[Drug damage to the kidney and efferent urinary pathways].
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To evaluate the effects of systemic bupivacaine on the baroreflex control of heart rate, we investigated the baroreflex sensitivity assessed with a pressor and a depressor test using phenylephrine and nitroglycerin in pentobarbital anesthetized dogs (n = 12). Intravenous injection of bupivacaine (mean plasma concentration of 2.4 +/- 0.9 micrograms.ml-1) caused a significant suppression of the baroreflex sensitivity, defined by the slopes of regression line (in msec of RR interval change per mmHg increase or decrease in systolic blood pressure). The sensitivity obtained with the pressor and the depressor tests decreased from 6.0 +/- 2.3 to 3.5 +/- 1.7, from 2.4 +/- 1.3 to 1.3 +/- 0.8 msec.mmHg-1, respectively (P < 0.01). Suppression of the baroreflex sensitivity during epidural anesthesia with bupivacaine could be due not only to cardiac sympathectomy but also to a direct effect of bupivacaine on the reflex arch including the receptors, the afferent nerve pathways, the CNS, the efferent pathway, and the effector organs. Therefore, the hemodynamic responses to reduction of blood pressure are likely to be inhibited by epidural bupivacaine.
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Electrical stimulation of the muscles of the thigh in the anaesthetized dog induces reflex changes of the aortic pressure and of the renal vascular tone. The afferent pathways is located in the somatic nerves of the stimulated limb, the efferent pathways is in the ortosympathetic nerves. Muscle contraction is necessary to activate the receptors, responsible for the reflex increase of the arterial pressure; this contraction is not necessary to activate the receptors responsible for the blood pressure decrease. It is probably that the former receptors play a role in the increase of the sympathetic tone during muscle exercise.
The afferent and the efferent pathways of the milk ejection reflex were studied in conscious lactating rats subjected to suckling after experiencing stereotaxically-controlled transections in the midbrain or hypothalamus. Extensive transections in midbrain or hypothalamus. Extensive transections in the midbrain or caudal hypothalamus blocked reflex milk ejection while less extensive cuts, sparing either the dorsal or the ventral fibers, did not. The frontal plane immediately caudal to the neurosecretory nuclei intersects both afferent and efferent fibers. All cuts at this plane, regardless of size, caused blockage whenever the neurosecretory fibers located at the lateral ventral hypothalamus were severed. A multiple cut in the near vicinity of both supraoptic nuclei caused blockage of milk ejection, probably by severing the combined neurosecretory tract originating in both the supraoptic and paraventricular nuclei. If the multiple cut was performed unilaterally, a blockage of milk ejection was not observed, indicating that reflex action can be sustained by preserving one side of the neurosecretory pathway. Simple cuts in the same region revealed that the efferent pathway takes on a caudo-medial direction towards the neurohypophysis. In the near vicinity of the infundibulum, simple cuts showed that the efferent fibers enter the infundibulum from the sides, and also established that the milk ejection reflex persisted even when a small number of fibers in the pituitary stalk remained intact. The results showed that the afferent pathway for the reflex is diffuse, while the efferent pathway is compact. Only complete transection of one of the two pathways caused blockage.
This paper is an account of the afferent and efferent projections of the nucleus sphericus (NS), which is the major secondary vomeronasal structure in the brain of the snake Thamnophis sirtalis. There are four major efferent pathways from the NS: 1) a bilateral projection that courses, surrounding the accessory olfactory tract, and innervates several amygdaloid nuclei (nucleus of the accessory olfactory tract, dorsolateral amygdala, external amygdala, and ventral anterior amygdala), the rostral parts of the dorsal and lateral cortices, and the accessory olfactory bulb; 2) a bilateral projection that courses through the medial forebrain bundle and innervates the olfactostriatum (rostral and ventral striatum); 3) a commissural projection that courses through the anterior commissure and innervates mainly the contralateral NS; and 4) a meager bilateral projection to the lateral hypothalamus. On the other hand, important afferent projections to the NS arise solely in the accessory olfactory bulb, the nucleus of the accessory olfactory tract, and the contralateral NS. This pattern of connections has three important implications: first, the lateral cortex probably integrates olfactory and vomeronasal information. Second, because the NS projection to the hypothalamus is meager and does not reach the ventromedial hypothalamic nucleus, vomeronasal information from the NS is not relayed directly to that nucleus, as previously reported. Finally, a structure located in the rostral and ventral telencephalon, the olfactostriatum, stands as the major tertiary vomeronasal center in the snake brain. These three conclusions change to an important extent our previous picture of how vomeronasal information is processed in the brain of reptiles.
