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PubMed1996

Stimulation of 5-HT3 receptors in the NTS inhibits the cardiac Bezold-Jarisch reflex response.

Intra-atrial administration of phenylbiguanide has been shown to trigger, through the stimulation of vagal afferent C-fibers, reflex bradycardia, hypotension, and sympathoinhibition classically known as the Bezold-Jarisch (B-J) reflex (O. Krayer. Naunyn-Schmiedeberg's Arch. Exp. Pathol. Pharmacol. 240: 361-368, 1961). The effects of microinjections, into the nucleus tractus solitarius (NTS), of serotonin (5-HT) and 1-(m-chlorophenyl)-biguanide (CPBG), a potent 5-HT3 receptor agonist, on these reflex responses were studied in urethananesthetized rats. 5-HT (600 and 900 pmol) and CPBG (10-150 pmol) produced a dose-dependent inhibition of the atropine-sensitive bradycardiac component of the B-J reflex. The effect of both agonists was reversed by prior local microinjection of the 5-HT3 receptor antagonists zacopride (100 pmol) and ondansetron (100 pmol), but not by that of the 5-HT2 receptor antagonist ketanserin (10 pmol) or the mixed 5-HT1/5-HT2 receptor antagonist methysergide (100 pmol). In contrast, CPBG (150 pmol) did not affect the B-J reflex inhibition of lumbar sympathetic nerve discharge. These results show that stimulation of NTS 5-HT3 receptors produced an inhibition of the cardiovagal component of the B-J reflex without affecting its sympathetic component. Because the stimulation of these receptors also inhibits the cardiac component of the baroreflex, the present data suggest the participation of NTS 5-HT3 receptors in the mechanisms that modulate cardiac reflex responses elicited by messages from different vagal afferents.

Animals↗
PubMed1999

5-HT(4) receptors in nucleus tractus solitarii attenuate cardiopulmonary reflex in anesthetized rats.

We determined whether the cAMP-protein kinase A (PKA) pathway modulation of the cardiopulmonary reflex was caused by activation of 5-HT(4) receptors at the level of the nucleus tractus solitarii (NTS) of the anesthetized rat. NTS microinjection of 5-methoxytryptamine (5-MeOT, 2.25 pmol, n = 13), a 5-HT-receptor agonist, attenuated the cardiopulmonary reflex-evoked bradycardia and tachypnea. Microinjection of RS-39604 (4.5 pmol, n = 6), a selective 5-HT(4)-receptor antagonist, blocked the attenuating effect of 5-MeOT. NTS microinjection of 8-bromoadenosine 3', 5'-cyclic monophosphate (8-BrcAMP, 9 nmol, 45 nl, n = 10), a membrane-permeant analog of cAMP, significantly attenuated the reflex bradycardia and tachypnea. Rp-adenosine 3',5'-cyclic monophosphorothioate (4.5 nmol, n = 6), a cAMP-dependent PKA inhibitor, had no effect on the cardiopulmonary reflex when microinjected into the NTS alone but when given before a microinjection of either 8-BrcAMP (n = 6) or 5-MeOT (n = 6) blocked the attenuating effect on the reflex-evoked bradycardia. Thus stimulation of 5-HT(4) receptors within the NTS depresses the reflex bradycardia components of the cardiopulmonary reflex via a cAMP-dependent PKA pathway.

5-Methoxytryptamine↗
PubMed2003

Hypothermia and hypoxia inhibit the Hering-Breüer reflex in the marsupial newborn.

