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PubMedDate not supplied

The theory of chronic deafferentation dysesthesias.

The chronic dysesthesias are abnormal disturbing somatic sensations, which are painful or non-painful. Their abnormality is revealed by their null or distorted psychophysical relationships; they occur spontaneously or can be peripherally induced by innocuous or noxious stimuli. Among nonverbal or mentally incompetent humans and also subhumans, these dysesthesias are expressed by patterns of escape or avoidance behaviors. There is no contemporaneous and necessary relationship with peripheral nociception. The basic mechanisms of these abnormalities have been obscure, and conventional modes of therapy have been unsuccessful. The origin of these chronic abnormalities is known to arise from lesions of peripheral or central components of the neural pathway for normal pain and temperature sensibility. The cause of these abnormalities is thought to reside in pathophysiological foci of excitability among deafferented central nocireceptive neurons. The spontaneous dysesthesias can occur after partial or total deafferentation. The peripherally induced dysesthesias occur after partial deafferentations, which include loss of small caliber myelinated afferents in cases of peripheral origin; and they are mediated via remaining afferent pathways. Little is known about the deafferented neurons in the brain, or the pertinent remaining central afferent pathways. More is now known about the pathophysiological effects of deafferentation on nonspecific nocireceptive neurons in the dorsal horn. These include morphological alterations, reduced inhibition, supersensitivity, hyperexcitability, and novel afferent excitation. Additional studies of chronic deafferentation in subhumans are necessary to provide further information and to test hypotheses concerning the chronic deafferentation dysesthesias.

Afferent Pathways↗
PubMed1996

Bilateral organization of parallel and serial pathways in the dentate gyrus demonstrated by current-source density analysis in the rat.

1. Membrane currents evoked in the dentate gyrus (DG) by stimulation of afferent pathways from the entorhinal cortex (EC) and contralateral DG were examined by current-source density (CSD) analysis in urethan-anesthetized rats. Stimulation of each afferent pathway evoked membrane currents with distinct spatial and temporal organization in the DG. CSD and anatomic analysis revealed that afferent input from the EC activated the DG bilaterally through parallel and serial pathways. The analysis provided a detailed description of the location, timing, and relative amplitude of evoked monosynaptic and multisynaptic currents in the DG. 2. Orthodromic stimulation of the perforant path (PP) evoked a large ipsilateral excitatory postsynaptic current (iEPSC) at a latency of 2.5-4 ms in the middle and outer stratum moleculare (STM) of the DG, and a population spike that was generated by an excitatory inward current at a latency of 5-9 ms in the stratum granulosum. 3. A variable, low-amplitude ipsilateral inward current followed the population spike at a latency of 13-16 ms in the inner STM, which is the site of synaptic terminals of the associational and commissural pathways arising from neurons in the hilus of the DG. Orthodromic stimulation of the commissural pathway from the hilus of the contralateral DG also evoked an inward current in the inner STM at a latency of 2-6 ms, which was 40-60% of the amplitude of the monosynaptic iEPSC. 4. Orthodromic stimulation of the EC evoked a low-amplitude contralateral excitatory postsynaptic current (cEPSC) at a latency of 3-6 ms in the outer and middle STM of the contralateral DG, which was generated by monosynaptic transmission in the sparse crossed pathway from the EC. In contrast to the variable, low-amplitude inward current in the inner STM that followed the iEPSC, the cEPSC was consistently followed by a large inward current at a latency of 8-14 ms in the inner STM of the contralateral DG. 5. The large inward current in the inner STM of the contralateral DG was abolished by transection of the PP ipsilateral and rostral to the stimulating electrode, but was unaffected by transection of the PP at a similar location in the hemisphere contralateral to the stimulating electrode. These observations suggested that this current was most likely generated by a multisynaptic pathway involving the ipsilateral PP and the commissural pathway arising from the hilus of the DG. 6. In conclusion, efferents from the EC activated the DG bilaterally by parallel and serial pathways. Parallel monosynaptic pathways from the EC activated homologous distal segments of granule cell dendrites bilaterally, by a massive input to the ipsilateral DG and a sparse input to the contralateral DG. Sequential propagation from the EC through a multisynaptic pathway that included the commissural pathway from the hilus of the DG bilaterally activated the proximal segments of granule cell dendrites at longer latencies. The amplitude of the multisynaptic currents generated by serial pathways in the proximal dendrites varied inversely with the amplitudes of the monosynaptic currents evoked by parallel pathways in the distal dendrites. These observations may have implications for synaptic integration, associative properties, and information processing in the DG.

