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PubMed2000

Electrically evoked fictive swimming in the low-spinal immobilized turtle.

Fictive swimming was elicited in low-spinal immobilized turtles by electrically stimulating the contralateral dorsolateral funiculus (cDLF) at the level of the third postcervical segment (D(3)). Fictive hindlimb motor output was recorded as electroneurograms (ENGs) from up to five peripheral nerves on the right side, including three knee extensors (KE; iliotibialis [IT]-KE, ambiens [AM]-KE, and femorotibialis [FT]-KE), a hip flexor (HF), and a hip extensor (HE). Quantitative analyses of burst amplitude, duty cycle and phase were used to demonstrate the close similarity of these cDLF-evoked fictive motor patterns with previous myographic recordings obtained from the corresponding hindlimb muscles during actual swimming. Fictive rostral scratching was elicited in the same animals by cutaneous stimulation of the shell bridge, anterior to the hindlimb. Fictive swim and rostral scratch motor patterns displayed similar phasing in hip and knee motor pools but differed in the relative amplitudes and durations of ENG bursts. Both motor patterns exhibited alternating HF and HE discharge, with monoarticular knee extensor (FT-KE) discharge during the late HF phase. The two motor patterns differed principally in the relative amplitudes and durations of HF and HE bursts. Swim cycles were dominated by large-amplitude, long-duration HE bursts, whereas rostral scratch cycles were dominated by large-amplitude, long-duration HF discharge. Small but significant differences were also observed during the two behaviors in the onset phase of biarticular knee extensor bursts (IT-KE and AM-KE) within each hip cycle. Finally, interactions between swim and scratch motor networks were investigated. Brief activation of the rostral scratch during an ongoing fictive swim episode could insert one or more scratch cycles into the swim motor pattern and permanently reset the burst rhythm. Similarly, brief swim stimulation could interrupt and reset an ongoing fictive rostral scratch. This shows that there are strong central interactions between swim and scratch neural networks and suggests that they may share key neural elements.

Animals↗
PubMed2003

Imipramine-induced antinociception in the formalin test. Receptor mechanisms involved and effect of swim stress.

This study concerned the effect of swim stress on imipramine-induced antinociception in mice. The data showed that intraperitoneal (i.p.) administration of different doses of imipramine (10-40 mg/kg) and 0.5-3 min of swim stress (17 degrees C) induced antinociception in the first and second phases of the formalin test. Low period of swim stress (10 s) with low doses of imipramine (2.5, 5 and 10 mg/kg i.p.), which did not have any effect by themselves, in combination showed antinociception in the second phase of the test. Either yohimbine (0.5 mg/kg i.p.) or naloxone (1 mg/kg i.p.) reversed the response induced by the combination of low doses of imipramine plus swim stress. Yohimbine (1 mg/kg i.p.) decreased the response of imipramine (20 mg/kg i.p.) but not that of 30 s swim stress in the second phase. However, naloxone (1 mg/kg i.p.) reduced the antinociception induced by imipramine (20 mg/kg i.p.) or 30 s swim stress in the second phase of the test, the combination of imipramine with swim stress was not altered by yohimbine or naloxone. Prazosin induced antinociception by itself in the first phase of the test and increased swim-stress-induced antinociception with no interaction. It is concluded that antinociception induced by imipramine in the second phase of formalin test may be mediated through alpha(2)-adrenoceptor antagonists. The results indicate that the responses of swim stress and imipramine may be mediated by an opioid mechanism, but the combination of both drugs induced higher antinociceptive effects.

Animals↗
PubMed2007

Central mechanisms underlying fish swimming.