The effects of lowering body temperature (T(b)) on metabolic rate, ventilation, and the strength of the Hering-Breüer expiratory promoting reflex (HB reflex; determined from an inhibitory ratio calculated from volumetric measurements of the respiratory rhythm) were examined in 18-day-old ectothermic pouch young of the tammar wallaby during normoxia or hypoxia (10% O(2)). Hypoxia and hypothermia, either singularly or combined, depressed metabolic rate. At all T(b), the hypoxic hyperventilation was associated with a significant hyperpnea. At pouch T(b) (36.5 degrees C) during normoxia, inflation of the lungs with -5 or -10 cmH(2)O extrathoracic pressure induced a significant HB reflex. Exposure to cold reduced the strength of the reflex, almost abolishing it at 28 degrees C. For T(b) above 28 degrees C, the reflex in hypoxia was always less than the corresponding normoxic value. Taken in context with the changes in metabolic state that occurred, these data in the ectothermic marsupial newborn suggest that the decline in the HB reflex during moderate hypothermia is the result of a direct effect of T(b) on vagal mechanisms rather than a temperature-driven decline in metabolic rate that should have acted to strengthen the HB reflex. Therefore, it seems that inputs inhibitory to breathing are more negatively affected during cold than those inputs that are excitatory.

Age Factors↗
PubMed2006

Reflexes from the lungs and airways: historical perspective.

Historical aspects of respiratory reflexes from the lungs and airways are reviewed, up until about 10 yr ago. For most of the 19th century, the possible reflex inputs into the "respiratory center," the position of which had been identified, were very speculative. There was little concept of reflex control of the pattern of breathing. Then, in 1868, Breuer published his paper on "The self-steering of respiration via the Nervus Vagus." For the first time this established the role of vagal inflation and deflation reflexes in determining the pattern of breathing. Head later extended Breuer's work, and Kratschmer laid a similar basis for reflexes from the nose and larynx. Then, 50-60 yr later, the development of the thermionic valve and the oscilloscope allowed recording action potentials from single nerve fibers in the vagus. In 1933, Adrian showed that slowly adapting pulmonary stretch receptors were responsible for the inflation reflex. Later, Knowlton and Larrabee described rapidly adapting receptors and showed that they mediated deep augmented breaths and the deflation reflex. Still later, it was established that rapidly adapting receptors were, at least in part, responsible for cough. In 1954, Paintal began his study of C-fiber receptors (J receptors), work greatly extended by the Coleridges. Since approximately 10 yr ago, when the field of this review stops, there has been an explosion of research on lung and airway receptors, many aspects of which are dealt with in other papers in this series.

Animals↗
PubMed2004

Effects of baclofen on spinal reflexes and persistent inward currents in motoneurons of chronic spinal rats with spasticity.

In the months after spinal cord injury, motoneurons develop large voltage-dependent persistent inward currents (PICs) that cause sustained reflexes and associated muscle spasms. These muscle spasms are triggered by any excitatory postsynaptic potential (EPSP) that is long enough to activate the PICs, which take > 100 ms to activate. The PICs are composed of a persistent sodium current (Na PIC) and a persistent calcium current (Ca PIC). Considering that Ca PICs have been shown in other neurons to be inhibited by baclofen, we tested whether part of the antispastic action of baclofen was to reduce the motoneuron PICs as opposed to EPSPs. The whole sacrocaudal spinal cord from acute spinal rats and spastic chronic spinal rats (with sacral spinal transection 2 mo previously) was studied in vitro. Ventral root reflexes were recorded in response to dorsal root stimulation. Intracellular recordings were made from motoneurons, and slow voltage ramps were used to measure PICs. Chronic spinal rats exhibited large monosynaptic and long-lasting polysynaptic ventral root reflexes, and motoneurons had associated large EPSPs and PICs. Baclofen inhibited these reflexes at very low doses with a 50% inhibition (EC50) of the mono- and polysynaptic reflexes at 0.26 +/- 0.07 and 0.25 +/- 0.09 (SD) microM, respectively. Baclofen inhibited the monosynaptic reflex in acute spinal rats at even lower doses (EC50 = 0.18 +/- 0.02 microM). In chronic (and acute) spinal rats, all reflexes and EPSPs were eliminated with 1 microM baclofen with little change in motoneuron properties (PICs, input resistance, etc), suggesting that baclofen's antispastic action is presynaptic to the motoneuron. Unexpectedly, in chronic spinal rats higher doses of baclofen (20-30 microM) significantly increased the total motoneuron PIC by 31.6 +/- 12.4%. However, the Ca PIC component (measured in TTX to block the Na PIC) was significantly reduced by baclofen. Thus baclofen increased the Na PIC and decreased the Ca PIC with a net increase in total PIC. By contrast, when a PIC was induced by 5-HT (10-30 microM) in motoneurons of acute spinal rats, baclofen (20-30 microM) significantly decreased the PIC by 38.8 +/- 25.8%, primarily due to a reduction in the Ca PIC (measured in TTX), which dominated the total PIC in these acute spinal neurons. In summary, baclofen does not exert its antispastic action postsynaptically at clinically achievable doses (< 1 microM), and at higher doses (10-30 microM), baclofen unexpectedly increases motoneuron excitability (Na PIC) in chronic spinal rats.

