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PubMedDate not supplied

Effects of morphine on somatocardiac sympathetic reflexes in spinalized cats.

The effects of morphine on sympathetic reflexes, recorded in the inferior cardiac nerve, to myelinated A and unmyelinated C afferent stimulation were tested in 17 acutely spinalized cats. Stable sympathetic A and C reflexes of short latency (approximately 30 ms and 140 ms in the case of the ulnar nerve, respectively) could be recorded in the inferior cardiac sympathetic nerve to stimulation of somatic A and C afferents in the ulnar and upper thoracic intercostal nerves, ipsilaterally. Spinal sympathetic A reflexes, which were primarily evoked from stimulation of A delta afferent fibers, could be elicited from more segmental levels than could sympathetic C reflexes. Additionally, smaller reflexes, only from A afferent fiber activation, were identified from stimulations on the contralateral side of the body. Small doses of morphine (0.02 mg kg-1, i.v.) proved to be ineffective at altering sympathetic A and C reflexes, while somewhat larger doses (0.2 mg kg-1, i.v.) produced a clear 62% decrease in C reflexes and a 33% decrease in A reflexes, Dosages of 1 and 2 mg kg-1 severely depressed both A and C reflexes. All of the above effects of morphine administration were completely and immediately reversible by naloxone (i.v.). The results are discussed with regard to the effects of morphine on sympathetic A and C reflexes in CNS intact, anesthetized cats.

Afferent Pathways↗
PubMed1992

Comparison of amplitude of human soleus H-reflex during sitting and standing.

The modulation of the H-reflex in the human soleus muscle under conditions of different length or of background EMG activity was compared in 7 healthy subjects under three conditions: sitting, standing with support, and standing without support. The amplitude of the H-reflex increased when the muscle was shortened in both the sitting and standing conditions. The degree of increase in H-reflex was smaller during standing than sitting for the same change in muscle length. The H-reflex was augmented according to the increase of the background EMG. The "reflex gain", the ratio of the increase in amplitude of the H-reflex to soleus muscle EMG activity, decreased on sitting, standing with support and standing without support, ranked in that order. From these observations, it is concluded that the H-reflex is modulated by both muscle length and the degree of postural stability. The modulation of the reflex could be interpreted in terms of gain compensation and would serve to stabilize posture. A decrease in reflex gain may be appropriate in stabilizing the spinal reflex feedback loop during standing, especially without support.

Adult↗
PubMed1995

Glutamate N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists administered into the brain stem depress the renal sympathetic reflex discharges evoked by single shock of somatic afferents in anesthetized rats.

The involvement of glutamate receptors in the central transmission of somatosympathetic reflexes was studied by examining, in anesthetized rats, the effects of MK-801, an N-methyl-D-aspartate (NMDA) receptor antagonist, and CNQX, a non-NMDA receptor antagonist, on two reflex components, the A- and C-reflexes evoked in the left sympathetic renal nerve by a single shock to the left tibial nerve. The A-reflex elicited by myelinated A fiber stimulation and the C-reflex elicited by unmyelinated C fiber stimulation were depressed, in a dose-dependent manner, following administration of either MK-801 or CNQX into the cisterna magna (i.c.m.). Intrathecal (i.t.) administration of MK-801 did not have any effect on either A- or C-reflexes, while i.t. administration of CNQX had a slight effect on the A-reflex (significantly on the A-reflex only when treated with the highest dose of 100 ng) and the C-reflex. These results indicate that both NMDA and non-NMDA receptors, stimulated by glutamate released possibly as a neurotransmitter, are involved in the central transmission pathways of somatosympathetic reflexes at the level of the brain stem, but not the spinal cord.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1990

A pharmacological analysis of the neuronal circuitry involved in distension-evoked enteric excitatory reflex.