Afferent Pathways↗
PubMed1982

Ventilatory responses to mechanical loads in cervical cord-injured humans.

Load compensation in 29 cervical cord-injured men was inferred from the difference between actual first-breath responses to graded elastic and resistive loads and those calculated assuming identical respiratory muscle pressure (Pmus) wave forms in the unloaded and loaded states (i.e., the passive prediction). At every load, respiratory frequency (f) and tidal volume (VT) responses from different individuals formed a continuum ranging from a weak VT defense coupled with an increased f to a strong VT defense coupled with a decreased f. Individual VT responses ranged from values smaller than the passive prediction to values exceeding control, suggesting that phrenic motoneuron output was not constant but decreased in some subjects and increased in others. In support of this hypothesis, 1) individual VT responses varied with inspiratory duration (TI; P less than 0.01); 2) TI responses indicated some subjects prematurely terminated their phrenic motoneuron output, whereas others prolonged it; 3) VT/TI responses suggested that some subjects modified the discharge frequency of their phrenic output; and 4) rib cage instability contributed insignificantly to these responses. These findings, which are similar to those reported for normal men, indicate that 1) afferent pathways from the rib cage and intercostal muscles are not required for the initiation of a range of ventilatory responses to loads; and 2) afferent pathways from the mouth, lung, and/or diaphragm are sufficient, by themselves, to modulate the duration, intensity, and timing of the phrenic discharge during the first loaded breath.

Afferent Pathways↗
PubMed2002

Activation of central terminal vanilloid receptor-1 receptors and alpha beta-methylene-ATP-sensitive P2X receptors reveals a converged synaptic activity onto the deep dorsal horn neurons of the spinal cord.

Using a spinal cord slice preparation and patch-clamp recordings from spinal cord dorsal horn neurons, we examined excitatory and inhibitory circuits connecting to lamina V neurons after the activation of afferent central terminal vanilloid receptor-1 (VR1) receptors and P2X receptors. We found that single neurons in lamina V often received excitatory inputs from two chemically defined afferent pathways. One of these pathways was polysynaptic from capsaicin-sensitive afferent terminals. In this pathway the capsaicin-sensitive afferent input first activated interneurons in superficial laminas, and then the excitatory activity was transmitted onto lamina V neurons. The second excitatory input was monosynaptic from alpha(beta)m-ATP-sensitive/capsaicin-insensitive afferent terminals. Both capsaicin-sensitive and alpha(beta)m-ATP-sensitive/capsaicin-insensitive pathways also recruited polysynaptic inhibitory inputs to lamina V neurons. Furthermore, we demonstrated that simultaneous activation of both capsaicin-sensitive afferent pathways and alpha(beta)m-ATP-sensitive/capsaicin-insensitive pathways could generate a temporal summation of excitatory inputs onto single lamina V neurons. These convergent pathways may provide a mechanism of sensory integration for two chemically defined sensory inputs and may have implications in different sensory states.

Action Potentials↗
PubMed2006

Peripheral ghrelin transmits orexigenic signals through the noradrenergic pathway from the hindbrain to the hypothalamus.

