TG-ISO4w group, which means that less O2 is needed to exert the same LV contractility, compared with the other groups. The increased ratio of SERCA2a/phospholamban returned to the level of the WT-control group only in the TG-ISO4w group. Longer-term up-regulation of mitochondrial transcription factor A for genes of mitochondrial enzymes producing ATP was observed in TG rats. In conclusion, longer-term overexpression of SERCA2a will be beneficial in the present cardiac failure model with down-regulated SERCA2a levels.

Evaluation of left ventricular mechanical work and energetics of normal hearts in SERCA2a transgenic rats.

Cardiac sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA2a) is responsible for most of the Ca(2+) removal during diastole and a larger Ca(2+) handling energy consumer in excitation-contraction (E-C) coupling. To understand the cardiac performance under long-term SERCA2a overexpression conditions, we established SERCA2a transgenic (TG) Wistar rats to analyze cardiac mechanical work and energetics in normal hearts during pacing at 300 beats/min. SERCA2a protein expression was increased in TGI and TGII rats (F2 and F3 of the same father and different mothers). Mean left ventricular (LV) end-systolic pressure (ESP) and systolic pressure-volume area (PVA; a total mechanical energy per beat) at midrange LV volume (mLVV) were significantly larger in TGI rats and were unchanged in TGII rats, compared to those in non-TG [wildtype (WT)] littermates. Mean myocardial oxygen consumption per minute for E-C coupling was significantly increased, and the mean slope of myocardial oxygen consumption per beat (VO(2))-PVA (systolic PVA) linear relation was smaller, but the overall O(2) cost of LV contractility for Ca(2+) is unchanged in all TG rats. Mean Ca(2+) concentration exerting maximal ESP(mLVV) in TGII rats was significantly higher than that in WT rats. The Ca(2+) overloading protocol did not elicit mitochondrial swelling in TGII rats. Tolerance to higher Ca(2+) concentrations may support the possibility for enhanced SERCA2a activity in TGII rats. In conclusion, long-term SERCA2a overexpression enhanced or maintained LV mechanics, improved contractile efficiency under higher energy expenditure for Ca(2+) handling, and improved Ca(2+) tolerance, but it did not change the overall O(2) cost of LV contractility for Ca(2+) in normal hearts of TG rats.

NHE-1 blockade reversed changes in calcium transient in myocardial slices from isoproterenol-induced hypertrophied rat left ventricle.

We previously reported that left ventricular (LV) slices from isoproterenol (ISO)-induced hypertrophied rat hearts showed an increase of energy expenditure due to remodeling of Ca(2+) handling in excitation-contraction coupling, i.e., suppressed SERCA2a activity and enhanced Na(+)/Ca(2+)exchanger-1 (NCX-1) activity. Na(+)/H(+) exchanger-1 (NHE-1) inhibitor (NHEI) has been demonstrated to exert beneficial effects in the development of cardiac remodeling. We hypothesized that a novel NHE-1 selective inhibitor, BIIB723 prevents remodeling of Ca(2+) handling in LV slices of ISO-induced hypertrophied rat hearts mediated by inhibiting NCX-1 activity. The significant shortening in duration of multi-cellular Ca(2+) transient in ISO group was normalized in ISO+BIIB723 group. The significant increase in amplitude of multi-cellular Ca(2+) waves (CaW) generated at high [Ca(2+)](o) of LV slices in ISO group was also normalized in ISO+BIIB723 group. However, the enhanced NCX-1 activity was not antagonized by BIIB723. We recently reported that ISO-induced down-regulation of a Ca(2+) handling protein, SERCA2a, was normalized by BIIB723. Therefore, it seems likely that BIIB723 normalized shortened multi-cellular Ca(2+) transient duration and increased CaW amplitude in LV slices mediated via normalization of SERCA2a activity. Furthermore, the results presented here suggest the multi-cellular Ca(2+) transient duration and CaW amplitude in LV slices might be better indices reflecting SERCA2a activity than SERCA2a protein expression level.

NHE-1 participates in isoproterenol-induced downregulation of SERCA2a and development of cardiac remodeling in rat hearts.