Isolated segments of guinea-pig small intestine were set up in a partitioned bath to study the enteric excitatory reflex evoked by distension. The gut was distended by a rubber balloon inserted at the aboral end and contractions of the circular muscle were recorded at the oral end. The oral and aboral ends of the gut were separated by an intermediate compartment of the bath. Inflation of the intraluminal balloon with 0.075-0.35 ml water elicited reproducible and distension-dependent contraction. This enteric orally directed (ascending) excitatory reflex was abolished by tetrodotoxin irrespective of the compartment in which it was applied. Hyoscine (0.3 microM) almost abolished the enteric excitatory reflex when it was applied to the oral compartment. This indicates that the transmission from the final motor neurons to the circular muscle is mainly cholinergic, acting via muscarinic receptors. Hyoscine had no effect on the enteric excitatory reflex when added to the intermediate compartment. When hyoscine was added to the aboral compartment, it decreased the enteric excitatory reflex elicited by low distension stimuli to 70% of control and decreased the enteric excitatory reflex elicited by higher distension stimuli to 95% of control. This indicates that ganglionic transmission involving muscarinic receptors at the site of distension in the aboral bath contributes to the enteric excitatory reflex. Hexamethonium (100 microm) greatly depressed the enteric excitatory reflex when applied to any compartment indicating that nicotinic transmission is most important in the afferent, intermediate and efferent components of the reflex and that the reflex pathway involves a polysynaptic chain of cholinergic interneurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Spinal substance P and N-methyl-D-aspartate receptors are coactivated in the induction of central sensitization of the nociceptive flexor reflex.

We have studied the effects and interactions of the neurokinin-1 receptor antagonist CP-96,345 and the N-methyl-D-aspartate receptor/channel blocker MK-801, both applied intravenously, on the flexor reflex and on the facilitation of the flexor reflex by conditioning stimulation of cutaneous C-afferents in decerebrate, spinalized, unanesthetized rats. The flexor reflex was evoked by subcutaneous electrical stimuli applied to the sural nerve innervation area 1/min at an intensity that activated C-fibers and was recorded as electromyogram from the ipsilateral hamstring muscles. The magnitude of the baseline flexor reflex was usually highly stable in the course of the experiments without experimental manipulations. The same stimulus was used as a conditioning train (0.9 Hz, 20 shocks) and caused a brief facilitation of the flexor reflex, which was maximal 0.5 and 1 min after stimulation (255.1 +/- 23.6% over baseline). During the course of the conditioning stimulus train, the reflex magnitude was gradually increased (wind-up). MK-801 (0.1 and 0.5 mg/kg) consistently depressed the polysynaptic flexor reflex. At a dose of 0.5 mg/kg, but not 0.1 mg/kg, MK-801 reduced the wind-up and blocked the facilitation of the flexor reflex induced by the conditioning stimulus by 90%. The facilitatory effect of 7 pmol intrathecal substance P was also partially reduced by MK-801. CP 96,345 (1 and 3 mg/kg) did not depress the flexor reflex, but dose-dependently antagonized reflex facilitation by the conditioning stimulus train, similarly to its antagonism of intrathecally applied 7 pmol substance P-induced facilitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Physiology and clinical applications of hand muscle reflexes.

Hand muscle reflexes to stretch or electric stimulation of mixed nerves consist of two main components, the short latency reflex (SLR, M1) or Hoffmann reflex (HR) and the long latency reflex (LLR, M2). The SLR is most likely a spinal, monosynaptic reflex and all the evidence presently available supports a transcortical pathway of the LLR. Investigations in normal subjects demonstrate that the LLR is a reflex mediated by fast conducting muscle and cutaneous afferents. Group II muscle afferents do not significantly contribute to this reflex and it cannot be explained by repetitive excitation of spinal oligosynaptic pathways. These findings should not be uncritically generalized to other muscle groups, because the central and peripheral mechanisms apparently differ according to the body region and mode of stimulation. The LLR of hand muscles is most likely involved in skillful movements of the fingers. It is believed to assist rapid compensatory responses to unexpected disturbances. In addition to the main component of the LLR, which is called LLR II, the study of electrically elicited thenar reflexes following stimulation of the median nerve disclosed further LLR components, the LLR I and the LLR III. The latter reflexes are rarely seen in normal subjects but have a significance in several diseases. Several abnormalities could be demonstrated in different diseases. Enhanced HR and reduced LLR are found in spasticity of various origin. Enhanced LLR I are frequently seen in Parkinson's disease, essential tremor and reflex myoclonus. Absent or reduced LLR II is found in Huntington's disease and in different focal brain lesions but not in symptomatic choreatic syndromes of other origin. Delayed latencies of the LLR II or absent LLR II have been described in multiple sclerosis. Enhanced LLR III may occur in cerebellar diseases. The method to elicit LLR of thenar muscles by electric stimulation may prove to be useful for clinical neurophysiology.