Ghrelin, a gastrointestinal peptide, stimulates feeding when administered peripherally. Blockade of the vagal afferent pathway abolishes ghrelin-induced feeding, indicating that the vagal afferent pathway may be a route conveying orexigenic ghrelin signals to the brain. Here, we demonstrate that peripheral ghrelin signaling, which travels to the nucleus tractus solitarius (NTS) at least in part via the vagus nerve, increases noradrenaline (NA) in the arcuate nucleus of the hypothalamus, thereby stimulating feeding at least partially through alpha-1 and beta-2 noradrenergic receptors. In addition, bilateral midbrain transections rostral to the NTS, or toxin-induced loss of neurons in the hindbrain that express dopamine beta hydroxylase (an NA synthetic enzyme), abolished ghrelin-induced feeding. These findings provide new evidence that the noradrenergic system is necessary in the central control of feeding behavior by peripherally administered ghrelin.

Animals↗
PubMed2005

Superior laryngeal and hypoglossal afferents tonically influence upper airway motor excitability in anesthetized rats.

Upper airway (UA) muscle activity is stimulated by changes in UA transmural pressure and by asphyxia. These responses are reduced by muscle relaxation. We hypothesized that this is due to a change in afferent feedback in the ansa hypoglossi and/or superior laryngeal nerve (SLN). We examined 1) the glossopharyngeal motor responses to UA transmural pressure and asphyxia and 2) how these responses were changed by muscle relaxation in animals where one or both of these afferent pathways had been sectioned bilaterally. Experiments were performed in 24 anesthetized, thoracotomized, artificially ventilated rats. Baseline glossopharyngeal activity and its response to UA transmural pressure and asphyxia were moderately reduced after bilateral section of the ansa hypoglossi (P < 0.05). Conversely, bilateral SLN section increased baseline glossopharyngeal activity, augmented the response to asphyxia, and abolished the response to UA transmural pressure. Muscle relaxation reduced resting glossopharyngeal activity and the response to asphyxia (P < 0.001). This occurred whether or not the ansa hypoglossi, the SLN, or both afferent pathways had been interrupted. We conclude that ansa hypoglossi afferents tonically excite and SLN afferents tonically inhibit UA motor activity. Muscle relaxation depressed UA motor activity after section of the ansa hypoglossi and SLN. This suggests that some or all of the response to muscle relaxation is mediated by alterations in the activity of afferent fibers other than those in the ansa hypoglossi or SLN.

Afferent Pathways↗
PubMed1996

Rectal afferent function in patients with inflammatory and functional intestinal disorders.

Chronic symptoms of abdominal pain and discomfort are reported by patients with inflammatory bowel disease (IBD) and functional disorders of the gut, such as Irritable Bowel Syndrome (IBS). It has recently been suggested that transient inflammatory mucosal events may result in long-lasting sensitization of visceral afferent pathways. To determine the effect of recurring intestinal tissue irritation on lumbosacral afferent pathways, and to identify a plausible mechanism that could account for the overlap in symptomatology between IBD and IBS, we compared rectal afferent mechanisms in patients with Crohn's disease (inflammation limited to the ileum) with those observed in patients with diarrhea-predominant IBS. Continuous volume ramp and phasic pressure step distension of a rectal balloon were performed in 9 healthy male control subjects, 12 male patients with isolated ileal Crohn's disease and 9 male patients with diarrhea-predominant IBS using an electronic visceral stimulation device. The response of rectal afferents to distension was evaluated by measuring thresholds for the perception of physiological (stool) and aversive (discomfort) sensations, viscerosomatic referral patterns, skin conductance responses, receptive relaxation, and rectoanal reflex responses. In response to slow ramp distension, thresholds for aversive sensations were significantly higher in Crohn's disease patients, but similar between the two other groups. In response to rapid phasic distension, IBS patients reported discomfort at lower distension pressures, while all other thresholds were similar between groups. Skin conductance responses to aversive distension were greatly reduced in Crohn's disease patients while IBS patients had greater responses when compared to normals. Changes in viscerosomatic referral patterns and receptive relaxation rate were similar in Crohn's disease and IBS patients. These findings demonstrate that chronic ileal inflammation is associated with increased thresholds for discomfort and greatly diminished systemic autonomic reflex responses. In contrast, IBS patients show lowered thresholds for discomfort associated with increased autonomic responses. The findings in Crohn's patients may result from descending bulbospinal inhibition of sacral dorsal horn neurons in response to chronic intestinal tissue irritation.