Impaired Ca(2+) handling is one of the main characteristics in heart failure patients. Recently, we reported abnormal expressions of Ca(2+)-handling proteins in isoproterenol (ISO)-induced hypertrophied rat hearts. On the other hand, Na(+)/H(+) exchanger (NHE)-1 inhibitor has been demonstrated to exert beneficial effects in ischemic-reperfusion injury and in the development of cardiac remodeling. The aims of the present study are to investigate the role of NHE-1 on Ca(2+) handling and development of cardiac hypertrophy in ISO-infused rats. Male Wistar rats were randomly divided into vehicle [control (CTL)] and ISO groups without or with pretreatment with a selective NHE-1 inhibitor, BIIB-723. ISO infusion for 1 wk significantly increased the ratios of heart to body weight and left ventricle (LV) to body weight and collagen accumulation. All of these increases were antagonized by coadministration with BIIB-723. The ISO-induced significant increase in LV wall thickness was suppressed significantly (P < 0.05) by BIIB-723. ISO-induced decreases in cardiac stroke volume and a total mechanical energy per beat index, systolic pressure-volume area at midrange LV volume, were normalized by BIIB-723. The markedly higher expression of NHE-1 protein in the ISO group than that in CTL group was suppressed (P < 0.05) by BIIB-723. Surprisingly, ISO induced downregulation of the important Ca(2+)-handling protein sarcoplasmic reticulum Ca(2+)-ATPase 2a, the expression of which was also normalized by BIIB-723 without changes in phosphorylated phospholamban (PLB)/PLB expression. We conclude that NHE-1 contributes to ISO-induced abnormal Ca(2+) handling associated with cardiac hypertrophy. Inhibition of NHE-1 ameliorates cardiac Ca(2+)-handling impairment and prevents the development of cardiac dysfunction in ISO-infused rats.

Synchronization analysis of voltage-sensitive dye imaging during focal seizures in the rat neocortex.

Seizures are often assumed to result from an excess of synchronized neural activity. However, various recent studies have suggested that this is not necessarily the case. We investigate synchronization during focal neocortical seizures induced by injection of 4-aminopyridine (4AP) in the rat neocortex in vivo. Neocortical activity is monitored by field potential recording and by the fluorescence of the voltage-sensitive dye RH-1691. After removal of artifacts, the voltage-sensitive dye (VSD) signal is analyzed using the nonlinear dynamics-based technique of stochastic phase synchronization in order to determine the degree of synchronization within the neocortex during the development and spread of each seizure event. Results show a large, statistically significant increase in synchronization during seizure activity. Synchrony is typically greater between closer pixel pairs during a seizure event; the entire seizure region is synchronized almost exactly in phase. This study represents, to our knowledge, the first application of synchronization analysis methods to mammalian VSD imaging in vivo. Our observations indicate a clear increase in synchronization in this model of focal neocortical seizures across a large area of the neocortex; a sharp increase in synchronization during seizure events was observed in all 37 seizures imaged. The results are consistent with a recent computational study which simulates the effect of 4AP in a neocortical neuron model.

Effects of formaldehyde on cardiovascular system in in situ rat hearts.

The aim of the present study was to examine the effects of formaldehyde solution on rat left ventricular function and compare it with those in hypertrophic hearts treated with isoproterenol by pressure-volume measurements with the catheter method. After 20-30 min. of intravenous infusion of 3.7% formaldehyde solution (FA) at 10 µl (3.7 mg)/kg/min, normal and hypertrophic hearts showed significant decreases in left ventricle end-systolic pressure (ESP), heart rate and cardiac output per minute, indicating an acute pumping failure. Hypertrophic hearts showed significantly smaller ESP, stroke volumes and cardiac output than those in normal hearts. Systolic pressure-volume area at midrange left ventricular volume (PVA(mLVV) : a mechanical work capability index) was significantly smaller than that in normal hearts and per cent of mean PVA(mLVV) versus pre-infusion mean value in hypertrophic hearts was significantly decreased compared to normal hearts 30 min. after FA infusion. The marked decrease in pH, base excess and no changes in PaO2 and PaCO2 suggest metabolic acidosis. The correction of metabolic acidosis with 9% NaHCO3 did not influence on the acute pumping failure, indicating that metabolic acidosis did not cause it. Ultrastructural observations revealed marked dilation of the sarcoplasmic reticulum with intact sarcolemmal membranes and no disintegration of muscle myofibrils. Ryanodine receptors and calcium (Ca²âº) pumps (SERCA2A) located in the sarcoplasmic reticulum have major roles in the cytosolic Ca²âº handling. Taken together, acute pumping failure by FA may derive from the impairment of Ca²âº handling in the cardiac excitation-contraction coupling.