Electric Stimulation↗
PubMed2004

Electrophysiological characterization of facilitated spinal withdrawal reflex to repetitive electrical stimuli and its modulation by central glutamate receptor in spinal anesthetized rats.

The present study is aimed to systematically investigate wind-up and after-discharge of the spinal withdrawal reflex assessed by recording single motor unit (SMU) electromyographic (EMG) response to different intensities [0.5-1.5xreflex threshold (T)] of repetitive [frequencies (0.5-200 Hz)] transcutaneous electrical stimuli for 5 s. The role of central glutamate receptors in modulation of the withdrawal reflex facilitation was observed and evaluated in order to explore the potential central mechanism. Stimulus intensities below reflex threshold, such as 0.8xT, but not 0.5xT, could by repetition elicit and facilitate withdrawal reflex. The facilitation (wind-up and after-discharge) of the withdrawal reflex is a result of central integration and is increased significantly for increasing stimulus intensity and frequency. Electrical stimuli at 3-5 Hz for 5 s are appropriate to elicit wind-up. In contrast, 10-20 Hz frequencies of electrical stimuli are adequate to evoke the after-discharge. For pharmacological intervention, suprathreshold (1.5xT) repeated (5 Hz) electrically evoked facilitated reflex (wind-up) were apparently depressed by intrathecal (i.t.) administration of MK-801 as well as CNQX (40 nmol/10 microl, respectively). However, wind-up of spinal reflexes evoked by subthreshold (0.8xT) electrical stimuli could only be depressed by the treatment with CNQX, not MK-801. The after-discharge of the withdrawal reflex elicited by 20 Hz electrical stimulation with either 0.8xT or 1.5xT intensity was depressed by i.t. treatment with CNQX. I.t. application of MK-801 only depressed 0.8xT the intensity of electrically evoked after-discharge. In conclusion, for the first time, the present study clearly demonstrates that, following the wind-up phase, the spinal withdrawal reflex pathways continue to fire spontaneously in a stimulus frequency- and intensity-dependent way (temporal and/or spatial summation). This inherited memory and the central non-N-methyl-d-aspartate (non-NMDA) receptor, but not the NMDA receptor, mainly involving pharmacological mechanisms, may play an important role in pathological conditions with spontaneous nociceptive firing. Furthermore, the after-discharge of the spinal reflex may be an important indicator for studies on central sensitization in many pathological pain conditions.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2004

Spinal neurons activated with the urethrogenital reflex in the male rat.

The urethrogenital (UG) reflex is a spinal ejaculatory-like reflex. The location of spinal neurons activated by the UG reflex was examined in the male rat using the immediate early gene, c-fos. In addition, co localization of neurons containing galanin and choline acetyl transferase (ChAT) and serotonin fibers with fos-immunoreactive (fos-I) nuclei was examined. Activation of the UG reflex resulted in a significant increase in fos positive nuclei in segments T13-S1, compared to controls in which the UG reflex was not activated. Spinal circuits involved in the UG reflex include neurons relaying afferent information from the pudendal sensory nerve, in the dorsal horn and medial cord of L5-S1. Interneurons specifically activated with the UG reflex were identified in the medial, intermediate and lateral gray. A small proportion of parasympathetic and sympathetic preganglionic neurons in the intermediolateral cell column (IML) of L5-S1 and IML and medial gray of T13-L2, respectively, was activated with the UG reflex. A significant increase in the number of galanin containing neurons expressing c-fos in the medial gray of L3-L4 was also observed with the UG reflex. Serotonin fibers and varicosities were found throughout the spinal cord and were especially dense in the ventral horn, IML and medial gray. Fos activated neurons were found in close apposition to serotonin fibers in the IML and medial gray. These studies demonstrate the multisegmental intraspinal circuitry responsible for ejaculatory-like responses and demonstrate the potential involvement of galanin, acetylcholine and serotonin in mediation of the UG reflex.

