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PubMed1984

[Connections of the laterodorsal nucleus of the thalamus in the monkey. Study of efferents].

Efferent pathways of the LD nucleus of the thalamus were studied in 6 Papio-papio baboons with the retrograde transport technique utilizing HRP. Injections were made in cingular and parietal cortex and hippocampal formation. Large projection from the LD to the cingular and subicular cortex were visualized as reciprocal connections. No pathway to parietal area 7 was found. The course of the fibers is via the fornix, the cingular bundle and the retro-lenticular portion of the internal capsule. The result of this study make it necessary to reconsider neuropathological hypotheses on memory.

Animals↗
PubMed1979

A critical period in the development of tectal neurons in the chick, as revealed by early enucleation.

To further study the existence of a critical trophic period in the development of the chick optic tectum, during which the presence of retinal synapses is essential to the continued growth of tectal neurons, we have unilaterally enucleated embryos between stages 14--20 and allowed survival until stages 35--43. If the critical trophic period is between stages 40--44, as previously reported, then we reasoned that early removal of the eye might not have any effect on tectal development until the critical period. We assessed tectal neuron survival by staining for degeneration in the efferent projections of tectal neurons. In early enucleates, degeneration was present from stages 37--43, and the severity of the degeneration was much reduced in comparison to animals enucleated during the critical period. These findings substantiate the proposition that there is a critical period late in chick tectal development. However, because the degeneration in tectal projections is less intense than in animals enucleated during the critical period, we suggest that the early enucleation has permitted axons from the remaining eye to be routed to the deafferented tectum, where they may help to sustain a portion of the tectal neurons through the critical period. Moreover, the somewhat earlier appearance of degeneration in tectal efferent pathways of early enucleates suggests that a subtle trophic relationship between retina and tectum may exist prior to stage 40, even though this relationship is not revealed when enucleations are performed later, as between stages 35--40 (ref. 17).

Age Factors↗
PubMed2006

Axonal plasticity is associated with motor recovery following amphetamine treatment combined with rehabilitation after brain injury in the adult rat.

Clinical and laboratory studies have suggested that amphetamine treatment when paired with rehabilitation results in improved recovery of function after stroke or traumatic brain injury. In the present study, we investigated whether new anatomical pathways developed in association with improved motor function after brain damage and amphetamine treatment linked with rehabilitation. Following a unilateral sensorimotor cortex lesion in the adult rat, amphetamine (2 mg/kg) was administered in conjunction with physiotherapy sessions on postoperative days two and five. Physiotherapy was continued twice daily for the first 3 weeks after injury, and then once daily until week six. Performance on skilled forelimb reaching and ladder rung walking was used to assess motor improvement. Our results show that animals with sensorimotor cortical lesions receiving amphetamine treatment linked with rehabilitation had significant improvement in both tasks. Neuroanatomical tracing of efferent pathways from the opposite, non-damaged cortex resulted in the novel finding that amphetamine treatment linked with rehabilitation, significantly increased axonal growth in the deafferented basilar pontine nuclei. These results support the notion that pharmacological interventions paired with rehabilitation can enhance neuronal plasticity and thereby improve functional recovery after CNS injury.

Amphetamine↗
PubMed2005

Possible neural mediation of the central effects of oxytocin on uterine motility.

The central nervous system contains the nuclei at the origin of autonomic and neuroendocrine pathways to the uterus. Although the anatomical basis of these pathways is known, the conditions of their recruitment and their interactions in the context of copulation remain to be explored. We tested the hypothesis that some central mechanisms could simultaneously recruit both pathways to the uterus. In this aim, we recorded intrauterine pressure changes in anesthetized female rats at the estrus stage after intracerebroventricular (ICV) administration of oxytocin (OT). Doses of 0.3-300 ng elicited increases of frequency and amplitude of uterine contractions. These effects were partly mimicked by the OT agonist [Thr(4),Gly(7)]OT but not by arginine vasopressin. They were blocked by the OT receptor antagonist atosiban delivered either ICV or intravenously. The latter suggests that ICV OT activated the systemic release of OT. The effects of OT were also blocked by hexamethonium, a ganglionic blocking agent, by atropine, a muscarinic receptor antagonist, and by N(omega)-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis. The results reveal that ICV OT recruits autonomic efferent pathways to the uterus. These results support our hypothesis that the activation of central nuclei can promote uterine contractility, and that OT may be a central coordinator of autonomic and neuroendocrine pathways. The hypothalamus, the source of direct OT-ergic projections to the pituitary, the brain stem, and the spinal cord, may be a target of central OT.