Although the basic swimming rhythm is created by central pattern generators (CPGs) located in each spinal segment, command signals from the brain should be indispensable for the activation of CPGs to initiate swimming. We hypothesized that the nucleus of medial longitudinal fascicles (Nflm) is the midbrain locomotor region driving swimming rhythms in teleosts. To test this hypothesis, we recorded neuronal activities from Nflm neurons in swimming carp and analyzed the cytoarchitecture of the nucleus. We identified two types of Nflm neurons exhibiting electric activities closely related to swimming rhythms. Remarkably, tonic neurons that continued firing during swimming were found. The Nflm and neighboring oculomotor nucleus contain about 600 neurons in total, and among them as many as 500 were labeled retrogradely by an intraspinal tracer implantation and 400 neurons showed glutamatergic immunoreactivity. They are the most likely candidates for the descending neurons as the origin of driving signals that initiate swimming. Double-labeling experiments demonstrated direct connections of Nflm neurons to spinal neurons consisting of the CPG. These data imply that most Nflm neurons possibly exert an excitatory drive to the spinal CPGs through the descending axons with excitatory transmitter(s), probably glutamate. Furthermore, we confirmed that the caudal part of Nflm and the rostral part of the oculomotor nucleus overlap rostrocaudally by approximately 200 mum. In connection with the control of swimming by the brain, we carried out experiments to clarify the efferent system of the cerebellum of the goldfish. Cerebellar efferent fibers terminated in most brain regions except for the telencephalon. Importantly, the cerebellum projected also to the Nflm, suggesting the involvement of this brain region in the control of swimming. We have also determined that in the carp so-called eurydendroid cells are cerebellar efferent neurons.

Animals↗
PubMed1990

Induction of the intermediate lobe pro-opiomelanocortin system with chronic swim stress and beta-adrenergic modulation of this induction.

Swimming at 25-30 degrees C for 30 min stimulates release of beta-endorphin from both the anterior and intermediate lobe of the pituitary in rats. Measurement of N-acetyl beta-endorphin-immunoreactivity (IR), which is specific for intermediate lobe secretion, indicates a 2- to 3-fold increase in N-acetyl beta-endorphin IR in plasma following this challenge. When swim is repeated on a daily basis, there is an increase in the amount of N-acetyl beta-endorphin IR released with repeated swim over time. As well as increased response to the swim challenge, these animals demonstrate an increase in the resting plasma levels of N-acetyl beta-endorphin IR and an increase in the intermediate lobe content of N-acetyl beta-endorphin IR. Molecular sieving of plasma from rats which were swum repeatedly demonstrates that this N-acetyl beta-endorphin IR consists of both larger molecular weight N-acetyl beta-endorphin IR, e.g. N-acetyl beta-endorphin1-31 and C-terminally shortened forms, e.g. N-acetyl beta-endorphin1-27. Administration of propranolol (3 mg/kg), a beta-adrenergic antagonist, 30 min before the onset of swim is able to block the intermediate lobe release of N-acetyl beta-endorphin IR with acute swim challenge. However, repeated administration of propranolol in conjunction with repeated swim is not able to block the swim stress-induced increase in plasma N-acetyl beta-endorphin IR or the increase in N-acetyl beta-endorphin IR content of the intermediate lobe. This is not due to decreased sensitivity to propranolol with repeated administration since in rats given chronic propranolol treatment an acute dose of propranolol is still able to block swim stress-induced release of N-acetyl beta-endorphin IR. Similarly, it is not due to a decreased efficacy of this dose of propranolol in rats which were swum chronically.

Animals↗
PubMed2003

Influence of seasonal temperature on the repeat swimming performance of rainbow trout Oncorhynchus mykiss.