Animals↗
PubMed2005

Gradual enlargement of human withdrawal reflex receptive fields following repetitive painful stimulation.

Dynamic changes in the topography of the human withdrawal reflex receptive fields (RRF) were assessed by repetitive painful stimuli in 15 healthy subjects. A train of five electrical stimuli was delivered at a frequency of 3 Hz (total train duration 1.33 s). The train was delivered in random order to 10 electrode sites on the sole of the foot. Reflexes were recorded from tibialis anterior, soleus, vastus lateralis, biceps femoris, and iliopsoas (IL). The RRF changes during the stimulus train were assessed during standing with even support on both legs and while seated. The degree of temporal summation was depending on stimulation site. At the most sensitive part of the RRF, a statistically significant increase in reflex size was seen after two stimuli while four stimuli were needed to observe reflex facilitation at less sensitive electrode sites. Hence, the region from which reflexes could be evoked using the same stimulus intensity became larger through the train, that is, the RRF was gradually expanding. Reflexes evoked by stimuli four and five were of the same size. No reflex facilitation was seen at other stimulus sites outside the RRF. In all muscles except in IL, the largest reflexes were evoked when the subjects were standing. In the ankle joint, the main withdrawal pattern consisted of plantar flexion and inversion when the subjects were standing while dorsi-flexion was prevalent in the sitting position. Up to 35 degrees of knee and hip flexion were evoked often leading to a lift of the foot from the floor during standing. In conclusion, a gradual expansion of the RRF was seen in all muscles during the stimulus train. Furthermore, the motor programme task controls the reflex sensitivity within the reflex receptive field and, hence, the sensitivity of the temporal summation mechanism.

Analysis of Variance↗
PubMed2004

Continuous wavelet transform in the evaluation of stretch reflex responses from surface EMG.

OBJECTIVE: This is the first reported use of the continuous wavelet transform (CWT) of the surface EMG (sEMG) to extract the reflex response to muscle stretch. We used a modulus-based method to estimate instantaneous amplitude-envelopes from ridges of the CWT (referred in this work as sEMG intensity) to extract the dynamic reflex response from sEMG. We tested the method on tendon reflexes where excellent temporal resolution is required to identify the different latency components, and on the tonic stretch reflex (tonic SR) response to an ongoing perturbation that characteristically has a low signal to noise ratio. METHODS: Eight subjects without neurological impairment were subjected to a series of archilles tendon taps and a 2 min continuous perturbation of the ankle using a pseudo-sinusoidal stretch profile containing frequencies from 0.1 to 8.0 Hz. The tendon reflexes were assessed in the soleus muscle at 10% of MVC and the tonic SR in tibialis anterior while the muscle was relaxed, at 5 and 10% of maximal voluntary contraction. Root mean square (RMS) and wavelet ridge extraction was applied to the sEMG signal to extract sEMG amplitudes (RMS) and intensities for all reflexes. To obtain the tonic SR, these estimates and those from the sEMG-RMS were subsequently cross-correlated with the perturbation record to yield 2 sets of estimates of reflex gain and coherence for comparison. RESULTS: The sEMG intensities were highly correlated with the torques resulting from a ramped voluntary contraction. Following tendon taps, the method resolved the M1, M2, M3 response components at accurate latencies and with more complete reconstruction of the components than RMS-derived estimates. The wavelet ridge estimates extracted the tonic SR from resting and contracting muscles with significantly higher coherence than RMS estimates. Reflex gain, when estimated from sEMG intensity or sEMG-RMS, demonstrated similar relationships to the perturbation frequency and background contraction level. When the sEMG intensity reflex gain estimates from different subjects were pooled, they showed significantly lower variance about the mean than gain estimates derived from the rectified sEMG. CONCLUSIONS: Wavelet-ridge extraction provides a valid approach to reflex evaluation from sEMG that does not depend on the absolute amplitude of the potentials measured at the EMG electrodes. This may have substantial advantages in more directly comparing responses between subjects on an absolute frequency scale without the need for normalisation against maximal contraction levels.

Electromyography↗
PubMed2006

The posture-related interaction between Ia-afferent and descending input on the spinal reflex excitability in humans.

