Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Efferent Pathways”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMed2005

Multiple defects in the formation of rat cortical axonal pathways following prenatal X-ray irradiation.

Prenatal X-ray irradiation is known to result in severe defects of neuronal migration and laminar formation in the cerebral cortex. We examined the formation of cortical afferent and efferent pathways in rats that had been exposed to X-ray irradiation (1.0 Gy) at embryonic day 14 (E14), by birthdating with bromodeoxyuridine (BrdU) and axonal labeling with 1-1'-dioctodecyl-3,3,3',3'- tetramethyl-indocarbocyanine perchlorate (DiI), in addition to immunohistochemical staining for various axonal markers including neurofilament, and cell adhesion molecules L1 and TAG-1. The results obtained were as follows. (i) The neuroepithelium formed germinal rosettes and concavities in the cortical anlage from 2 days after irradiation. Neurons generated in the neuroepithelium accumulated to form subcortical heterotopia and obstructed pathway formation in the intermediate zone, resulting in an aberrant trajectory of TAG-1-immunoreactive cortical efferent axons. (ii) In rats exposed to X-ray irradiation at E14, cystic cavities were formed in the cortex-striatum boundary region between E15 and E17, probably because of delayed cell death of neurons generated at E14. These cavities transiently interrupted both cortical afferent (L1-positive) and efferent (TAG-1-positive) axons. (iii) X-ray irradiation at E14 partially destroyed subplate neurons (transient targets of thalamic afferent axons) and disturbed the arrangement of the subplate layer. This resulted in a misrouting of neurofilament- and L1-immunoreactive thalamocortical axons that obliquely traversed the cortical plate to run up to the superficial layer. The present study demonstrates for the first time that X-ray irradiation during initial cortical development causes multiple defects in the formation of cortical afferent and efferent pathways.

Age Factors↗
PubMed2004

Recent advances in laryngeal sensorimotor control for voice, speech and swallowing.

PURPOSE OF REVIEW: This article reviews advances in knowledge on laryngeal sensorimotor control affecting the assessment, understanding, and treatment of laryngeal motor control disorders in voice, speech, and swallowing. Three topics are covered: new knowledge on laryngeal innervation and central nervous system control from basic research studies, the role of laryngeal sensation in normal swallowing and dysphagia in patients, and new approaches to the restoration of laryngeal motor control after recurrent laryngeal nerve disorders. RECENT FINDINGS: A significant advance this year was tracing the efferent pathways from the cortex to the brainstem in monkeys. This provided new information on subcortical and brainstem connections in the laryngeal efferent pathways. Laryngeal sensory feedback continued to receive attention, and the role of sensory feedback in the control of the pharyngeal phase of swallowing is now well established. Further developments in neuromotor monitoring of the recurrent laryngeal nerve during thyroidectomy were seen, and a large case series recommended that these techniques become standard practice for surgery for thyroid benign recurrence or malignancy. Finally, the first tissue engineering papers in the field of vocal fold tissue and nerve restoration were published this year, beginning an exciting new approach to restoration of laryngeal motor control. SUMMARY: Considerable attention has been given to laryngeal muscle physiology, denervation, and sensation in neurolaryngology. Relatively limited understanding is available regarding the central nervous system integrative control of laryngeal function for speech, respiration, and swallowing.

Animals↗
PubMed2000

Evidence that long-lasting potentiation in limbic circuits mediating defensive behaviour in the right hemisphere underlies pharmacological stressor (FG-7142) induced lasting increases in anxiety-like behaviour: role of benzodiazepine receptors.