Animals↗
PubMed2003

Central nuclei mediating estrogen-induced changes in autonomic tone and baroreceptor reflex in male rats.

The current investigation examines the significance of estrogen in central cardiovascular regulatory nuclei in modulating autonomic tone and baroreceptor reflex function. Experiments were done in anaesthetized male Sprague-Dawley rats. Changes in autonomic tone were assessed by monitoring vagal and renal efferent nerve activities before and following bilateral injection of estrogen into select central autonomic nuclei. In the first study, selective blockade of neurotransmission through the central nucleus of the amygdala (CNA), lateral hypothalamic area (LHA) and ventral posteromedial thalamic nucleus (VPM) using the local anaesthetic lidocaine was done to determine which nuclei were involved in mediating the autonomic changes observed following bilateral injections of estrogen into the insular cortex (IC). In the second study, the role of the parabrachial nucleus (PBN) in mediating the autonomic changes observed following bilateral estrogen injections into the CNA, LHA, VPM and IC was determined by blocking neurotransmission through the PBN using lidocaine.Injections of estrogen into the IC produced a significant increase in renal sympathetic nerve activity (RSNA; from 10+/-2 to 24+/-4 microV/sec; p<0.05). This estrogen-induced increase in RSNA was significantly attenuated when lidocaine was pre-injected into the LHA, CNA or PBN (55+/-6, 33+/-4 and 91+/-7% decrease respectively; p<0.05) but not when injected into the VPM (16+/-6% decrease; p>0.05). Injection of estrogen into the CNA resulted in a significant decrease in RSNA (48+/-5%; p<0.05) whereas estrogen injection into the LHA resulted in a significant increase (28+/-4%; p<0.05) in RSNA. Pre-injection of lidocaine into the PBN resulted in complete blockade of the autonomic changes observed following estrogen injection into the CNA but did not affect the changes observed following estrogen injection into the LHA. These results suggest that estrogen acting in forebrain and midbrain cardiovascular nuclei activated efferent pathways which synapse in the LHA, CNA and/or PBN prior to projecting to autonomic preganglionic nuclei to affect autonomic tone. These nuclei may therefore provide an added level of processing and/or integration of the autonomic response(s) following activation by local or systemic estrogen.

Amygdala↗
PubMed2002

Reflections of efferent activity in rotational responses of chinchilla vestibular afferents.

To study presumed efferent-mediated responses, we determined if afferents responded to head rotations that stimulated semicircular canals other than the organ being innervated. To minimize stimulation of an afferent's own canal, its plane was placed nearly orthogonal to the rotation plane. Otolith units were tested in a horizontal head position with the ear placed near the rotation axis to minimize linear forces. Under these circumstances, angular-velocity trapezoids (2-s ramps, 2-s plateau) evoked excitatory responses for both rotation directions. These type III responses were considerably larger in decerebrate than in anesthetized preparations. In addition to their being exclusively excitatory, the responses resembled those obtained with electrical stimulation of efferent pathways in including per-stimulus and more prolonged post-stimulus components and in being larger in irregularly discharging than in regularly discharging units. Responses, which were not seen for rotations <80 degrees/s, grew as velocity increased between 80 and 500 degrees/s but were seldom larger than 20 spikes/s. Complete section of the VIIIth nerve abolished type III responses, leaving conventional afferent responses intact. To study the separate contributions of canals on the two sides, responses were compared when the labyrinths were intact and when the ipsilateral or contralateral horizontal canal was mechanically inactivated. Both sides contributed to the efferent-mediated responses. That afferents could be influenced from the contralateral labyrinth was confirmed with the use of unilateral galvanic currents. Following inactivation, excitatory responses were produced by rotations exciting or inhibiting the intact horizontal canal with the responses resulting from excitatory rotations being much larger. Such a response asymmetry is consistent with a semicircular-canal origin for the type III responses. A similar asymmetry was seen in the post-stimulus responses to contralateral cathodal (excitatory) and anodal (inhibitory) galvanic currents. We conclude that the efferent system receives a sufficiently powerful vestibular input from both the ipsilateral and contralateral labyrinths to affect afferent discharge.