Acute Disease↗
PubMed2003

Progressive adaptation of the soleus H-reflex with daily training at walking backward.

When untrained subjects walk backward on a treadmill the amplitude of the soleus H-reflex in midswing is equal to or exceeds the value in stance. This is a surprising result because during the swing phase of backward walking the soleus is inactive and its antagonist, the tibialis anterior, is active. We suggested that the high amplitude of the soleus H-reflex in late swing reflects task uncertainties, such as estimating the moment of foot contact with the ground and losing balance. In support of this idea we show that when untrained subjects held on to handrails the unexpected high-amplitude H-reflex during midswing was no longer present. We therefore asked whether daily training at this task without grasping the handrails would adaptively modify the H-reflex modulation pattern. In this event, within 10 days of training for 15 min daily, the anticipatory reflex activity at the beginning of training was gradually abated as the subjects reported gaining confidence at the task. However, when adapted subjects were made to walk backward with their eyes shut, the anticipatory reflex activity in midswing returned immediately. The reflex changes as a result of training were not due to changes in the motor activity or kinematics; they are likely part of the motor program controlling backward walking. This adaptive phenomenon may prove to be a useful model for studying the neural mechanisms of motor learning and adaptive plasticity in humans and may be relevant to rehabilitation programs for neurological patients.

Adaptation, Physiological↗
PubMed2006

Contribution of M-waves and H-reflexes to contractions evoked by tetanic nerve stimulation in humans.

Tetanic neuromuscular stimulation evokes contractions by depolarizing motor axons beneath the stimulating electrodes. However, we have shown that extra torque can develop due to the discharge of spinal neurons recruited by the evoked sensory volley. The present experiments investigated whether extra torque in the ankle plantar- and dorsiflexors was associated with enhanced H-reflexes. The tibial and common peroneal nerves were stimulated using 7-s trains (20 Hz for 2 s, 100 Hz for 2 s, 20 Hz for 3 s). Extra torque was defined as significantly more torque during 20-Hz stimulation after the 100-Hz burst (time2) than before it (time1). In 9 of 11 subjects, extra plantarflexion torque developed during stimulation just above motor threshold. In these nine subjects, torque increased from 8 to 13% MVC (time1 to time2), the soleus H-reflex increased from 13 to 19% Mmax and the M-wave of approximately 2% Mmax did not change significantly. To evoke extra dorsiflexion torque, greater stimulation intensities were required. In 6 of 13 subjects, extra torque developed at intensities that evoked an M-wave of 5-20% Mmax at time1. In these six subjects, torque doubled from 2 to 4% MVC (time1 to time2), whereas tibialis anterior (TA) H-reflexes and M-waves did not change significantly (H-reflex from 0.8 to 2% Mmax; M-wave from 12 to 14% Mmax). In 7 of 13 subjects, extra torque developed at higher stimulation intensities (35-65% Mmax). In these seven subjects, torque increased from 13 to 20% MVC, whereas TA H-reflexes and M-waves were not significantly different (H-reflex from 0.7 to 1% Mmax; M-wave from 49 to 54% Mmax). Thus enhanced H-reflexes contributed to extra plantarflexion, however, other factors generated extra dorsiflexion.