The hypothesis that benzodiazepine receptors mediate initiation of lasting behavioural changes induced by FG-7142 was supported in this study. Behavioural changes normally induced by FG-7142 were blocked by prior administration of the competitive benzodiazepine receptor blocker, Flumazenil. When cats were subsequently given FG-7142 alone, the drug produced lasting behavioural changes in species characteristic defensive responses to rodent and cat vocal threat. FG-7142 also induced long-lasting potentiation (LLP) of evoked potentials in a number of efferent pathways from the amygdala in both hemispheres. Flumazenil given prior to FG-7142 blocked LLP in all but one of the amygdala efferent pathways, suggesting benzodiazepine receptor dependence of initiation of LLP. Three physiological changes were most closely correlated with behavioural changes. LLP in the right amygdalo-ventromedial hypothalamic (VMH) and amygdalo-periacqueductal gray (PAG) pathways coincided closely with behavioural changes, as did a reduced threshold for the right amygdalo-VMH evoked potential. Administration of Flumazenil after FG-7142 returned defensive behaviour to pre FG-7142 baseline levels in a drug-dependent manner. At the same time LLP only in the right amygdalo-PAG pathway was reduced by Flumazenil. LLP in other pathways and amygdalo-VMH threshold were unaltered by Flumazenil. Moreover, covariance analyses indicated that increased defensiveness depended solely on LLP in the right amygdalo-PAG. These findings support the view that maintenance of lasting increases in defensive behaviour depend upon LLP of excitatory neural transmission between amygdala and lateral column of the PAG in the right hemisphere. Moreover, FG-7142 may be a useful model of the effects of traumatic stressors on limbic system function in anxiety, especially in view of the recent data in humans implicating right hemispheric function in persisting negative affective states in post-traumatic stress disorder.

Aggression↗
PubMed1984

Central inhibition of milk ejection in the rabbit: involvement of hippocampus and subiculum.

Removal of discrete parts of the forebrain of the anaesthetized lactating rabbit by suction caused repeated milk-ejection responses. These were associated with transection or removal of the subiculum, which represents the major efferent pathway from the hippocampal formation to the diencephalon. It is suggested that the hippocampus may exert a tonic, inhibitory influence over oxytocin release, that this inhibition may represent a cascade of events which originates in the brainstem and culminates in the subiculum and that removal of this inhibition may lead to release of oxytocin.

Afferent Pathways↗
PubMedDate not supplied

[The neuronal network of the hippocampus: a morphological analysis].

The use of new methods of morphologic analysis made it possible to detail significantly already known insights and to formulate the new ones concerning the hippocampal construction. This review discusses in detail the principles of structural organization of all intrahippocampal interneuronal connections and projections to the hippocampus from entorhinal cortex. Also, other afferent and efferent pathways and connections of polymorphic neurons of hippocampus are studied. Revision of the lamellar principle of hippocampal organization and involvement of inhibitory system in restricting an excitation propagation along the hippocampus is discussed.

Afferent Pathways↗
PubMed1985

Dorsal midbrain syndrome: clinical and oculographic findings.

We report clinical and oculographic findings in seven patients with the dorsal midbrain syndrome (Parinaud's syndrome). All presented with limited upward voluntary gaze and convergence nystagmus with attempted upward voluntary gaze. Quantitative analysis of vertical eye movements documented characteristic abnormalities of saccades with relative preservation of reflex eye movements (ie, vestibular, optokinetic, and visual-vestibular). Vertical saccade velocity was only slightly decreased in five patients with tumors, indicating that the vertical burst neurons in the mesencephalic reticular formation and their efferent pathways to the oculomotor neurons were minimally damaged. On the other hand, two patients with probable brainstem encephalitis exhibited marked slowing of vertical saccades, indicating that the burst neurons, or their efferent pathways to the oculomotor neurons, were severely damaged.

Adolescent↗
PubMed1981

Anatomical evidence for the influence of degenerating pathways on regenerating optic fibers following surgical manipulations in the visual system of the goldfish.

We have used [3H]proline radioautography to trace regenerating optic fibers in the goldfish following: (1) the removal of the right tectal lobe and the right eye, and (2) the removal of both tectal lobes. Our results indicate that following the removal of the right tectal lobe and the right eye, both the denervated tectal efferent pathways, and the denervated visual pathways and terminal zones of the enucleated eye were penetrated by the regenerating optic fibers. In addition, following bilateral lobectomy, the denervated tectal efferent pathways were bilaterally penetrated by the regenerating fibers. Since, in both types of operations, these denervated pathways and terminal zones should undergo degeneration, our results support the suggestion that the presence of degenerating axonal debris and proliferating glia may play an important role in guiding regenerating optic fibers in the visual system of the goldfish.