The question of whether automatic, sensory processes can be modified by selectively directing attention to stimuli was addressed by comparing effects on brainstem reflexes that share a common efferent pathway but have distinct afferent limbs. Subjects judged the duration of brief but intense blink-eliciting tones (Experiment 1) or weak tones preceding a blink-eliciting air puff at interstimulus intervals producing blink inhibition (Experiment 2). Tones occurred unpredictably at left, right, or midline loci; designation of the target location varied across blocks of trials. Latency of blinks to lateralized blink-eliciting targets was facilitated selectively, and the magnitude of blinks evoked by air puff following lateralized prestimulus targets was inhibited selectively. There was no evidence for a midline selective effect. Results appear to support a preset differential processing of stimuli in sensory pathways at low, possibly subcortical, levels and the consequent modification of obligatory, automatic processes.
In dogs anaesthetized with chloralose, distension of small balloons in the right upper and middle pulmonary vein-atrial junctions, to stimulate left atrial receptors, caused an increase in heart rate and an increase in activity in efferent sympathetic nerve fibers in cardiac branches of the right stellate ganglion. Cooling of the cervical vagi in steps reduced the magnitude of the responses in these sympathetic nerve fibres. In four dogs, the response in six preparations of sympathetic nerves was slightly reduced with the vagi at 18 degrees C and markedly reduced or abolished at 12 degrees C. In these nerves there was no significant response to distension of the balloons when the cervical vagi were cooled to 9 degrees C. The effect of cooling the vagi was the same as the previously shown effect of cooling on the increase in activity in myelinated afferent vagal fibres and the increase in heart rate during stimulation of atrial receptors. It is concluded that the increase in activity in efferent sympathetic cardiac nerve fibres during distension of small balloons in the pulmonary vein-atrial junctions involves receptors discharging into myelinated vagal nerve fibres; receptors which discharge into non-myelinated vagal nerves of afferent sympathetic nerve fibres are not involved in this response. Thus, the efferent sympathetic nerve fibres studied are likely to represent the efferent pathway of the response of an increase in heart rate to distension of the small balloons.
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.
Contraversive turning movements of the head were elicited in alert cats by unilateral electrical stimulation of the entopeduncular nucleus. To determine the relative functional importance of ascending and descending pathways activated by the stimulation, the animals were submitted to thalamocortical or midbrain lesions and to combinations of the two lesions interrupting the pathways. Head turning was hindered considerably only after combinations of the two lesions and not after either lesion alone. Taking into account the results of previous studies, showing that most efferent fibers of the entopeduncular nucleus branch to the thalamus and to the midbrain, it is concluded that not only one but two main efferent pathways, corresponding to each branch, are used by the entopeduncular nucleus to control motoneurons, each pathway carrying enough redundant information to mediate head turning.
Layer 5 (L5) pyramidal neurones constitute a major sub- and intracortical output of the somatosensory cortex. This layer 5 is segregated into layers 5A and 5B which receive and distribute relatively independent afferent and efferent pathways. We performed in vivo whole-cell recordings from L5 neurones of the somatosensory (barrel) cortex of urethane-anaesthetized rats (aged 27-31 days). By delivering 6 deg single whisker deflections, whisker pad receptive fields were mapped for 16 L5A and 11 L5B neurones located below the layer 4 whisker-barrels. Average resting membrane potentials were -75.6 +/- 1.1 mV, and spontaneous action potential (AP) rates were 0.54 +/- 0.14 APs s(-1). Principal whisker (PW) evoked responses were similar in L5A and L5B neurones, with an average 5.0 +/- 0.6 mV postsynaptic potential (PSP) and 0.12 +/- 0.03 APs per stimulus. The layer 5A sub- and suprathreshold receptive fields (RFs) were more confined to the principle whisker than those of layer 5B. The basal dendritic arbors of layer 5A and 5B cells were located below both layer 4 barrels and septa, and the cell bodies were biased towards the barrel walls. Responses in both L5A and L5B developed slowly, with onset latencies of 10.1 +/- 0.5 ms and peak latencies of 33.9 +/- 3.3 ms. Contralateral multi-whisker stimulation evoked PSPs similar in amplitude to those of PW deflections; whereas, ipsilateral stimulation evoked smaller and longer latency PSPs. We conclude that in L5 a whisker deflection is represented in two ways: focally by L5A pyramids and more diffusely by L5B pyramids as a result of combining different inputs from lemniscal and paralemniscal pathways. The relevant output evoked by a whisker deflection could be the ensemble activity in the anatomically defined cortical modules associated with a single or a few barrel-columns.
