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Reflex Changes (reflex + change)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

The inhibitory effect of a chewing task on a human jaw reflex

MUSCLE AND NERVE, Issue 6 2010
Pauline Maillou BDS
Abstract This study was undertaken to investigate whether an inhibitory jaw reflex could be modulated by experimentally controlled conditions that mimicked symptoms of temporomandibular disorders. Reflecting on previous work, we anticipated that these conditions might suppress the reflex. Electromyographic recordings were made from a masseter muscle in 18 subjects, while electrical stimuli were applied to the upper lip. An inhibitory reflex wave (mean latency 47 ms) was identified and quantified. Immediately following an accelerated chewing task, which in most cases produced muscle fatigue and/or pain, the size of the reflex wave decreased significantly by about 30%. The suppression of inhibitory jaw reflexes by fatigue and pain may result in positive feedback, which may contribute to the symptoms of temporomandibular disorders. Future studies of temporomandibular disorder sufferers will help to determine whether such reflex changes reflect the underlying etiology and/or are a result of the temporomandibular disorder itself. Muscle Nerve, 2010 [source]

Proceedings of the Australian Physiological and Pharmacological Society Symposium: The Hypothalamus HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND CARDIOVASCULAR REGULATION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2001
Emilio BadoerArticle first published online: 10 DEC 200
SUMMARY 1. The hypothalamic paraventricular nucleus (PVN) is an important integrative site within the brain composed of magnocellular and parvocellular neurons. It is known to influence sympathetic nerve activity. 2. The parvocellular PVN contains neurons that project to the intermediolateral cell column of the thoraco,lumbar spinal cord (IML). This defines the PVN as an autonomic ,premotor nucleus', one of only five present within the brain. 3. Another projection arising from the PVN is a prominent innervation of the pressor region of the rostral ventrolateral medulla (RVLM), also a premotor nucleus. The distribution of the PVN neurons projecting to the RVLM is similar to that of the PVN neurons that project to the IML. 4. It has been found that up to 30% of spinally projecting neurons in the PVN also send collaterals to the RVLM. Thus, there are neurons in the PVN that can: (i) directly influence sympathetic nerve activity (via PVN,IML connections); (ii) indirectly influence sympathetic nerve activity (via PVN,RVLM connections); and (iii) both directly and indirectly influence sympathetic nerve activity (via neurons with collaterals to the IML and RVLM). 5. In the rat, results of studies using the protein Fos to identify activated neurons in the brain suggest that neurons in the PVN with projections to the IML or RVLM may be activated by decreases in blood volume. 6. In conclusion, the PVN can influence sympathetic nerve activity. Within the PVN are neurons with anatomical connections that enable them to affect sympathetic nerve activity either directly, indirectly or via both mechanisms (via collaterals). Studies that have examined the role of specific subgroups within the PVN suggest that PVN neurons with connections to the IML or to the RVLM may play a role in the reflex changes in sympathetic nerve activity that are involved in blood volume regulation. [source]

Neural Regulation Of Renal Blood Flow: A Re-Examination

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2000
Simon C Malpas
SUMMARY 1. The importance of renal sympathetic nerve activity (RSNA) in the regulation of renal function is well established. However, it is less clear how the renal vasculature responds to the different mean levels and patterns of RSNA. While many studies have indicated that small to moderate changes in RSNA preferentially regulate renin secretion or sodium excretion and only large changes in RSNA regulate renal blood flow (RBF), other experimental evidence suggests that small changes in RSNA can influence RBF 2. When RSNA has been directly measured in conjunction with RBF, it appears that a range of afferent stimuli can induce reflex changes in RBF. However, many studies in a variety of species have measured RBF only during stimuli designed to reflexly increase or decrease sympathetic activity, but have not recorded RSNA. While this approach can be informative, it is not definitive because the ability of the vasculature to respond to RSNA may, in part, reflect the resting level of RSNA and, therefore, the vasoconstrictive state of the vasculature under the control conditions. 3. Further understanding of the control of RBF by RSNA has come from studies that have analysed the underlying rhythms in sympathetic nerve activity and their effect on the cardiovascular system. These studies show that the frequency,response characteristic of the renal vasculature is such that higher frequency oscillations in RSNA (above 0.6 Hz) contribute to setting the mean level of RBF. In comparison, lower frequency oscillations in RSNA can induce cyclic vasoconstriction and dilation in the renal vasculature, thus inducing oscillations in RBF. 4. In summary, the present review discusses the neural control of RBF, summarizing evidence in support of the hypothesis that RBF is under the influence of RSNA across the full range of RSNA. [source]

Pattern Formation And Rhythm Generation In The Ventral Respiratory Group

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2000
Donald R McCrimmon
SUMMARY 1. There is increasing evidence that the kernel of the rhythm-generating circuitry for breathing is located within a discrete subregion of a column of respiratory neurons within the ventrolateral medulla referred to as the ventral respiratory group (VRG). It is less clear how this rhythm is transformed into the precise patterns appearing on the varied motor outflows. 2. Two different approaches were used to test whether subregions of the VRG have distinct roles in rhythm or pattern generation. In one, clusters of VRG neurons were activated or inactivated by pressure injection of small volumes of neuroactive agents to activate or inactivate groups of respiratory neurons and the resulting effects on respiratory rhythm and pattern were determined. The underlying assumption was that if rhythm and pattern are generated by neurons in different VRG subregions, then we should be able to identify regions where activation of neurons predominantly alters rhythm with little effect on pattern and other regions where pattern is altered with little effect on rhythm. 3. Based on the pattern of phrenic nerve responses to injection of an excitatory amino acid (DL -homocysteate), the VRG was divided into four subdivisions arranged along the rostrocaudal axis. Injections into the three rostral regions elicited changes in both respiratory rhythm and pattern. From rostral to caudal the regions included: (i) a rostral bradypnoea region, roughly associated with the Bötzinger complex; (ii) a dysrhythmia/tachypnoea area, roughly associated with the pre-Bötzinger complex (PBC); (iii) a second caudal bradypnoea area; and, most caudally, (iv) a region from which no detectable change in respiratory motor output was elicited. 4. In a second approach, the effect of unilateral lesions of one subregion, the PBC, on the Breuer,Hering reflex changes in rhythm were determined. Activation of this reflex by lung inflation shortens inspiration and lengthens expiration (TE). 5. Unilateral lesions in the PBC attenuated the reflex lengthening of TE, but did not change baseline respiratory rhythm. 6. These findings are consistent with the concept that the VRG is not functionally homogeneous, but consists of rostrocaudally arranged subregions. Neurons within the so-called PBC appear to have a dominant role in rhythm generation. Nevertheless, neurons within other subregions contribute to both rhythm and pattern generation. Thus, at least at an anatomical level resolvable by pressure injection, there appears to be a significant overlap in the circuitry generating respiratory rhythm and pattern. [source]