Animals↗
PubMed2006

Contextual modulation of cochlear hearing desensitization depends on the type of loud sound trauma.

In ears in which cochlear efferent pathways were cut and with testing done under anaesthetic conditions that preclude middle ear muscle activity (so as to examine the "intrinsic" effects of loud sound on the cochlea without any confounding effect of efferent pathways to the auditory periphery), atraumatic background white noise (WN) increases cochlear hearing loss (temporary threshold shifts, TTSs) induced by a traumatic pure tone but reduces TTSs caused by traumatic 5-kHz wide narrow band (NB) sound. The short-duration moderately intense traumata used in these studies most likely cause TTSs by affecting cochlear mechanics and these WN modulatory effects, exerted directly on the cochlea's intrinsic susceptibility to TTSs, are not predicted by any current description of cochlear mechanics. Here it is demonstrated that background WN reduces trauma-induced TTSs with even a relatively small increase in trauma bandwidth beyond that of a pure tone, discounting the alternative that contextual modulatory effects transition systematically along a continuum as trauma bandwidth increases from a pure tone to a broader bandwidth (albeit 2 kHz-wide NB) trauma. These results have implications for cochlear mechanics as the TTSs due to the traumatic sound of this study are most likely due to changes in cochlear mechanics but are not easily explained by what is currently known of cochlear mechanics.

Acoustic Stimulation↗
PubMed2004

Brainstem and basal ganglia lesions in xeroderma pigmentosum group A.

Xeroderma pigmentosum group A (XPA) is a hereditary disorder characterized by cutaneous symptoms and progressive neurodegeneration. Since XPA patients exhibit peripheral neuropathy, neuronal deafness, rigidity, dysphagia, and laryngeal dystonia, it is indispensable for investigation of the neurodegeneration to analyze brainstem and basal ganglia lesions clinically and pathologically; we have previously shown the role of oxidative stress in the development of basal ganglia lesions. Here we immunohistochemically examined the expression of neurotransmitters, calcium-binding proteins, and neuropeptides in the brainstem, basal ganglia, and thalamus in 5 XPA autopsy cases. In the brainstem, immunoreactivity for tyrosine hydroxylase, tryptophan hydroxylase, and calbindin-D28K was severely reduced throughout the brainstem in all the XPA cases. Nevertheless, the expressions of parvalbumin, substance P, and methionine-enkephalin in the brainstem were comparatively preserved; the exception being reduced immunoreactivity for them in the cochlear and dorsal column nuclei in 3 cases. The large cell neurons in the putamen were preferentially reduced, the immunoreactivity for tyrosine hydroxylase reflecting the dopaminergic afferent and efferent pathways was severely affected, and the expression of 3 calcium binding proteins (i.e. parvalbumin, calbindin-D28K, and calretinin) was disturbed in various ways. The expression of substance P and methionine-enkephalin, which are involved in the efferent pathways in the basal ganglia, in the globus pallidus and substantia nigra was spared. It is speculated that the selective damage to the dopamine system in the basal ganglia and the disturbed monoaminergic expression in the brainstem could be related to clinical abnormalities such as the rigidity, laryngeal dystonia, and several neurophysiological changes. Functional analysis of autopsy brains will facilitate clarification of the pathogenesis of the neurodegeneration in XPA.

Adolescent↗
PubMed2001

Identification of efferent neural pathways from the lamina terminalis activated by blood-borne relaxin.