Adult↗
PubMed1983

Dynamics of neck-to-forelimb reflexes in the decerebrate cat.

We have studied the neck-to-forelimb reflex evoked by head rotation around the longitudinal axis (roll) in the long and medial heads of triceps brachii of decerebrate, acutely labyrinthectomized cats. Reflexes were measured by recording mass electromyogram (EMG). As expected from the work of others, they were reciprocal in the two limbs, with excitation in the limb toward which the chin rotates. The reflex was sufficiently linear for a sinusoidal analysis. Although there was sometimes adaptation at stimulus frequencies of 0.1 Hz and below, response phase at these frequencies was usually in phase with position, and gain was flat. At higher frequencies there was some sensitivity to the velocity of the stimulus: gain increased with a slope of 10 dB/decade and phase advanced in some cats but not in others. Gain at low frequencies of head rotation, expressed as percent modulation of EMG, was typically 1%/deg or less. Reflexes evoked by head rotation in triceps and in the neck extensor splenius capitis have different dynamics. It remains to be determined whether this difference is due to activation of different receptors. We compared the dynamics of roll reflexes evoked by stimulation of neck receptors with those of vestibular reflexes evoked by tilt of the whole animal (23). Taking into account dynamics and gain, the two reflexes should cancel at low frequencies, as predicted by others. Above 0.2 Hz, cancellation becomes less effective.

Animals↗
PubMed1986

Phase-dependent reversal of reflexes mediated by the thoracocoxal muscle receptor organ in the crayfish, Pacifastacus leniusculus.

Both negative feedback, resistance reflexes and positive feedback, assistance reflexes are mediated by the thoracocoxal muscle receptor organ (TCMRO) in the crayfish, depending on the central excitability of the preparation. In this paper we present evidence that the velocity-sensitive afferent T fiber of the TCMRO may elicit either resistance or assistance reflexes in different preparations. In preparations displaying assistance reflexes, the S and T fibers of the TCMRO exert reciprocal effects on leg motor neurons (MNs). The S fiber excites promotor MNs (negative feedback) and inhibits remotor MNs, the T fiber excites remotor MNs (positive feedback) and inhibits promotor MNs. During reciprocal motor output of promotor and remotor MNs, reflexes mediated by the TCMRO are modulated in a phase-dependent manner. The TCMRO excites promotor MNs during their active phases (negative feedback) but inhibits them during their reciprocal phases. Remotor MNs are excited by the TCMRO during their active phases (positive feedback). It is proposed that depolarizing central inputs that occur in the S and T fibers at opposite phases of the motor output cycle (21) facilitate the output effects of each afferent in alternation, effectively mediating a phase-dependent shift between the effects of one afferent and the other. The implications of central modulation of reflex pathways and the possible functions of positive and negative feedback reflexes during locomotion are discussed.

Animals↗
PubMed1990

Stiffness regulation by reflex action in the normal human hand.