While the temperature dependence of exercise performance in fishes is reasonably well documented, information on the temperature dependence of metabolic recovery and reperformance is scant. This study examined the recovery of swimming performance after exhaustive exercise in rainbow trout Oncorhynchus mykiss at seasonal temperatures ranging from 5 to 17 degrees C and explored the relationship between performance and preceding metabolic state. The primary objective of the study was to test the hypothesis that increased temperature increases the capability of rainbow trout to repeat a critical swimming speed (U(crit)), as assessed by two consecutive critical swimming speed tests separated by a 40 min rest interval. An additional expectation was that certain plasma ionic, metabolic and humoral parameters would be correlated with how well fish reperformed and so plasma levels of lactate, potassium, ammonia, osmolality, sodium and cortisol, as well as hematocrit, were monitored before, during and after the swim challenges via an indwelling cannula in the dorsal aorta. As expected, performance in the first U(crit) test (U(crit1)) was positively related to temperature. However, the relationship between U(crit1) and reperformance (U(crit2)) was not dependent on acclimation temperature in a simple manner. Contrary to our expectations, U(crit2) was less than U(crit1) for warm-acclimated fish (14.9+/-1.0 degrees C), whereas U(crit2) equaled U(crit1) for cold-acclimated fish (8.4+/-0.9 degrees C). Cold-acclimated fish also exhibited a lower U(crit1) and less metabolic disruption compared with warm-acclimated fish. Thus, while warm acclimation conferred a faster U(crit1), a similar swimming speed could not be attained on subsequent swim after a 40 min recovery period. This finding does not support the hypothesis that the ability of rainbow trout to reperform on U(crit) test is improved with temperature. Both plasma lactate and plasma potassium levels were strongly correlated with U(crit1) performance. Therefore, the higher U(crit1) of warm-acclimated fish may have been due in part to a greater anaerobic swimming effort compared with cold-acclimated fish. In fact, a significant correlation existed between the plasma lactate concentration prior to the start of the second test and the subsequent U(crit2) performance, such that U(crit2) decreased when a threshold plasma lactate level of around 12.2 mmol l(-1) was surpassed for the initial swim. No other measured plasma variable showed a significant relationship with the U(crit2) performance. We conclude that warm-acclimated fish, by apparently swimming harder and possibly more anaerobically compared with cold-acclimated fish, were unable to recovery sufficiently well during the fixed recovery period to repeat this initial level of performance, and this poorer repeat performance was correlated with elevations in plasma lactate levels.

Acclimatization↗
PubMed2006

Effect of temperature on maximum swimming speed and cost of transport in juvenile European sea bass (Dicentrarchus labrax).

This study is an attempt to gain an integrated understanding of the interactions between temperature, locomotion activity and metabolism in the European sea bass (Dicentrarchus labrax). To our knowledge this study is among the few that have investigated the influence of the seasonal changes in water temperature on swimming performance in fish. Using a Brett-type swim-tunnel respirometer the relationship between oxygen consumption and swimming speed was determined in fish acclimatised to 7, 11, 14, 18, 22, 26 and 30 degrees C. The corresponding maximum swimming speed (U(max)), optimal swimming speed (U(opt)), active (AMR) and standard (SMR) metabolic rates as well as aerobic metabolic scope (MS) were calculated. Using simple mathematical functions, these parameters were modelled as a function of water temperature and swimming speed. Both SMR and AMR were positively related to water temperature up to 24 degrees C. Above 24 degrees C SMR and AMR levelled off and MS tended to decrease. We found a tight relationship between AMR and U(max) and observed that raising the temperature increased AMR and increased swimming ability. However, although fish swam faster at high temperature, the net cost of transport (COT(net)) at a given speed was not influence by the elevation of the water temperature. Although U(opt) doubled between 7 degrees C and 30 degrees C (from 0.3 to 0.6 m s(-1)), metabolic rate at U(opt) represented a relatively constant fraction of the animal active metabolic rate (40-45%). A proposed model integrates the effects of water temperature on the interaction between metabolism and swimming performance. In particular the controlling effect of temperature on AMR is shown to be the key factor limiting maximal swimming speed of sea bass.

Analysis of Variance↗
PubMed2000

The influence of temperature on power production during swimming. II. Mechanics of red muscle fibres in vivo.