The ovarian hormone relaxin, in addition to its role in pregnancy, exerts an action on the brain to influence oxytocin and vasopressin secretion, water drinking, and cardiovascular function. Intravenous (i.v.) infusion of relaxin causes an acute water drinking response, confirming its role as a dipsogenic hormone. The aim of this study was to determine whether neurones in the lamina terminalis, which project to the hypothalamic paraventricular and supraoptic nuclei, are activated by elevated levels of circulating relaxin in conscious rats. Immunocytochemistry combined with retrograde neuronal tracing with cholera toxin B subunit conjugated to cholera toxin B (CTB-gold) was used to identify populations of neurones responding with elevated cells of Fos protein to i.v. relaxin administration and which project to these specific hypothalamic sites. Neurones exhibiting Fos were present in the outer parts of the subfornical organ (SFO), the dorsal part of the organum vasculosum (OVLT), the supraoptic nucleus and the paraventricular nucleus. These did not occur in control rats with i.v. infusions of isotonic saline. Approximately 90% of neurones concentrated in the outer parts of the SFO and in the dorsal OVLT showed both retrogradely transported CTB-gold and Fos in response to i.v. infusion of relaxin. These data support a role for relaxin acting on the brain to regulate body fluid and electrolyte homeostasis by activating neural pathways subserving water drinking, vasopressin and oxytocin secretion.

Animals↗
PubMed1989

[Dacryocystorhinostomy with temporary intubation using a Hatt set].

During the period between June 1987 and March 1988 the authors performed 10 dacryocystorhinostomies with temporary intubation of the new efferent pathways, using a Hatt set. Three patients removed the set themselves during the early postoperative period. The authors evaluate thus seven successful intubations lasting two months. The observation period is six to eighteen months. In six patients the new efferent pathways are patent without signs of epiphora not even when lacrimation is irritated. One patient developed during the postoperative period torpid rhinitis persisting for two months and a block at the junction of the canaliculi. The results even in this small group are encouraging and the authors assume that temporary intubation with a Hatt set, which was very well tolerated by the patients, will enhances the success of this promising operation.

Dacryocystorhinostomy↗
PubMed1996

Extracellular matrix in early cortical development.

Studies of the distribution and production of ECM components during development of the cerebral cortex have suggested several hypotheses regarding their functional role. In the earliest stages of cortical development, fibronectin is produced by cells in the ventricular zone throughout the telencephalic vesicle, where it may serve as a part of the local environment that supports cell division and determines cell fate. Fibronectin is also distributed along radial glial processes. It is closely associated with preplate neurons, as are chondroitin sulfate proteoglycans and several other ECM components. This association continues as preplate cells are divided into the marginal zone and subplate by the invasion of cortical plate neurons, suggesting that ECM, preplate cells and radial glia serve as a scaffold for cortical plate formation. Fibronectin is also produced by migrating neurons, but only by those moving into specific cortical domains, suggesting that it may help neurons destined for specific targets discriminate between adjacent glial guides. A recently defined ECM-like protein, reelin, is absent or abnormal in the reeler mutant mouse in which cortical neurons are severely malpositioned. Reelin is produced by marginal zone cells and is therefore appropriately located to serve as a stop signal for migrating neurons. Axons leaving the cortical plate cross the CSPG-rich subplate, then turn to follow a path containing much less CSPG. In contrast, the cortical trajectory of thalamic axons is centered on the subplate, indicating that CSPGs in the subplate are not a barrier to axon outgrowth and may instead be serving as guidance cues that distinguish afferent from efferent pathways. Neurocan, a CNS-specific CSPG with many molecular features that indicate roles in cell-cell and cell-substrate interactions, is the only CSPG defined to date whose distribution supports a role in distinguishing afferent from efferent pathways.

Animals↗
PubMed2000

Central control of the cardiovascular and erection systems: possible mechanisms and interactions.