1. The torque and electromyographic (EMG) responses to stretch of the first dorsal interosseous muscle (externally imposed joint rotation) were recorded in five normal human subjects. The total measured stiffness was decomposed into three individual stiffness components; passive, intrinsic, and reflex. 2. The passive component was measured with the subject relaxed. Compared with the total response at the height of short latency reflex action, the passive component comprised 6-32% of the total stiffness recorded at an initial torque level of 20 N-cm [15-39% maximum voluntary contraction (MVC)]. The passive response also reflected a significant acceleration component during rapid joint rotation due primarily to digit inertia. 3. The intrinsic stiffness component, attributed to the mechanical properties of the active muscle fibers, was estimated by recording the response to joint rotation with the muscle activated in a distributed manner using a single intramuscular electrode. The dynamic stiffness (measured at the end of a ramp displacement) and the static stiffness (measured 1 s after onset of the displacement) both scaled in a straight-line manner with the initial torque level. This relationship held whether the initial torque level was varied by changes in recruitment or temporal summation. 4. The reflex component was calculated by subtracting the passive and the estimated intrinsic component from the total response. The timing of the EMG signal recorded during measurement of the total response and the fact that the estimated intrinsic component matched the total active response over the first 65-100 ms after displacement onset supported the case that this was the true reflex component. The peak of the reflex activity occurred 155-360 ms after displacement onset and, at this peak, accounted for 18-44% of the total stiffness (at an initial torque level of 20 N-cm). 5. Over the low to intermediate torque range employed, we observed that both intrinsic muscle stiffness and total stiffness increased with initial torque. Because total stiffness increased more rapidly than intrinsic stiffness, the difference between them (equal to reflex stiffness) also increased with initial torque. Furthermore, when the total active response trials (passive stiffness removed) were shifted vertically so that the initial torque levels matched, it was seen that reflex action did not reduce the stiffness range to less than the stiffness range encountered for the intrinsic response alone.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1991

Changes in central delay of soleus H reflex after facilitatory or inhibitory conditioning in humans.

1. Central delay (CD) changes after facilitatory or inhibitory conditioning of the soleus H reflex have been investigated in a group of normal subjects as a function of the conditioning and test stimulus intensities and also as a function of the Hmax/Mmax ratio. Both facilitation and inhibition of the reflex response have been obtained by conditioning stimulation of the ipsilateral tibial nerve at suitable conditioning-test stimulus intervals. CD changes have been extrapolated from the variations of the time interval between afferent and efferent neural volleys underlying the H reflex, directly recorded from the sciatic nerve. 2. The CD was significantly decreased by facilitatory and increased by inhibitory conditioning. Facilitatory CD changes were positively related to test stimulus strength (at a given conditioning stimulus intensity) and negatively related to conditioning stimulus strength (at a given test stimulus intensity). Both trends were reversed after inhibitory conditioning. The effectiveness of facilitatory conditioning was positively related to the individual Hmax/Mmax ratio whereas a negative relationship could be observed after inhibitory conditioning. 3. Also, the "conditioning threshold" (the minimal conditioning stimulus strength affecting the reflex size) and the "maximal conditioning effect" (the conditioning stimulus intensities leading to either the saturation of the facilitatory effect or the suppression of the reflex response) were significantly related to the Hmax/Mmax ratio. 4. We suggest that temporal changes in the H reflex pathway after facilitatory or inhibitory conditioning stimuli depend both on the size of the motoneuronal pool underlying the reflex response, as determined by the test stimulus intensity, and on the individual excitability of the motoneuronal pool, as defined by the Hmax/Mmax ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Transient reversal of the stretch reflex in human arm muscles.

1. Load perturbation responses can violate the law of reciprocal innervation between antagonist muscles under particular conditions. Thus flexor and extensor muscles of wrist and elbow joints are reflexly coactivated by the impact of a ball on the hand during a catching task. The aim of this study was to determine whether reflex coactivation can be preset within the central nervous system (CNS) or whether it is entirely due to the peripheral stimulus. To this end, we studied the behavior of stretch reflex responses of arm muscles evoked by torque motor perturbations applied before and during the catching task. 2. Subjects were instructed to catch a ball dropped from 1.6 m. A torque motor delivered perturbations to the elbow joint, resulting in angular motion at both elbow and wrist joints because of their dynamic mechanical coupling. Two series of experiments were performed that differed in the perturbation waveform. In the first series, a single torque pulse could be randomly applied at different times during the task. The corresponding responses were recovered by subtracting the average of the unperturbed trials from the averages of perturbed trials. In the second series of experiments, a train of pseudorandom pulses was applied continuously during each trial. The time-varying impulse responses were computed at 20-ms intervals by cross-correlation methods. 3. The pattern of the short-latency electromyographic responses evoked by either single pulses or pseudorandom perturbations obeyed the law of reciprocal innervation of antagonist muscles under basal conditions. However, the pattern of the responses evoked by the same perturbations around the time of ball impact on the hand consisted of a substantial coactivation of both stretched and shortening muscles. Reflex coactivation resulted from response patterns that differed at different joints. At the elbow, reflex coactivation resulted from a transient reversal of the direction of the short-latency responses of flexor muscles, with little changes of the responses of extensor muscles. At the wrist, instead, reflex coactivation resulted from simultaneous changes in the response waveform of both flexor and extensor muscles. 4. The peripheral conditions associated with the applied perturbations were constant before the time of ball impact. Thus, because the changes of the stretch reflex responses began before that time, they must have been generated within the CNS. It is here hypothesized that the reversal of the reflex responses is centrally gated by switching from the pathways of reciprocal inhibition to those of coactivation of antagonist alpha-motoneurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Arm↗
PubMed1995