Anesthesia↗
PubMed1982

The defence-arousal system and its relevance for circulatory and respiratory control.

It was proposed some fifty years ago that the visceral and hormonal changes accompanying fear and rage reactions can best be understood as adaptations which prepare an organism to cope with an emergency and specifically to perform the extreme muscular exertion of flight or attack. This is well exemplified by the pattern of cardiovascular response which is characteristic of the alerting stage of these reactions and consists of an increase in cardiac output directed mainly to the skeletal muscles. This group of behavioural responses has been collectively termed the defence reaction. The regions of the hypothalamus and brainstem which organize it have been mapped. They function as a reflex centre for the visceral components of the altering response as well as initiating the behavioural response. So far as the cardiovascular system is concerned, this is a preparatory reflex and not compatible with short-term homeostasis. Indeed, the baroreceptor reflex, which is homeostatic, is strongly inhibited. By contrast, the chemoreceptor reflex is facilitated. The input from peripheral chemoreceptors is itself an alerting stimulus. The visceral alerting response has been studied in most detail in the cat, but there is evidence for the same cardiovascular pattern and an accompanying group of respiratory changes in other mammalian species (rat, rabbit, dog, monkey and man). On the efferent pathway for the cardiovascular response pattern, there is a group of relay neurones near the ventral surface of the caudal medulla, which seem important for the maintenance of arterial blood pressure. The visceral alerting system may therefore be continually engaged to some extent in the awake state, as well as being acutely activated in response to novel, and especially to noxious, stimuli.

Animals↗
PubMed1995

The efferent innervation of outer hair cells in humans: physiological investigations.

We report on a case of reversible pontine deafness caused by multiple sclerotic lesions in the pons, and describe six experiments in humans, in whom we recorded transient otoacoustic emissions and distortion products. Our findings indicate an inhibitory effect of efferent innervation on the motility of outer hair cells in humans. Otoacoustic emissions increased in patients with unilateral deafness after the central part of the efferent pathway was destroyed (pontine deafness). Otoacoustic emissions also increased in patients with myasthenia gravis after the administration of an acetylcholinesterase inhibitor. General myotonia (Batter-Curschmann-Steinert Syndrome) resulted in mild sensorineural hearing loss, and in the absence of contralateral inhibition of otoacoustic emissions. Otoacoustic emissions decreased gradually under general anesthesia with muscle relaxation. Contralateral acoustic stimulation was seen during anaesthesia with muscle relaxation.

Acoustic Stimulation↗
PubMed2000

The cerebellar and thalamic degeneration in Fukuyama-type congenital muscular dystrophy.

We report a male autopsy case of Fukuyama-type congenital muscular dystrophy (FCMD), with unusual neuropathological findings. The patient was a Japanese man aged 26 years at the time of death. He had shown severe psychomotor retardation and muscular dystrophy since early infancy, and was diagnosed as having FCMD at the age of 5 years. He died of respiratory failure. The main neuropathological finding was extensive cerebral and cerebellar cortical dysplasia, characteristic of this disorder. In addition, degeneration of the cerebellar efferent pathway, including the dentate nucleus, superior cerebellar peduncle, and red nucleus, and that of the lateral thalamic nucleus were observed. These findings suggest the possibility that the long survival can clarify the latent neurodegeneration in the cerebellum and thalamus in FCMD, in addition to congenital malformations. The system degeneration should be carefully evaluated in the pathological examination of this disorder.