We found previously that scup (Stenotomus chrysops) reduce neither their stimulation duration nor their tail-beat frequency to compensate for the slow relaxation rates of their muscles at low swimming temperatures. To assess the impact of this 'lack of compensation' on power generation during swimming, we drove red muscle bundles under their in vivo conditions and measured the resulting power output. Although these in vivo conditions were near the optimal conditions for much of the muscle at 20 degrees C, they were far from optimal at 10 degrees C. Accordingly, in vivo power output was extremely low at 10 degrees C. Although at 30 cm s(-)(1), muscles from all regions of the fish generated positive work, at 40 and 50 cm s(-)(1), only the POST region (70 % total length) generated positive work, and that level was low. This led to a Q(10) of 4-14 in the POST region (depending on swimming speed), and extremely high or indeterminate Q(10) values (if power at 10 degrees C is zero or negative, Q(10) is indeterminate) for the other regions while swimming at 40 or 50 cm s(-)(1). To assess whether errors in measurement of the in vivo conditions could cause artificially reduced power measurements at 10 degrees C, we drove muscle bundles through a series of conditions in which the stimulation duration was shortened and other parameters were made closer to optimal. This sensitivity analysis revealed that the low power output could not be explained by realistic levels of systematic or random error. By integrating the muscle power output over the fish's mass and comparing it with power requirements for swimming, we conclude that, although the fish could swim at 30 cm s(-)(1) with the red muscle alone, it is very unlikely that it could do so at 40 and 50 cm s(-)(1), thus raising the question of how the fish powers swimming at these speeds. By integrating in vivo pink muscle power output along the length of the fish, we obtained the surprising finding that, at 50 cm s(-)(1), the pink muscle (despite having one-third the mass) contributes six times more power to swimming than does the red muscle. Thus, in scup, pink muscle is crucial for powering swimming at low temperatures. This overall analysis shows that Q(10) values determined in experiments on isolated tissue under arbitrarily selected conditions can be very different from Q(10) values in vivo, and therefore that predicting whole-animal performance from these isolated tissue experiments may lead to qualitatively incorrect conclusions. To make a meaningful assessment of the effects of temperature on muscle and locomotory performance, muscle performance must be studied under the conditions at which the muscle operates in vivo.

Animals↗
PubMed2001

Caudal differential pressure as a predictor of swimming speed of cod (Gadus morhua).

We report the results of an experiment designed to investigate the feasibility of using differential pressure to estimate the swimming speed and metabolic rate of Atlantic cod (Gadus morhua). Seven cod were fitted with a miniature differential pressure sensor mounted on one side of the caudal peduncle immediately anterior to the base of the caudal fin rays. Relationships between differential pressure, tailbeat frequency, tailbeat amplitude, swimming speed and rate of oxygen consumption ((O(2))) were determined as a function of the swimming speed of cod swimming at 5 degrees C in a recirculating 'Brett-style' respirometer. Tailbeat differential pressure, tailbeat amplitude and tailbeat frequency were highly correlated with swimming speed. The average or integrated pressure ranged from 0 to 150 Pa for speeds up to 0.8 m s(-1) (1.1 L s(-1), where L is total body length), while the 'pressure difference' (maximum minus minimum pressure) ranged from 0 to 900 Pa. Small changes in swimming speed of less than 0.05 m s(-1) were readily detected as differences in tailbeat pressure. Burst swimming in the respirometer resulted in huge pressure 'bursts' of up to 5000 Pa 'pressure difference'. The rate of oxygen consumption increased exponentially and was highly correlated with swimming speed (r(2)=0.77). The rate of oxygen consumption was also correlated with tailbeat integrated pressure (r(2)=0.68) and with differential pressure (r(2)=0.43); regression correlations were always greater for individuals than for combined data from all cod. The results detailed in this study indicate that an ultrasonic differential pressure transmitter would enable accurate estimates of the swimming speed, rates of oxygen consumption and activity patterns of free-ranging fish in nature.

Animals↗
PubMed2005

The role of hair in swimming of laboratory mice: implications for behavioural studies in animals with abnormal hair.