Ventral respiratory group bulbospinal inspiratory neurons participate in vestibular-respiratory reflexes.

1. The vestibular system responds to accelerations of the head and produces reflex responses that serve a variety of compensatory functions. The neuronal circuitry that mediates vestibulo-respiratory reflexes is largely unknown. The purpose of the present study was to investigate the possible role of bulbospinal inspiratory neurons located in the para-ambigual region of the ventral respiratory group (VRG) in mediating these reflexes. Experiments were carried out in cats that were decerebrated, paralyzed, and artificially ventilated. 2. Activation of the vestibular nerve by electrical stimulation produced prominent bilateral reflex responses recorded from the phrenic nerve, which supplies the diaphragm. The responses could be complex and consisted of a decrease and/or increase in nerve discharge. 3. Extracellular recordings were made from 35 VRG inspiratory neurons that were antidromically activated from the upper cervical spinal cord. Almost one-half of these neurons (15/35, 43%) responded to vestibular stimulation. The neuronal response patterns were consistent with VRG inspiratory neurons contributing to the vestibular reflex response simultaneously recorded from the phrenic nerve. 4. The present results indicate that approximately one-half of VRG bulbospinal inspiratory neurons contribute to vestibulo-respiratory reflexes. These findings are in contrast to our recent neuroanatomic and electrophysiological studies which revealed a paucity of vestibular inputs to the dorsal respiratory group (DRG) located in the ventrolateral nucleus of the solitary tract. Thus there appears to be a difference between inspiratory neurons in the DRG and VRG in regard to participating in vestibulo-respiratory reflexes.

Animals↗
PubMed1996

Modulation of human soleus H reflex in association with voluntary clenching of the teeth.

1. To determine the effects of motor activity in the jaw on more general motor behavior, we examined the modulation of the soleus H reflex in association with voluntary clenching of the teeth in healthy adult volunteers. 2. The amplitude of the H reflex increased remarkably during teeth clenching. The increase during maximal teeth clenching was greater than that induced either by maximal voluntary isometric contraction of the wrist extensors or by maximal voluntary clenching of the fists. 3. The increase in amplitude of the soleus H reflex showed a positive correlation with the strength of teeth clenching, as monitored by recording electromyographic (EMG) activity from the masseter muscle. 4. The increase in amplitude of the H reflex associated with teeth clenching started before the onset of the EMG activity of the masseter muscle, reached a peak shortly after the onset, and then declined to a plateau that continued in parallel with the masseter EMG until the end of teeth clenching. 5. The increase in amplitude of the H reflex in association with teeth clenching was partially decreased during the inhibitory masseteric reflex evoked by innocuous electrical stimulation of the lip. 6. It is concluded that the soleus H reflex is facilitated in association with voluntary teeth clenching, and that descending influences from the cerebral cortex, as well as peripheral afferent impulses from the oral-facial region, are involved in this facilitation. It is proposed that oral motor activity can exert strong influences on the motor activity of the other parts of the body.