Adult↗
PubMedDate not supplied

Sympathetic skin response in Parkinson's disease.

Sudomotor function in 83 patients with Parkinson's disease (PD) was evaluated using the sympathetic skin response (SSR) and sweat response to intradermal acetylcholine (ACh) injection. The incidence of abnormal SSRs (36.1%) increased, and the size of the response decrease with the severity of the illness. Neither the incidence of abnormal SSRs nor the amplitudes of the responses were influenced by levodopa or an anticholinergic agent. The SSR therefore can be used to evaluate the sudomotor efferent pathway in PD patients. In all the patients who had no SSR response, the local sweat response to ACh showed a reduced number of excitable sweat glands and low sweat volume. One patient, whose local sweat response to ACh was markedly impaired, had unmyelinated and acetylcholinesterase-positive fiber densities that were in the normal range in his biopsied sural nerve. The abnormal sweat response to ACh is considered to reflect the dysfunction of postganglionic sympathetic fibers in PD patients.

Acetylcholine↗
PubMed1990

Efferent connections of the A1 noradrenergic cell group: a DBH immunohistochemical and PHA-L anterograde tracing study.

Immunohistochemical localization of the catecholamine biosynthetic enzymes tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), and phenylethanolamine N-methyltransferase (PNMT) was employed to reveal the anatomical organization of the A1 noradrenergic cell group in the caudal ventrolateral medulla oblongata of the rat. Subsequently, the supraspinal efferent axonal projections of A1 were investigated with a view to elucidating the anatomical substrates underlying its postulated function in central fluid and cardiovascular homeostasis. Within the caudal medulla, DBH-positive/PNMT-negative (noradrenergic) neurons were observed extending bilaterally through the ventrolateral medullary reticular formation from upper cervical spinal cord levels to the level of the area postrema. At the rostral pole of A1, its neurons intermingled with PNMT-immunoreactive perikarya of the more rostrally situated C1 adrenergic cell group. Discrete injections of the anterogradely transported plant lectin Phaseolus vulgaris leucoagglutinin (PHA-L) into A1 resulted in terminal labeling in a number of presumptive efferent target sites including the nucleus of the solitary tract, rostral ventrolateral medulla, dorsal parabrachial nucleus, Kolliker-Fuse nucleus, central grey, dorsomedial nucleus of the hypothalamus, perifornical region, zona incerta, lateral hypothalamus, paraventricular nucleus of the hypothalamus, supraoptic nucleus, bed nucleus of the stria terminalis, and organum vasculosum of the lamina terminalis. Tissue sections adjacent to those reacted for PHA-L were processed immunohistochemically for DBH to determine if anterogradely labeled terminals were localized in regions that demonstrated appropriate immunoreactivity. The majority of regions in which PHA-L terminal labeling was present also exhibited moderate to intense DBH activity. These experiments provide neuroanatomical evidence for direct efferent pathways from the A1 noradrenergic cell group to a number of supraspinal sites that have been reliably implicated in the neural circuitry underlying the central regulation of fluid and cardiovascular homeostasis. Furthermore, the results suggest a selective anatomical interrelation between A1 and sites in the basal forebrain and hypothalamus in which vasopressinergic neurons have been previously demonstrated. It is postulated that the noradrenergic A1 projections observed in this investigation represent the morphological substrate through which A1 exerts a significant influence on cardiovascular regulatory mechanisms.

Animals↗
PubMed1996

[Inhibitory effect of substance P of caudate nucleus on gastric motility via substantia nigra and dorsal vagal nucleus mediated by vagus nerve].