Animal swimming tests, such as the forced swim test, are extensively used in biomedical research to study rodent behaviour. Hair and skin exposed to water may be an important factor affecting the performance in this test. Since various hair and skin abnormalities are not uncommon in genetically modified or drug-treated laboratory animals, this test may be inappropriate for these animals. Because on occasions it is necessary to screen their swimming behaviour, in the present study we aimed to assess the role of hair in swimming of laboratory rodents in the forced swim test, widely used in behavioural research. For this, we shaved laboratory mice (129S1 strain) and compared their swimming patterns with those of unshaven controls. Overall, shaving mice did not affect their swimming behaviours in the 5 min forced swim test. Our results indicate that hair condition is not an important factor in the forced swim test for this mouse strain, and suggest that this test may have wider utility for behavioural analyses of mice with abnormal hair.

Animals↗
PubMed1993

[Cardiorespiratory responses during flume swimming and treadmill running in swimmers].

The present study was designed to compare cardiorespiratory responses of swimmers to swimming and running. Six male trained college swimmers performed maximal work test (progressive method) in flume swimming and treadmill running. VEmax during swimming (128.3 +/- 20.6 l/min) was about 4% lower than during running (133.2 +/- 9.9 l/min). VO2max during swimming (3628 +/- 228 ml/min) was significantly higher than during running (3408 +/- 222 ml/min). HRmax during swimming (191 +/- 8 beats/min) was significantly lower than during running (198 +/- 6 beats/min). VO2 at ventilatory threshold (VT) during swimming (2177 +/- 183 ml/min) was significantly higher than during running (1699 +/- 214 ml/min). %VO2max at VT during swimming (60.1 +/- 4.2%) was significantly about 10% higher than during running (49.8 +/- 4.4%). These results suggest that subjects of this study have specific cardiorespiratory adaptation to swimming from a long period of swim training.

Adult↗
PubMed1999

Long-term regulation of locus ceruleus sensitivity to corticotropin-releasing factor by swim stress.

Corticotropin-releasing factor (CRF) acts as a putative neurotransmitter in the locus ceruleus (LC) to mediate its activation by certain stressors. In this study, we quantified LC sensitivity to CRF 24 h after swim stress, at a time when behavioral depression that is sensitive to antidepressants is apparent. Rats were placed in a tank with 30 cm (swim stress) or 4 cm water and 24 h later, either behavior was monitored in a forced swim test or LC discharge was recorded. Swim stress rats were more immobile than control animals in the swim test. LC neurons of swim stress rats were sensitized to low doses of CRF (0.1-0.3 microgram i.c.v.) that were ineffective in control animals and were desensitized to higher doses. Swim stress selectively altered LC sensitivity to CRF because neither LC spontaneous discharge nor responses to other agents (e.g., carbachol, vasoactive intestinal peptide) were altered. Finally, the mechanism for sensitization was localized to the LC because neuronal activation by low doses of CRF was prevented by the intracerulear administration of a CRF antagonist. CRF dose-response curves were consistent with a two-site model with similar dissociation constants under control conditions but divergent dissociation constants after swim stress. The results suggest that swim stress (and perhaps other stressors) functionally alters CRF receptors that have an impact on LC activity. Stress-induced regulation of LC sensitivity to CRF may underlie behavioral aspects of stress-related psychiatric disorders.

Action Potentials↗
PubMed1991

Validation of the 12-min swim as a field test of peak aerobic power in young men.

The purposes of this study were to validate the 12-min swim as a field test of VO2max and to compare its validity with that of the 12-min run. Thirty-six young men completed 12-min swim, 12-min run, tethered swimming (TS) VO2peak, and treadmill running (TR) VO2peak tests within 3 wk. Mean (+/- SD) 12-min swim and run distances were 581 +/- 88 and 2797 +/- 290 m, and mean TS and TR VO2peak values were 50.3 +/- 6.2 and 57.2 +/- 5.5 ml.kg BW-1.min-1, respectively. Correlation coefficients and standard errors of estimate for predictions of TS VO2peak from the 12-min swim (0.40 and 5.7 ml.kg BW-1.min-1) and run (0.74 and 4.2 ml.kg BW-1.min-1) and for predictions of TR VO2peak from the 12-min swim (0.38 and 5.1 ml.kg BW-1.min-1) and run (0.88 and 2.6 ml.kg BW-1.min-1) indicated that the 12-min run was a more accurate predictor of TS or TR VO2peak than the 12-min swim. We conclude that the 12-min swim has relatively low validity as a field test of peak aerobic power and that it should not be considered an equally valid alternative to the 12-min run in young male recreational swimmers. However, the accuracy of predicting VO2peak from the 12-min swim is as good as some other commonly used methods, and, therefore, it may be adequate for fitness classification in situations in which a high level of accuracy is not needed.