Adult↗
PubMed2006

A genetic approach for investigating vagal sensory roles in regulation of gastrointestinal function and food intake.

Sensory innervation of the gastrointestinal (GI) tract by the vagus nerve plays important roles in regulation of GI function and feeding behavior. This innervation is composed of a large number of sensory pathways, each arising from a different population of sensory receptors. Progress in understanding the functions of these pathways has been impeded by their close association with vagal efferent, sympathetic, and enteric systems, which makes it difficult to selectively label or manipulate them. We suggest that a genetic approach may overcome these barriers. To illustrate the potential value of this strategy, as well as to gain insights into its application, investigations of CNS pathways and peripheral tissues involved in energy balance that benefited from the use of gene manipulations are reviewed. Next, our studies examining the feasibility of using mutations of developmental genes for manipulating individual vagal afferent pathways are reviewed. These experiments characterized mechanoreceptor morphology, density and distribution, and feeding patterns in four viable mutant mouse strains. In each strain a single population of vagal mechanoreceptors innervating the muscle wall of the GI tract was altered, and was associated with selective effects on feeding patterns, thus supporting the feasibility of this strategy. However, two limitations of this approach must be addressed for it to achieve its full potential. First, mutation effects in tissues outside the GI tract can contribute to changes in GI function or feeding. Additionally, knockouts of developmental genes are often lethal, preventing analysis of mature innervation and ingestive behavior. To address these issues, we propose to develop conditional gene knockouts restricted to specific GI tract tissues. Two genes of interest are brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), which are essential for vagal afferent development. Creating conditional knockouts of these genes requires knowledge of their GI tract expression during development, which little is known about. Preliminary investigation revealed that during development BDNF and NT-3 are each expressed in several GI tract regions, and that their expression patterns overlap in some tissues, but are distinct in others. Importantly, GI tissues that express BDNF or NT-3 are innervated by vagal afferents, and expression of these neurotrophins occurs during the periods of axon invasion and receptor formation, consistent with roles for BDNF or NT-3 in these processes and in receptor survival. These results provide a basis for targeting BDNF or NT-3 knockouts to specific GI tract tissues, and potentially altering vagal afferent innervation only in that tissue (e.g., smooth muscle vs. mucosa). Conditional BDNF or NT-3 knockouts that are successful in selectively altering a vagal GI afferent pathway will be valuable for developing an understanding of that pathway's roles in GI function and food intake.

Afferent Pathways↗
PubMed1978

Afferent and efferent fiber connections of the carp torus longitudinalis.

The efferent and afferent pathways of the carp torus longitudinalis were studied by means of degeneration and retrograde HRP methods. Efferent projections were only seen in the most superficial layer of the ipsilateral optic tectum (stratum fibrosum marginale). Afferent pathways to the torus longitudinalis were found to originate mainly in the valvula cerebelli. Degenerating fibers course in the tractus mesencephalocerebellaris posterior within the valvula, and join the tractus mesencephalocerebellaris anterior in the tegmentum. The fibers which ascend in the tract gradually invade the optic tectum through which they are distributed to the torus longitudinalis. The remaining fibers pass through the posterior commissure and terminate in the torus longitudinalis at the rostral end of the tract. Degenerating terminals were also seen in the torus longitudinalis when lesions were made in the optic tectum, tectal commissure, torus semicircularis, and in the area between the valvula and the corpus cerebelli. The possibility of projections from these areas is discussed depending upon the results of the retrograde HRP method.