Effects of lesion of bilateral hypothalamus (LH), substantia nigra and dorsal vagal nucleus as well as their efferent pathway on the inhibition of gastric myoelectric fast wave and gastric motility due to injection of substance P (SP) to caudate nucleus were studied in rats. The experimental results showed that this induced inhibition was independent of the presence of intact LH but abolished by lesioning substantia nigra, dorsal vagal nucleus or vagus nerve. Depletion of sympathetic transmitter by reserpine did not affect the occurrence of the inhibition. Thus, it appears that the gastric inhibitory effect of caudate nucleus SP is mediated via substantia nigra and dorsal vagal nucleus to vagus nerve.

Animals↗
PubMed1987

The cerebellar corticonuclear projection from lobule Vb/c of the cat anterior lobe: a combined electrophysiological and autoradiographic study. II. Projections from the vermis.

The present study is an investigation of the efferent pathways from Purkinje cells within particular sagittal zones of the vermal region of the cat cerebellar cortex. A combined electrophysiological/autoradiographic technique was used, in which a small volume (10-120 nl) of 3H-leucine was injected into the centre of a chosen cortical zone after the mediolateral extent of the zone had been delimited electrophysiologically on the basis of its climbing fibre input. Study of the uptake and orthograde transport of labelled material by the Purkinje cells showed that the smallest injections gave rise to injection sites which were restricted to a single zone and to terminal labelling which was very reproducible between cases. Larger injections usually resulted in spread of labelled material to neighbouring zones but the resultant distribution of terminal labelling was nevertheless consistent with that arising from smaller injections. The x zone, which receives climbing fibre input transmitted from the ipsilateral forelimb via a dorsal funiculus spino-olivo-cerebellar pathway (DF-SOCP), was found to project to the junctional region between nucleus fastigius and nucleus interpositus posterior (NIP). The b zone, which lies laterally in the vermis and receives climbing fibre input transmitted from both forelimbs (and both hindlimbs) via a slower conducting SOCP, was found to project, not to the cerebellar nuclei proper, but to the ipsilateral lateral vestibular nucleus. The projection of the third zone within the vermis, the a zone, was not examined but it is generally agreed that this zone projects mainly to nucleus fastigius.

Animals↗
PubMed1975

Amygdalar participation in tonic ACTH secretion in the rat.

The role of the amygdaloid complexes in the compensatory hypersecretion of ACTH following adrenalectomy was studied in the adult male rat. Unilateral or bilateral radiofrequency or knife-cut lesions were placed in the amygdalae, their efferent pathways or the septal region. Three weeks following adrenalectomy resting plasma ACTH concentrations were measured by radioimmunoassay. Bilateral lesions of a direct medial-projecting portion of the ventral amygdalo-hypothalamic pathway blocked the compensatory hypersecretion of ACTH following adrenalectomy. A unilateral complete amygdalar lesion coupled with destruction of the same direct amygdalo-hypothalamic pathway on the opposite side had the same positive effect. In contrast, unilateral destruction of the direct amygdalo-hypothalamic projections, ablation of the septum, or bilateral destruction of the stria terminalis did not block hypersecretion of ACTH following adrenalectomy. These data suggest that the amygdalae and their direct hypothalamic projections, but not the stria terminalis or septum, are essential for the hypersecretion of ACTH following adrenalectomy. Furthermore, one amygdaloid complex appears sufficient for this effect. It is possible that the amygdalae act as a central nervous system 'glucocorticoid-sensor' in the modulation of ACTH secretion in the rat.

Adrenalectomy↗
PubMed1994

Dissociation of behavioral changes in rats resulting from lesions of the habenula versus fasciculus retroflexus and their possible anatomical substrates.

Lesions in either the habenula or its primary efferent pathway, the fasciculus retroflexus (FR), impaired avoidance responding. However, lesions of only the FR provided a persistent elevation of locomotor activity. Immunocytochemical study of the interpeduncular nucleus (IPN) through injection of retrograde tracers into the IPN and the overlying ventral tegmental area indicated that habenular lesions spared both rostral habenula and forebrain projections to the caudal midbrain, but these projections were axotomized by FR lesions. Rostral sparing of the habenula resulted in normal peptidergic staining in the IPN, and normal cholinergic innervation was absent. Performance of individual rats in behavioral tests was consistent with variations in anatomical sparing. Such considerations may account for previous discrepancies in functional effects of habenular lesions.