Adult↗
PubMed1987

Sex difference in naloxone antagonism of swim stress-induced antinociception in mice.

A 30 sec swim in water at 30 degrees C reduced the number of abdominal constrictions produced in mice by the intraperitoneal injection of acetic acid. In male mice this reduction in abdominal constrictions induced by swim stress was not affected by prior subcutaneous administration of naloxone hydrochloride. However, in the female mice naloxone hydrochloride administered 5 min, 10 min, or 15 min before the 30 sec swim dose-dependently antagonized the effect of swim stress on the abdominal constriction response to i.p. acetic acid. In view of the possibility that female mice may perceive the stress at different intensity from those of the male, the effects of different swimming durations on female mice were also studied. It was found that a 15 sec swim in water at 30 degrees C was sufficient to induce antinociceptive response to i.p. acetic acid. The antinociceptive effect was greater if the duration of swim was extended to 60 sec. In both instances, prior administration of naloxone dose-dependently reduced the antinociceptive effect induced by swimming. These results suggest sex difference in the involvement of endogenous opioid system in swim stress-induced antinociception in mice.

Acetates↗
PubMed1980

[Changes of locomotor activities, lipid peroxide levels and their related enzyme activities in rat loaded with swimming exercise (author's transl)].

The changes of locomotor activities in rat loaded with swimming exercise were recorded by our newly devised apparatus. In addition, changes of lipid peroxide levels and their related enzyme activities in rat brain, liver as well as blood were studied. The results obtained were as follows: 1. The locomotor activities in rat recorded by the apparatus showed the same patterns as that reported by the other researchers. 2. After the loading of swimming, locomotor activities in rat during the dark period decreased significantly as compared to those of the control. 3. The levels of TBARS (thiobarbituric acid reactive substance), SOD (superoxide dismutase) and GSH-px (glutathione peroxidase) in rat liver elevated after the swimming exercise in the first group, which was sacrificed after loading with one treatment (about 5 hours) exercise of swimming. 4. The level of TBARS in rat brain elevated after the swimming exercise in the second group, which was sacrificed after loading with two treatment exercise of swimming. 5. The level of TBARS in plasma decreased, and GSH-px, GR (glutathione reductase) and catalase in red blood cells elevated in the third group, which was sacrificed after two-hour rest following the loading with two treatment exercise of swimming. It is indicated that our newly devised apparatus is useful for monitoring locomotor activities in rat, and that the fatigue in rat caused by swimming load can be shown in terms of changes in the above activities. The elevation of the level of TBARS during the swimming exercise observed in tissues of the brain and liver may suggest that the lipid peroxidation will reflect a certain state of fatigue in rat.

Animals↗
PubMed1994

[Helminth and protozoan findings in the water of school swimming pools].

In the year 1993 repeated parasitological examinations of water and the equipment of an indoor school swimming pool were made. The sanitary and hygienic regime of the swimming pool was not respected and parasitological findings corresponded to this fact. Examinations of the swimming pool revealed the presence of helminths--Ascaris lumbricoides, Enterobius vermicularis and Taenia saginata, as well as of protozoa--Giardia intestinalis and Entamoeba coli. The parasites were detected in samples taken under operation conditions from free water, from walls of the swimming pool an from its equipment, as well as from the sediment in sand filters. The authors pointed out that increased occurrence of parasites was connected with exceeding of swimming pool capacity. They noted also massive occurrence of non-pathogenic protozoa in water and sediment of the swimming pool, which was considered an indicator of increased pollution. They drew attention to the possibility of infection with intestinal parasites present in the swimming pool water. The conditions are discussed which enable parasites to reach the stage in which they are can infect bathing people and cause parasitoses in them. The authors suggested which places of a swimming pool should be examined in the course of parasitological investigations. They took steps to prevent contamination of swimming pool water with developmental stages of parasites and to prevent their maturation.