The spinoreticulocerebellar (SRC) tract is an indirect spinocerebellar tract formed by the reticular formation (RF), which is connected to the cerebellum and spinal cord. The RF receives ascending fibers to both the spinal enlargement and sends descending fibers to the cerebellum. This study demonstrated that the connectivity of the neurons in the RF is concerned to the cerebellum and spinal cord using the anterograde projection with biotinylated dextran amine (BDA) and retrograde labeling with wheatgerm agglutinin-horseradish peroxidase (WGA-HRP). Until now, a preliminary study in mammals has dealt with the afferent and efferent pathways in separating groups of neurons in the RF. There are only few reports on chickens. This study examined the SRC tract in chickens. Following bilateral injections we injected BDA into chicken spinal cord (lumbosacral enlargement) and WGA-HRP into the cerebellum. Both of single- and double-labeled cells were found within the RF. The spinoreticular axons were mainly distributed from the potomedullary junction to the rostral medulla in the rostro-caudally RF levels, for example, nucleus of reticularis (n. r.) pontis oralis,locus coeruleus, n. r. pontis caudalis, n. r. pars gigantocellularis, n. r. gigantocellularis and n. r. parvocellularis. Reticulocerebellar labeling by the WGA-HRP was found in the same place as well as that of the BDA-projection. We observed that the proportion and location of double labeling cells in the chicken were almost similar in each level, comparing to the rodents. These results suggest that the reticular formation is strongly related to the spinoreticulocerebellar tract in chickens.
Sympathetic efferent pathways and alpha-adrenergic receptivity were investigated in one patient with spinal cord transection (D1 level) and orthostatic hypotension. The lack of increase in catecholamine plasma levels during orthostasis and the paradoxical pressor effect of clonidine (2 micrograms/kg orally) suggested complete interruption of efferent sympathetic pathways. The pressor response to exogenous noradrenaline was significantly higher in the patient than in 6 normal controls (0.09 vs 0.72 micrograms.kg-1), indicating supersensitivity of vascular alpha-adrenoceptors. The platelet alpha 2-adrenergic receptor number, measured with [3H]yohimbine, was 507 in the patient vs 178 fmol.mg-1 protein in controls. The increase in systolic blood pressure induced by 10 mg midodrine, a specific alpha 1-agonist, was significantly higher in the patient (delta = 56 mm Hg) than in controls (delta = 15 mm Hg). The results indicate that in the patient there was alpha-adrenergic supersensitivity both of alpha 1- and alpha 2-adrenoceptors. This led to successfully oral treatment of the orthostatic hypotension with clonidine 150 micrograms bd and midodrine 10 mg bd.
The mammalian circadian timing system has three principal components; (1) photoreceptors and visual pathways mediating entrainment; (2) a pacemaker, the suprachiasmatic nucleus of the hypothalamus; and (3) efferent pathways coupling the suprachiasmatic nucleus to effector systems exhibiting circadian function. In most mammals there are two visual entraining pathways, a direct retinohypothalamic pathway terminating in the suprachiasmatic nucleus, for which the transmitter is unknown, and a secondary visual pathway, the geniculohypothalamic tract, from the intergeniculate leaflet of the lateral geniculate to the suprachiasmatic nucleus that is neuropeptide Y-producing. These pathways end in a distinct subdivision of the suprachiasmatic nucleus characterized by the presence of vasoactive intestinal polypeptide neurons. A second suprachiasmatic nucleus division does not receive visual afferents and is characterized by vasopressin neurons. The efferent projections of the suprachiasmatic nucleus are very restricted, predominantly to the hypothalamus. Although we have much less information on the human circadian timing system than on that of other animals, it seems clear that the human conforms to the general animal pattern in most features. There are, however, two significant differences. First, the largest neural component of the human suprachiasmatic nucleus is a population of neurotensin neurons found throughout the nucleus. Few, if any, neurotensin neurons are found in monkey or other mammals. Second, the human suprachiasmatic nucleus contains a large number of neuropeptide Y neurons located where the plexus arising from geniculate neuropeptide Y neurons is found in other mammals. This is unique and suggests that the geniculohypothalamic projection may be bypassed in the human. It also may imply that the functional organization of the human SCN is fundamentally different from that of other mammals. The function of the circadian timing system is to coordinate the activities of a series of homeostatic regulatory mechanisms with the control of behavioral state in a temporal pattern that facilitates adaptive behavior, including reproduction (Fig. 9). The function of this system, then, is to provide the appropriate physiological and behavioral background to facilitate adaptation and survival.