Adult↗
PubMed1996

Role of ventral respiratory group bulbospinal expiratory neurons in vestibular-respiratory reflexes.

1. Activation of the vestibular system produces reflex modulation of expiratory muscle activity. The purpose of the present study was to investigate the possible role of bulbospinal expiratory (E) neurons located in the caudal ventral respiratory group (VRG) in mediating vestibulo-respiratory reflexes. Experiments were carried out in decerebrated, paralyzed, and artificially ventilated cats. 2. Electrical stimulation of the vestibular nerve (VN), using short trains of current pulses, elicited bilateral reflex responses on abdominal muscle nerves (ABDNs). This response was not affected by lesions of the cochlear nuclei made by kainic acid injections. The ABDN response typically consisted of a combination of short-latency excitation and long-latency inhibition on the ipsilateral side and, in contrast, a combination of short-latency inhibition and long-latency excitation on the contralateral side. 3. Extracellular recordings were made from 43 caudal VRG bulbospinal E neurons that were activated antidromically from the contralateral upper lumbar spinal cord. More than 80% of these neurons responded to either ipsi- and/or contralateral VN stimulation. The neuronal response consisted of either a combination of excitation and inhibition or only inhibition. The majority of neurons had response patterns appropriate to contribute to the response observed on the contralateral ABDN; however, the latency of the VRG E neuron response was too long to initiate the ABDN response. 4. To further evaluate the contribution of caudal VRG E neurons to the vestibulo-abdominal reflex, ABDN responses were compared before and after sectioning the axons of caudal VRG bulbospinal E neurons where they cross the midline between the obex and first cervical spinal segment. These midsagittal lesions abolished expiratory modulation of ABDN discharge. The lesions also decreased the amplitude of the vestibular-evoked ABDN response but could not abolish the response. The postlesion amplitude was decreased on average to approximately 70% of prelesion values. 5. In conclusion, although the present results indicate that the majority of caudal VRG bulbospinal E neurons respond appropriately to contribute to the vestibulo-abdominal reflex, the reflex largely is unaffected by the removal of caudal VRG E input. The additional descending inputs that are important for mediating the reflex remain to be investigated and may include vestibulospinal and/or reticulospinal tracts.

Abdominal Muscles↗
PubMed2000

Kinetic and frequency-domain properties of reflex and conditioned eyelid responses in the rabbit.

Eyelid position and the electromyographic activity of the orbicularis oculi muscle were recorded unilaterally in rabbits during reflex and conditioned blinks. Air-puff-evoked blinks consisted of a fast downward phase followed sometimes by successive downward sags. The reopening phase had a much longer duration and slower peak velocity. Onset latency, maximum amplitude, peak velocity, and rise time of reflex blinks depended on the intensity and duration of the air puff-evoking stimulus. A flashlight focused on the eye also evoked reflex blinks, but not flashes of light, or tones. Both delayed and trace classical conditioning paradigms were used. For delayed conditioning, animals were presented with a 350-ms, 90-dB, 600-Hz tone, as conditioned stimulus (CS). For trace conditioning, animals were presented with a 10-ms, 1-k/cm(2) air puff, as CS. The unconditioned stimulus (US) consisted of a 100-ms, 3-k/cm(2) air puff. The stimulus interval between CS and US onsets was 250 ms. Conditioned responses (CRs) to tones were composed of downward sags that increased in number through the successive conditioning sessions. The onset latency of the CR decreased across conditioning at the same time as its maximum amplitude and its peak velocity increased, but the time-to-peak of the CR remained unaltered. The topography of CRs evoked by short, weak air puffs as the CS showed three different components: the alpha response to the CS, the CR, and the reflex response to the US. Through conditioning, CRs showed a decrease in onset latency, and an increase in maximum amplitude and peak velocity. The time-to-peak of the CR remained unchanged. A power spectrum analysis of reflex and conditioned blink acceleration profiles showed a significant approximately 8-Hz oscillation within a broadband of frequencies between 4 and 15 Hz. Nose and mandible movements presented power spectrum profiles different from those characterizing reflex and conditioned blinks. It is concluded that eyelid reflex responses in the rabbit present significant differences from CRs in their profiles and metric properties, suggesting different neural origins, but that a common approximately 8-Hz neural oscillator underlies lid motor performance. According to available data, the frequency of this putative oscillator seems to be related to the species size.