The separate and combined depressive effects induced by vibration and standing on the soleus H-reflex have been studied by administering Achilles' tendon vibration in prone position and during stance. Without vibration, H-reflex amplitude was larger under prone than standing condition. Vibration reduced the reflex both in prone position and even more during stance. When vibration was superimposed to inclined stance (greater EMG background), the reflex was reduced of the same absolute amount as when it was superimposed to normal stance. When vibration was superimposed on stance with minimal or no background EMG, the reflex disappeared. These results confirm that both upright posture and vibration have a strong depressive effect on the H-reflex. They also show that muscle activity during stance is enough for overcoming the reflex depression. These findings provide information about the origin of the disfacilitatory effects on the monosynaptic reflex pathway, contribute to the understanding of the posture-related mechanisms responsible for the modulation of the spinal reflex excitability, and allow arguing in favour of a minor but adaptable role for the short latency stretch reflex in the control of quiet unperturbed stance.

Adult↗
PubMed2004

5-HT receptors involved in opioid-activated descending inhibition of spinal withdrawal reflexes in the decerebrated rabbit.

The role of 5-HT(1B/1D), 5-HT(2) and 5-HT(3) receptors in mediating descending inhibition of spinal reflexes activated by application of fentanyl to the fourth ventricle has been studied in rabbits decerebrated under N(2)O/isoflurane anaesthesia. In the control state, intraventricular fentanyl (3-30 microg kg(-1)) depressed, to an equal extent, short- and long-latency reflexes in the medial gastrocnemius muscle nerve evoked by electrical stimulation of all sural nerve afferents. Inhibition of reflexes resulted from a decreased base line excitability in the reflex pathway accompanied by a reduction in the rate of temporal summation of responses. Fentanyl-induced suppression of short- and long-latency reflexes was significantly reduced after intrathecal administration of the selective 5-HT(2)-receptor antagonist ICI 170,809 (300 microg). The same dose of the selective 5-HT(1B/1D) blocker GR 127,935 reduced inhibition from intraventricular fentanyl only for long-latency reflexes (i.e. those parts of the response for which the afferent drive is provided mainly by Adelta and C-fibre afferents). The 5-HT(3) antagonist tropisetron (also 300 microg intrathecal) did not significantly alter the descending inhibition of reflexes evoked by fentanyl. Both GR 127,935 and tropisetron reduced temporal summation of reflexes per se, effects that were reversed by intraventricular fentanyl. These data suggest that the descending pathway(s) activated by intraventricular fentanyl liberate 5-HT in the spinal cord to inhibit withdrawal reflexes by acting at 5-HT(2) and 5-HT(1B/1D), but not 5-HT(3) receptors. 5-HT(1B/1D), and to a lesser extent 5-HT(3) receptors also appear to have a role in modulating temporal summation of reflexes evoked by repetitive stimuli.

Afferent Pathways↗
PubMed1999

Assessing the laryngeal cough reflex and the risk of developing pneumonia after stroke.

OBJECTIVE: To determine the effectiveness of a new reflex cough test, using nebulized tartaric acid, in the evaluation of the laryngeal cough reflex and the development of aspiration pneumonia. STUDY DESIGN: In this two-phase study, the cough test assessed the cough reflex in 161 stroke subjects. Phase 1 was a double-blinded prospective study of 40 subjects scheduled to have both modified barium swallow and the reflex cough test. Phase 1 subjects with an abnormal cough test showed an increased pneumonia incidence, and therefore, phase 2 was not blinded. In phase 2, 121 subjects were evaluated using the cough test; 38 received a modified barium swallow. Test results were compared using the Fisher exact test. RESULTS: A total of 131 subjects from both phases had a normal reflex cough test; none developed pneumonia (p < .01). Thirty subjects from both phases had abnormal reflex cough test results; 5 developed pneumonia. Modified barium swallow findings did not reliably indicate the risk for developing pneumonia. Specificity of a normal reflex cough test was 100%. CONCLUSION: The reflex cough test reliably evaluated the laryngeal cough reflex and the associated risk of developing aspiration pneumonia in stroke patients. Testing the laryngeal cough reflex may significantly reduce morbidity, mortality, and costs in stroke patients.

Aged↗
PubMed1997

Trigeminal autonomic pathways involved in nociception-induced reflex cardiovascular responses.