Sexual activity is accompanied by vascular changes mediated by parasympathetic and sympathetic outflow to the peripheral organs. The brain stem and spinal cord contain the neurons that innervate the cardiovascular system and the penis. Heart rate and blood pressure increase, suggesting a decrease of the cranial parasympathetic outflow and an increase of the activity of sympathetic efferent pathways. In contrast, penile erection occurs in response to increased activity of the sacral parasympathetic innervation and a decreased activity of sympathetic pathways. A modulation of the balance between sympathetic and parasympathetic activities may result from an adaptation of an intraspinal network that (1) would be the recipient of peripheral and supraspinal information; and (2) would coordinate the activity of the different efferent pathways. A variety of nuclei in the medulla, pons, and hypothalamus contain premotor neurons that exert an influence on brain stem and spinal autonomic motoneurons. These descending pathways release amines (noradrenaline, adrenaline, serotonin, dopamine) and peptides. A fine tuning of brain stem and spinal activity is made possible by the great variety of receptor subtypes through which these neuromediators act. More recently, the role of nitric oxide, synthesized and released by different cell populations, has been evaluated in the brain and spinal control of the cardiovascular system and penile erection. Depending on its central neural target, nitric oxide may either activate or inhibit the cardiovascular system. In contrast, its role on the central control of penile erection is only excitatory.

Animals↗
PubMed2002

In vivo approach to the cellular mechanisms for sensory processing in sleep and wakefulness.

1. The present review analyzes sensory processing during sleep and wakefulness from a single neuronal viewpoint. Our premises are that processing changes throughout the sleep-wakefulness cycle may be at least partially evidenced in single neurons by (a) changes in the phase locking of the response to the hippocampal theta rhythm, (b) changes in the discharge rate and firing pattern of the response to sound, and (c) changes in the effects of the neurotransmitters involved in the afferent and efferent pathways. 2. The first part of our report is based on the hypothesis that the encoding of sensory information needs a timer in order to be processed and stored, and that the hippocampal theta rhythm could contribute to the temporal organization. We have demonstrated that the guinea pig's auditory and visual neuronal discharge exhibits a temporal relationship (phase locking) to the hippocampal theta waves during wakefulness and sleep phases. 3. The concept that the neural network organization during sleep versus wakefulness is different and can be modulated by sensory signals and vice versa, and that the sensory input may be influenced by the CNS state, i.e., asleep or awake, is introduced. During sleep the evoked firing of auditory units increases, decreases, or remains similar to that observed during quiet wakefulness. However, there has been no auditory unit yet that stops firing as the guinea pig enters sleep. Approximately half of the cortical neurons studied did not change firing rate when passing into sleep while others increased or decreased. Thus, the system is continuously aware of the environment. We postulate that those neurons that changed their evoked firing during sleep are also related to still unknown sleep processes. 4. Excitatory amino acid neurotransmitters participate in the synaptic transmission of the afferent and efferent pathways in the auditory system. In the inferior colliculus, however, the effects of glutamate's mediating the response to sound and the efferent excitation evoked by cortical stimulation failed to show differences in sleep and wakefulness. 5. Considering that neonates and also infants spend most of the time asleep, the continuous arrival of sensory information to the brain during both sleep phases may serve to "sculpt" the brain by activity-dependent mechanisms of neural development, as has been postulated for wakefulness.

Action Potentials↗
PubMed2001

Pupillary disturbances in multiple sclerosis: correlation with MRI findings.

UNLABELLED: Autonomic nervous system disturbances such as pupillary abnormalities have rarely been evaluated in multiple sclerosis (MS). However, pupillary impairment is not uncommon in MS and its origin is still unclear. The aim of this study was to investigate pupillary disturbances in MS and to try to correlate pupillary defects with spinal cord and brainstem magnetic resonance imaging (MRI) findings. We prospectively studied 45 MS patients and 30 normal subjects. METHODS: The pupillary contraction latency and the amplitude of contraction were recorded by pupillometry. We also determined afferent and efferent pathway defects by comparing the direct and consensual pupillary reflexes. We evaluated brainstem and spinal cord demyelinating lesions and spinal cord cross-sectional area on MRI. At least one pupillometric parameters were significantly impaired in 60% of patients and in none of the controls. We did not find any correlation between pupillary defect and demyelinating lesions on MRI. The most frequent abnormality was efferent pathway shift and this was correlated with spinal cord atrophy (P<0.02). These results confirm that the autonomic nervous system, and especially pupillary function, is frequently impaired in MS. The parasympathetic system is most commonly affected and this is most likely linked to axonal loss (demonstrated by spinal cord atrophy) rather than to demyelinating lesions.