A comparison of the mechanical effect of arm swing and countermovement on the lower extremities in vertical jumping.

The purposes of this study were to quantify and compare how arm swing and countermovement affect lower extremity torque and work during vertical jumping and to gain insight into the mechanisms that enable the arm swing and countermovement to increase jump height. Five participants maximally performed two types of vertical squat jumps with (SJA) and without (SJ) an arm swing and two types of countermovement vertical jumps with (CJA) and without (CJ) an arm swing. The participants jumped from a force platform and all performances were videotaped with a high-speed video camera (200 Hz). Jump heights, joint torques and work were calculated by combining kinematic and kinetic data. It was found that of the four jumping conditions, the participants jumped highest when they used an arm swing with countermovement (i.e., CJA). The increase of the countermovement jump height with an arm swing is the result of the increase of the lower extremity work. In the hip joint, the increase in torque caused by the countermovement predominantly occurred at the beginning of the propulsion phase, while the increase in torque caused by the arm swing occurred in the rest of the propulsion phase. A key finding of our study is that arm swing and countermovement have independent effects on lower extremity work, and their effects are additive in CJA to produce greater jump height.

Isoproterenol-induced hypertrophied rat hearts: does short-term treatment correspond to long-term treatment?

In consideration of clinical implications, it is often complained that short-term experimental diseased heart models do not mimic long-term diseased hearts that are often clinically encountered. The aim of the present study was (i) to compare the left ventricular function between rat cardiac hypertrophy models treated with isoproterenol for 3 days (Iso 3d) and 7 days (Iso 7d) by pressure-volume measurements with a catheter method, and (ii) to follow up the left ventricular function in the same model treated with Iso up to 16 weeks with a less-invasive echocardiography. An infusion of either Iso (1.2 mg x kg(-1) x day(-1) for 3 days-16 weeks) or vehicle (saline 24 microl x day(-1) for 3 days-16 weeks; Sa group) was performed by subcutaneously implanting an osmotic minipump. There were no significant differences in the systolic pressure-volume area at midrange left ventricular volume (PVA(mLVV): a mechanical work capability index) between Iso 3d and 7d groups, though PVA(mLVV) in both groups was significantly reduced from that in the Sa group. From echocardiography, the left ventricular function of the hypertrophy models at 3 days, 1 week, and 2 weeks was unchanged, but the model at a term longer than 4 weeks resulted in prolonged systolic failure. The results indicated that (i) no marked differences in the left ventricular mechanical work capability were found between the Iso 3d and 7d groups, and that (ii) only a 3-day Iso infusion induced the hypertrophy model similar in shape and function to that induced by a 2-week Iso infusion. We concluded that the 3-day model was sufficient.

Imaging cortical electrical stimulation in vivo: fast intrinsic optical signal versus voltage-sensitive dyes.

We applied high-temporal-resolution optical imaging utilizing both the fast intrinsic optical signal (fIOS) and voltage-sensitive dyes (VSDs) to observe the spatiotemporal characteristics of rat somatosensory cortex during electrical stimulation. We find that changes in both the fIOS and VSD signals occur rapidly (<30 ms) after the stimulus is applied, suggesting that both membrane depolarization and transmembrane ion movement occur shortly after the stimulus, preceding the more gradual physiological changes in oxygen consumption revealed by the slower component of the intrinsic optical signal. We find that the VSD signal spreads through a much larger area of cortex than the fIOS.

Transitions between multistable states as a model of epileptic seizure dynamics.

Epileptic seizures are generally considered to result from excess and synchronized neural activity. Additionally, changes in amplitude and frequency are often seen in local field potential or electroencephalogram recordings during a seizure event. To investigate how seizures initiate, and how dynamical changes occur during seizure progression, we develop a neocortical network model based on a model suggested by Wilson [J. Theor. Biol. 200, 375 (1999)]. We propose a possible mechanism for seizure initiation as a bifurcation, and suggest that experimentally observed changes in field potential amplitude and frequency during the course of a seizure may be explained by noise-induced transitions among multistable states.