Reflex cardiovascular responses elicited by noxious oro-facial stimulation are well known but the neural pathways that underlie trigeminal cardiovascular reflex reactions remain to be elucidated. In previous studies, we have shown that noxious electrical stimulation of the mandibular incisor in the anesthetized rat elicits increases in mean arterial blood pressure and heart rate (Allen, G.V., Barbrick, B. and Esser, M.J., Trigeminal parabrachial connections: possible pathway for nociception-induced cardiovascular reflex responses, Brain Res., 715 (1996) 125-135). In this study, microinjections of the presynaptic blocker, cobalt chloride, or the anesthetic agent, lidocaine, were made into selected brainstem sites to identify neural pathways that are involved in mediation of the reflex pressor responses. Ipsilateral and bilateral injections of chemical blocker into the dorsomedial spinal trigeminal nucleus, pars caudalis, lateral parabrachial nucleus and the rostral ventral lateral medulla/caudal A5 region attenuated the reflex cardiovascular response. Bilateral injections of cobalt chloride into the dorsomedial subnucleus caudalis resulted in 70-100% attenuation of the reflex pressor response. Bilateral injections of cobalt chloride and/or lidocaine into the lateral parabrachial nucleus or the rostral ventral lateral medulla/A5 region resulted in 43-57% and 44-100% attenuation of the reflex pressor response, respectively. There were no significant differences in the degree or duration of attenuation of the reflex pressor responses produced by cobalt chloride compared to that produced by lidocaine injections. The reflex pressor responses usually returned to baseline levels approximately 60 min following injection of the chemical blocker substance. The results indicate that noxious electrical stimulation of the mandibular incisor elicits a reflex increase in mean arterial blood pressure which is initially mediated in the dorsomedial spinal trigeminal nucleus, pars caudalis and is subsequently mediated in the lateral parabrachial nucleus and the rostral ventral lateral medulla/caudal A5 region.

Animals↗
PubMed2000

Crossed linguo-buccal reflex in post-stroke patients.

A pathological crossed orofacial reflex, called crossed linguo-buccal reflex in the present study, was observed in approximately 1/3 of post-stroke patients with central facial palsy. Stroking with pressure two or three times with a split wooden tongue-blade to the tongue or palate contralateral to the central facial palsy elicited a reflex movement consisting of retraction of the angle of mouth and medio-posterior withdrawal of the buccal mucosa on the paretic side. Seventy-seven patients with central hemifacial palsy caused by a unilateral cerebral lesion were examined clinically, electromyographically and by computed tomography (CT) and magnetic resonance imaging (MRI). In addition, three men with bilateral cerebral lesions and bilateral crossed linguo-buccal reflexes were electromyographically examined. Twenty-two patients with unilateral cerebral lesions had this reflex. It was found that this reflex was most frequently observed in patients with a capsulo-caudate lesion involving the head of the caudate nucleus, the anterior limb and genu of the internal capsule. The electromyogram of the reflex showed increased activity in the orbicularis oris, depressor anguli oris, risorius, zygomaticus major and buccinator muscles on the paretic side with a long latency (254-856 ms), and a prolonged after-discharge after the stimulation. Reciprocal inhibition was observed in patients with bilateral positive reflexes. These findings suggest that liberation of the polysynaptic brainstem reflex in the medulla oblongata and pons from the indirect corticobulbar inhibition may underlie the occurrence of the crossed linguo-buccal reflex in post-stroke patients.

Adult↗
PubMed1998

Effects of prenatal morphine and cocaine exposure on spinal sexual reflexes in male and female rats.

Previous studies demonstrated that in utero exposure to morphine or cocaine differentially alters adult sexual behaviors, which are dependent on circulating gonadal hormones in male and female rats. In the present study, the effects of in utero morphine and cocaine exposure on the urethrogenital reflex were examined. The urethrogenital reflex is thought to be a hormone-independent spinal sexual reflex in both males and females. This reflex is tonically inhibited by supraspinal neurons but can be consistently evoked by urethral stimulation in the spinally transected animals. Prenatal morphine or cocaine exposure did not remove the supraspinal inhibition of the urethrogenital reflex in spinally intact male or female rats. In spinally transected animals, the urethrogenital reflex was qualitatively similar in all groups. However, morphine-exposed males required a stronger stimulus to elicit the urethrogenital reflex but once elicited, the frequency of the urethrogenital reflex was significantly higher compared to either controls or cocaine-exposed males. In contrast, in female rats, neither prenatal morphine nor cocaine exposure had any effect on the urethrogenital reflex. Thus, the urethrogenital reflex appears to be differentially affected by prenatal exposure to morphine in males and females.