Animals↗
PubMed1997

The neuronal basis of the behavioral choice between swimming and shortening in the leech: control is not selectively exercised at higher circuit levels.

Swimming and the whole-body shortening reflex are two incompatible behaviors performed by the medicinal leech Hirudo medicinalis. We set out to examine the neuronal basis of the choice between these behaviors, taking advantage of the fact that the neuronal circuit underlying swimming is relatively well understood. The leech swim circuit is organized hierarchically and contains three interneuronal levels, including two upper levels of "command-like" neurons. We tested the responses of the swim circuit neurons to stimuli that produced shortening, using reduced preparations in which neurophysiological recording could be performed while behaviors were elicited. We found that the majority of the swim circuit neurons, including most of the command-like cells and all of the cells at the highest hierarchical level of the circuit, were excited by stimuli that produced shortening as well as by stimuli that produced swimming. Only a subset of neurons, at levels below the top, were inhibited during shortening; these included one of the command-like cells and an oscillator cell (an interneuron that is part of the central pattern generator for swimming). These results imply that the control of the choice between swimming and shortening is not exercised selectively at the higher levels of the swim circuit.

Action Potentials↗
PubMed1997

Removal of spike frequency adaptation via neuromodulation intrinsic to the Tritonia escape swim central pattern generator.

For the mollusc Tritonia diomedea to generate its escape swim motor pattern, interneuron C2, a crucial member of the central pattern generator (CPG) for this rhythmic behavior, must fire repetitive bursts of action potentials. Yet, before swimming, repeated depolarizing current pulses injected into C2 at periods similar those in the swim motor program are incapable of mimicking the firing rate attained by C2 on each cycle of a swim motor program. This resting level of C2 inexcitability is attributable to its own inherent spike frequency adaptation (SFA). Clearly, this property must be altered for the swim behavior to occur. The pathway for initiation of the swimming behavior involves activation of the serotonergic dorsal swim interneurons (DSIs), which are also intrinsic members of the swim CPG. Physiologically appropriate DSI stimulation transiently decreases C2 SFA, allowing C2 to fire at higher rates even when repeatedly depolarized at short intervals. The increased C2 excitability caused by DSI stimulation is mimicked and occluded by serotonin application. Furthermore, the change in excitability is not caused by the depolarization associated with DSI stimulation or serotonin application but is correlated with a decrease in C2 spike afterhyperpolarization. This suggests that the DSIs use serotonin to evoke a neuromodulatory action on a conductance in C2 that regulates its firing rate. This modulatory action of one CPG neuron on another is likely to play a role in configuring the swim circuit into its rhythmic pattern-generating mode and maintaining it in that state.

Action Potentials↗
PubMed1993

Simultaneous swim-up/swim-down of sperm in assisted reproduction procedures.

PURPOSE: High-quality motile human spermatozoa were obtained following treatment of semen by simultaneous swim-up into medium and swim-down into an isotonic 40% Percoll solution. RESULTS: This procedure was significantly better than the swim-up method and comparable to discontinuous Percoll gradient centrifugation. Recovery rates of motile sperm were 35% for swim-up, 65% for Percoll gradient centrifugation, and 73% for swim-up/swim-down. CONCLUSION: The swim-down sperm was inferior to the swim-up sperm in its upward migration capacity but superior in morphology. Spermatozoa obtained by the swim-up/swim-down procedure demonstrated fertilizing ability in IVF, and clinical pregnancies were established. The simultaneous swim-up/swim-down procedure offers an alternative efficient method of simple separation of high-quality motile sperm for various assisted reproduction techniques.

Cell Separation↗