Air Movements↗
PubMed2000

Abeta fibers mediate cutaneous reflexes during human walking.

During human gait, transmission of cutaneous reflexes from the foot is controlled specifically according to the phase of the step cycle. These reflex responses can be evoked by nonnociceptive stimuli, and therefore it is thought that the large-myelinated and low-threshold Abeta afferent fibers mediate these reflexes. At present, this hypothesis is not yet verified. To test whether Abeta fibers are involved the reflex responses were studied in patients with a sensory polyneuropathy who suffer from a predominant loss of large-myelinated Abeta fibers. The sural nerve of both patients and healthy control subjects was stimulated electrically at a nonnociceptive intensity during the early and late swing phases while they walked on a treadmill. The responses were studied by recording electromyographic (EMG) activity of the biceps femoris (BF) and tibialis anterior (TA) of the stimulated leg. In both phases, large facilitatory responses were observed in the BF of the healthy subjects. These facilitations were reduced significantly in the BF of the patients, indicating that Abeta fibers mediate these reflexes. In TA similar results were obtained. The absolute response magnitude across the two phases was significantly smaller for the patients than for the healthy subjects. The TA responses for the healthy subjects were on average facilitatory during early swing and suppressive during end swing. Both facilitations and suppressions were considerably smaller for the patients, indicating that both types of responses are mediated by Abeta fibers. It is concluded that low-threshold Abeta sensory fibers mediate these reflexes during human gait. The low threshold and the precise phase-dependent control of these responses suggest that these responses are important in the regulation of gait. The loss of such reflex activity may be related to the gait impairments of these patients.

Adolescent↗
PubMed1988

Central modulation of baroreceptor reflex response to phenylephrine by dihydropyridines in rats.

The effects of two dihydropyridine derivatives, the calcium channel agonist BAY k 8644 or the antagonist PN 200-110, on the central nervous components of the baroreceptor reflex control of heart rate during activation of baroreceptors by phenylephrine (2 micrograms i.v.) were studied in pentobarbital-anesthetized normotensive (Wistar) rats and spontaneously hypertensive rats (SHR). To rule out an effect on peripheral vessels or on the sinoauricular node (or on both), BAY k 8644 and PN 200-110 were administered intracerebroventricularly (i.c.v.) at doses that did not change blood pressure. Baroreceptor reflex sensitivity was calculated as the slope of the relationship between systolic arterial pressure and heart period. Baroreceptor reflex sensitivity increased with time following the onset of anesthesia. In SHR, injection of BAY k 8644 (3 micrograms/kg i.c.v.) suppressed the time-dependent increase in baroreceptor reflex sensitivity. The inhibitory effect of BAY k 8644 (3 micrograms/kg i.c.v.) on the time-dependent increase in baroreceptor reflex sensitivity was suppressed by pretreatment with PN 200-110 (0.6 microgram/kg i.c.v.) but not with the solvent, indicating that the central effect of BAY k 8644 occurred at the level of specific dihydropyridine binding sites. In addition, the inhibitory effect of BAY k 8644 (3 micrograms/kg i.c.v.) on the time-dependent increase in baroreceptor reflex sensitivity was suppressed by pretreatment with the muscarinic antagonist atropine methylnitrate (80 micrograms/kg i.c.v.) but not with the solvent. In normotensive rats, the time-dependent increase in baroreceptor reflex sensitivity was not significantly altered by BAY k 8644 (3 micrograms/kg i.c.v.).(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