Animals↗
PubMed1983

Morphological and electrophysiological properties of giant interneurons during the postembryonic development of the cockroach CNS.

The giant interneurons (GIN) of the central nervous system of the cockroach undergo two major physiological changes during the postembryonic development period: (A) a gradual decrease in the safety factor for action potential propagation across the GIN in the metathoracic ganglion (T3); and (B) a marked decrease in the number of afferent pathways innervating the GIN in T3 (Spira and Yarom). Analysis of the morphological structure of the GINs, by intracellular injection of cobalt ions and by cross-sections prepared for light and electron microscope, reveals that despite the extensive growth of the GINs during the postembryonic developmental period, the main structural outline of the fibers is not altered. In adult preparations, however, the GIN diameter narrows 25-26% in ganglion T3, while in early nymphal stages the reduction is only 8-10%. The difference in the extent of narrowing of the fibers in adult and nymphal stages is the major factor that accounts for the development of a low safety factor region for impulse propagation across T3. Analysis of the passive membrane properties of the GIN reveals that the electrotonic length of the GIN segment in T3 is identical in adult and nymphal stages. It is concluded that the functional disappearance of afferents innervating the GINs in T3 is a consequence of decreased transmission efficacy along the afferent pathways.

Afferent Pathways↗
PubMed1999

Vestibular evoked myogenic potentials in humans: a review.

The human vestibule has preserved an ancestral sound sensitivity and it has been suggested that a reflex could originate from this property, thus inducing cervical muscle microcontractions secondary to strong acoustic stimulations. This reflex is assumed to originate in the saccule, the afferent pathways being either the vestibulocochlear nerve or the inferior vestibular nerve, and the efferent pathways the vestibulospinal tract. Averaging these muscular responses allows vestibular evoked myogenic potentials (VEMPs) to be obtained. The responses consist of two alternatively positive and negative successive waves (p13-n23, p33-n43). The characteristics of this reflex are defined in the literature as follows: it has been established that VEMP amplitude depends on muscular tension. All studies give concording evidence that in healthy subjects the first component of VEMP is more consistent than the second. Binaural stimulation is always responsible for responses of greater amplitude than those obtained from monaural stimulation. Following monaural stimulation, however, VEMPs are either of greater amplitude on the muscle ipsilateral to the stimulation or of the same amplitude on both muscles. There is consensus in the literature demonstrating that VEMP amplitude depends on stimulus intensity: the threshold of VEMP occurrence is clearly above auditory level but varies from one individual to the next. In the 1970s, recordings performed in cases of specific audiovestibular defects suggested that the reflex receptor could be the saccule. More recent studies suggest that the cochlea too could be involved in the response. Likewise, while a number of studies tend to demonstrate that VEMPs depend on vestibular integrity, others suggest that afferent pathways could be of both cohlear and vestibular origin. Finally, while it has been suggested that VEMP efferent pathways travel through the vestibulospinal tract, whether it is the lateral or the medial vestibulospinal tract that is concerned remains to be clarified. A few points regarding VEMP receptors and afferent and efferent pathways call for further investigation. They are inaccurate for use in routine vestibular examination. Once precise receptor localization and pathways are clarified, VEMP recording will provide both a straightforward non-invasive exploration of each vestibule independently and an attractive method by which to explore otolithic receptors and vestibulospinal pathways.

Acoustic Stimulation↗
PubMedDate not supplied

[Activation of sanogenesis mechanisms in central nervous system disorders].

Brain dysfunctions develop in brain injuries. Drug therapy is aimed at restitution processes which are often insufficient for recovery of impaired functions. Activation of the compensatory mechanisms of damaged and intact hemispheres will modify the time and qualitative characteristics of the restitution period. With this aim in view, transcranial electromagnetic stimulation in physiological range of efferent pathways and audiovisual stimulation of afferent pathways are recommended.