Adult↗
PubMed1971

Reflex effects on the heart of stimulating left atrial receptors.

1. Stimulation of left atrial receptors, by distension of the pulmonary vein/left atrial junctions, is known to cause a reflex increase in heart rate; the efferent pathway is known to be solely in the sympathetic nerves.2. In expectation of a concomitant positive inotropic response the effect of stimulating the left atrial receptors on the inotropic state of the left ventricle was studied, using as a known sensitive index of inotropic changes the maximal rate of rise of pressure in the left ventricle (dP/dt max).3. Stimulation of left atrial receptors resulted in an increase in heart rate but there were no significant concomitant changes in dP/dt max.4. It is concluded that activity in this discrete efferent pathway does not include an inotropic effect on the left ventricle and therefore the reflex involves only those sympathetic nerves which innervate the sinu-atrial node.5. The possible function of atrial receptors in the regulation of heart volumes is discussed.

Animals↗
PubMed2005

Brain damage after heat stroke.

Cerebellar syndromes and radiologic cerebellar atrophy after hyperpyrexia have occasionally been reported, mostly in neuroleptic malignant syndromes, but neuropathologic studies are extremely rare. We studied 3 patients (a 74-year-old woman, a 63-year-old man, and an 80-year-old man) who had heat stroke during heat waves in France. One patient had generalized seizures and died 28 hours after admission. The other patients survived one month and 2 months after admission; both had palatal myoclonus, and in one case, magnetic resonance imaging showed high signal intensity in the cerebral peduncles. The main neuropathology in the 3 cases was severe diffuse loss of Purkinje cells associated with heat shock protein 70 expression by Bergmann glia. In situ end labeling was negative in surviving Purkinje cells, suggesting that the mechanism of neuronal death was not apoptosis. Degeneration of Purkinje cells axons resulted in myelin pallor of the white matter of the folia and of the hilum of the dentate nuclei. DNA internucleosomal breakages were identified by in situ end labeling in the dentate nuclei and centromedian nuclei of the thalamus and were associated with degeneration of the cerebellar efferent pathways: superior cerebellar peduncles, decussation of the superior cerebellar peduncles (Wernekinck commissure), and dentatothalamic tract. These findings suggest that the mechanisms of neuronal death in the dentate nuclei and centromedian nuclei of the thalamus was different from that in Purkinje cells and more likely resulted from deafferentation. Ammon's horn and other areas susceptible to hypoxia were spared. These observations confirm the selective vulnerability of Purkinje cells to heat-induced injury and involvement of the cerebellar efferent pathways in palatal myoclonus.

Aged↗
PubMed1989

[Cold pressor test in the evaluation of autonomic neuropathy].

Neurogenic orthostatic hypotension is due to interruption of the baroreceptor reflex. To optimize the pharmacological therapy in this clinical setting the lesion should be carefully pinpointed and the degree of denervation established. To this purpose 7 patients with autonomic failure underwent ambulatory intraarterial monitoring, which showed the reversal of the normal 24-hour blood pressure (BP) pattern. During daytime BP gradually rose from its lowest point early in the morning to a peak during late evening. No BP fall was observed during sleep. Tilting test, Valsalva maneuver, hyperventilation, cold pressor test, handgrip and pharmacological tests showed interruption of the efferent pathway of the reflex. The BP fall 60 seconds after assuming the orthostatic position significantly correlated with the BP response to the cold pressor test (r = 0.89; p less than 0.01), while it did not with the BP changes during hand grip and hyperventilation and with the orthostatic increase of heart rate. Therefore, the BP response to the cold pressor test seems the most reliable indicator of the degree of autonomic dysfunction in the lesions of the efferent pathway of the reflex.

Aged↗