Animals↗
PubMed1998

Developmental and injury induced plasticity in the micturition reflex pathway.

The storage and periodic elimination of urine are dependent upon neural circuits in the brain and spinal cord that co-ordinate the activity of the urinary bladder, the urethra and the striated urethral sphincter. This study utilized anatomical, electrophysiological and pharmacological techniques to examine: (1) the organization of the parasympathetic excitatory reflex mechanisms that control the urinary bladder of the rat and the cat; and (2) the changes in these reflexes during postnatal development and after spinal cord injury. In normal adult cats and rats, the parasympathetic excitatory input to the bladder is dependent upon a spinobulbospinal reflex pathway that is activated by myelinated (Adelta) bladder afferents and that passes through an integrative center (the pontine micturition center, PMC) in the rostral brain stem. Transneuronal tracing studies using pseudorabies virus as well as physiological methods have revealed that the PMC is located in close proximity to the locus coeruleus. Single unit recordings indicate that neurons in the PMC respond to afferent input from the bladder and are excited prior to or during reflex bladder contractions. Glutamic acid is the major excitatory transmitter in the micturition reflex pathway. Glutamatergic transmission which is mediated by AMPA/kainate and NMDA receptors can be modulated by a variety of other transmitters. In neonatal animals, a spinal micturition reflex is activated by somatic afferent fibers from the perigenital region. This reflex is suppressed during postnatal development, but can be unmasked in adult animals following spinal cord injury. Spinal injury also causes the emergence of a spinal bladder-to-bladder reflex which in the cat is activated by capsaicin-sensitive C-fiber bladder afferents. Patch clamp studies in spinal cord slice preparations indicate that developmental and spinal cord injury induced plasticity in sacral parasympathetic reflex pathways is due in part to alterations in glutamatergic excitatory transmission between interneurons and preganglionic neurons. Changes in the electrical properties of bladder afferent pathways may also contribute to the reorganization of bladder reflexes in paraplegic animals.

Animals↗
PubMed2002

Modulation of viscero-somatic H-reflex during bladder filling: a possible tool in the differential diagnosis of neurogenic voiding dysfunctions.

OBJECTIVE: Despite evidence that the activation of visceral afferents modulates spinal motoneurone activity in humans, the circuits responsible for this modulation remain unclear. The aim of the present study was to assess the effect of urinary bladder filling on the excitability of somatic spinal motoneurones in patients affected by overactive bladder secondary to neurogenic and non-neurogenic causes in both patients with bladder underactivity and normal subjects by means of a urodynamic evaluation. METHODS: In order to evaluate the influence of bladder filling on somatic reflexes, we studied the H-reflex evoked by electrical stimuli applied to the tibial nerve at the popliteal fossa and recorded from the soleus muscle. The H-reflex was tested in the following conditions: (1). empty bladder; (2). medium bladder filling; (3). maximum bladder filling; (4). five minutes after bladder emptying. The H-reflex amplitude at empty bladder was considered as the control value. RESULTS: In healthy subjects, we observed a progressive reduction in the H-reflex amplitude during bladder filling. In spinal cord-injured patients affected by a neurogenic overactive bladder, bladder filling failed to inhibit the H-reflex amplitude; a decrease in the H-reflex amplitude similar to that displayed by normal subjects was observed in patients with a non-neurogenic overactive bladder. By contrast, H-reflex behavior was unmodified in neurogenic underactive bladder patients and was similar to normal subjects in psychogenic underactive patients. CONCLUSIONS: As behavior of the H-reflex varies during bladder filling in neurogenic and non-neurogenic overactive bladder patients as well as in neurogenic and non-neurogenic underactive bladder patients, H-reflex modulation may be considered a useful tool in the differential diagnosis of voiding dysfunctions.

Adult↗