Afferent Pathways↗
PubMed2006

Parallel thalamic pathways for whisking and touch signals in the rat.

In active sensation, sensory information is acquired via movements of sensory organs; rats move their whiskers repetitively to scan the environment, thus detecting, localizing, and identifying objects. Sensory information, in turn, affects future motor movements. How this motor-sensory-motor functional loop is implemented across anatomical loops of the whisker system is not yet known. While inducing artificial whisking in anesthetized rats, we recorded the activity of individual neurons from three thalamic nuclei of the whisker system, each belonging to a different major afferent pathway: paralemniscal, extralemniscal (a recently discovered pathway), or lemniscal. We found that different sensory signals related to active touch are conveyed separately via the thalamus by these three parallel afferent pathways. The paralemniscal pathway conveys sensor motion (whisking) signals, the extralemniscal conveys contact (touch) signals, and the lemniscal pathway conveys combined whisking-touch signals. This functional segregation of anatomical pathways raises the possibility that different sensory-motor processes, such as those related to motion control, object localization, and object identification, are implemented along different motor-sensory-motor loops.

Afferent Pathways↗
PubMed2005

A spinal cord pathway connecting primary afferents to the segmental sympathetic outflow system.

The sympathetic innervation of lumbar dorsal root ganglia (DRGs) and the possible presence of spinal cord circuits connecting primary sensory afferents to the sympathetic outflow to DRGs were investigated. We used simultaneous tracing of the sympathetic input to and sensory output from DRGs. Adult male rats received unilateral microinjections of the Bartha strain of pseudorabies virus into four lumbar DRGs. At 24 h post-inoculation, productive infection was detected in both DRG neurons and sympathetic postganglionic neurons. Infection of spinal cord neurons was first observed in sympathetic preganglionic neurons of the intermediolateral column. Subsequently, the infection spread to the contralateral intermediolateral column, the area around the central canal and the superficial dorsal horn layers. To investigate the relationship between infected spinal cord neurons and primary afferents from the corresponding DRGs, we injected pseudorabies virus for retrograde tracing together with cholera toxin B for anterograde tracing. We found that infected LIV/LV and LX neurons were in close apposition to cholera toxin B labeled afferents. Importantly, immunohistochemical detection of bassoon, a pre-synaptic zone protein, identified such contacts as synapses. Together, this suggests synaptic contacts between primary sensory afferents and neurons regulating sympathetic outflow to corresponding DRGs.

Afferent Pathways↗
PubMed1985

Central pathways relaying cardiovascular afferent information to amygdala.

It has been suggested that cardiovascular information to the amygdala is relayed through the paraventricular nucleus of the hypothalamus (PVH) and the parabrachial nucleus (PB;7). To test this possibility spontaneously firing units in the amygdala of 12 chloralose-anesthetized cats were monitored for changes in firing frequency during electrical stimulation of PVH and PB and for their responsiveness to baroreceptor (BA) and chemoreceptor (CA) activation. In the ipsilateral amygdala 27 of 140 units responded to PVH stimulation, 9 of which also responded to CA and none to BA, whereas 46 of 150 units responded to PB stimulation, 11 of which also responded to CA and 2 to BA. To demonstrate the relative contribution of the PVH and PB in relaying cardiovascular information to the amygdala, in an additional six cats, the effect of neuronal block and lesions of these two nuclei on potentials evoked in the amygdala by stimulation of the buffer nerves was tested. Reversible neuronal block with injections of procaine in the PB significantly attenuated these evoked potentials. Electrolytic and chemical (kainic acid) lesions in the same PB sites also were effective in attenuating the responses. The potentials were unaltered by injection of procaine in the PVH. These results indicate that the PB is a site of relay of chemoreceptor and of some baroreceptor information from the medulla to the amygdala.

Afferent Pathways↗