Animals↗
PubMed2003

Electrophysiologic evaluation of lumbosacral single nerve roots using compound muscle action potentials.

Transcutaneous electrical stimulation applied to the vertebral column produces compound muscle action potentials (CMAPs) from the leg muscles. Using this method, we evaluated the efferent pathways of the lumbosacral nerve roots. The subjects were 26 healthy volunteers and 31 patients with lumbar disc herniation (LDH). CMAP recordings were obtained from the bilateral vastus medialis, tibialis anterior, extensor digitorum brevis, and abductor hallucis muscles using low-output-impedance stimulation. In normal subjects, the CMAP latency increased linearly with the distance between the stimulating electrode and the recording electrode, with little difference in latency between the left and the right sides in each subject. The CMAP amplitude was significantly lower in the patients with LDH, and the latency was also prolonged when the stimulating electrode was placed above the lesion. This technique may thus be a useful noninvasive method for assessing lumbosacral nerve root function in patients with LDH.

Action Potentials↗
PubMed1994

Lesions of the central gray block the sensitization of the acoustic startle response in rats.

The amplitude of the acoustic startle response (ASR) in rats is increased after administration of footshocks, a phenomenon termed sensitization. The neural circuitry underlying this kind of modulation of the ASR is only partly understood. It has been shown that the central nucleus of the amygdala (cA) and its efferent pathway to the caudal pontine reticular nucleus (PnC), an essential part of the primary startle circuit, is important for the sensitization of the ASR. It was unclear, however, whether the amygdaloreticular pathway directly transfers the effects of footshocks onto the PnC, or whether there exists a relay nucleus within this pathway. The present study tested the hypothesis that the midbrain central gray (CG) is important for the sensitization of the ASR. Neuroanatomical tracing experiments indicate that a descending projection from the medial part of the cA might form synapses in the region of the midbrain CG, where a descending projection to the PnC takes its origin. We lesioned the dorsal and lateral part of the CG with the neurotoxin quinolinic acid and measured the effects of this lesion on the sensitization of the ASR by footshocks. Lesions confined to the dorsal and lateral parts of the CG totally blocked the sensitization of the ASR, without affecting the ASR amplitude in the absence of sensitizing stimuli. These findings suggest a crucial role of the CG for the sensitization of the ASR. The present data are reconciled with other findings from our laboratory and from the literature and we discuss possible mechanisms underlying the mediation of the sensitization of the ASR in rats.

Acoustic Stimulation↗
PubMed1995

Three-dimensional reconstruction of the rubrocerebellar premotor network of the turtle.

Neuroanatomical studies have demonstrated that the organization of the reptilian rubrocerebellar limb premotor network is similar to that of mammals. This network is composed of prominent recurrent connections among the red nucleus, lateral cerebellar nucleus and lateral reticular nucleus. In this paper the rubrocerebellar system of the turtle was three-dimensionally reconstructed to permit detailed examination of its anatomical organization. Each nucleus and its major efferent pathway was imaged and reconstructed from separate anatomical cases. Section images were used to draw tissue boundaries, mark cell positions and locate axonal trajectories. For each nucleus, drawings of section images containing labeled cells were stacked in the rostrocaudal direction using anatomical landmarks, and a graphic model of the surface was constructed using the method of triangulation. An ellipsoid of equal concentration was computed for each nucleus to ascertain their three-dimensional boundaries and location within the brainstem. To examine the entire rubrocerebellar network, a template of the turtle brainstem and cerebellum was constructed. The component nuclei of the rubrocerebellar network and their axonal projections were then spatially warped onto the template reconstruction on a section by section basis. The final three-dimensional reconstruction of the turtle rubrocerebellar limb premotor network could be rotated in space, allowing proper visualization of the anatomical details of this system. Furthermore, we were able to mathematically section through the reconstruction to obtain brainstem slices with differing orientations and thickness.

Animals↗