Tectal efferent neurons were retrogradely filled from extracellular injections of horseradish peroxidase (HRP) into pathways efferent from the tectum. Tectorotundal neurons have cylindrical dendritic trees, 80-100 microns in diameter, that extend vertically across the central and superficial tectal layers. Apical and basal dendrites are laden with complex appendages. The axon gives rise to an intratectal, collateral arbor that extends horizontally into the stratum griseum centrale beyond the cell's dendritic tree. The parent axon exits the tectum laterally in the tectothalamic tract. Tectogeniculate neurons also have narrow, radially oriented, and highly branched apical dendrites, but their basal dendrites are infrequently branched and lack appendages. An intratectal axon collateral forms a small, spherical arbor overlapping the apical dendrites in sublayer c of the stratum fibrosum et griseum superficiale. The parent axon ascends vertically and just below the stratum opticum turns rostrad to follow the optic fibers to the diencephalon. Tectoisthmi neurons have small somata and thin, radial dendrites that arborize below the pial surface in the stratum zonale. An intratectal axon collateral forms a spatially restricted arbor ventral to the soma in register with the dendritic tree. Tectoisthmobulbar neurons have dendrites that arborize extensively in sublayer a of the stratum fibrosum et griseum superficiale. The axon exits the tectum without collateralizing and joins a small-caliber component of the ventral tectobulbar tract. Ipsilateral tectobulbar neurons have stellate dendritic fields, 150-250 microns in diameter, that are restricted to the deep layers of the tectum. Sparsely branched dendrites are appendage-free but bear many short, fine spicules. The axon initially ascends from the soma and recurves into the stratum album centrale without collateralizing before joining a medium-caliber component of the ventral tectobulbar tract. Crossed tectobulbar neurons have large, stellate dendritic trees with diameters ranging from 200 to 500 microns. Like ipsilateral tectobulbar neurons, their dendrites are appendage-free but bear spicules. Their thick-caliber axons exit the tectum without collateralizing and course deep in the stratum album centrale to reach the dorsal tectobulbar tract.
It has been proposed that the vagus nerve plays a role in mediating cholecystokinin-8 (CCK-8) effect on such gastric functions as motility, emptying and gastric acid secretion. To examine the contribution of the efferent pathways in realizing these effects, efferent mass activity in the ventral gastric vagal nerve in Sprague-Dawley rats was recorded. Intravenous infusion of CCK-8 (0.1-1 nmol) suppressed the efferent activity. The effect of CCK-8 was significantly reduced in animals with total subdiaphragmatic vagotomy in comparison to those with partial vagotomy. Intravenous infusion of CCK(A) receptor antagonist L-364,718 (1-100x10(-6) g) blocked the response of vagal efferent activity to 0.1 nmol CCK-8, but the CCK(B) receptor antagonist L-365,260 (1-100x10(-6) g) did not in the conditions of either partial or total vagotomy. Intracisternal infusion of L-364,718 (1x10(-6) g) blocked the response of vagal efferent activity to 0.1 nmol CCK-8 i.v. Infusion of exogenous CCK-8 did not affect the activity of supradiaphragmatic vagal afferents. The results suggest that the effect of systemically administered CCK-8 on vagal efferent activity is mediated by both peripherally (subdiaphragmatically) and centrally localized CCK(A) receptors.
Distension of small balloons in the venous-atrial junctions results in an increase in heart rate, urinary flow and sodium excretion. Two types of atrial receptors are described: one type, histologically known, discharging into myelinated fibers, and a second type, discharging into nonmyelinated ("C") fibers. These responses are mediated by the myelinated fibers. Experiments have shown that simulation of receptors discharging into the large myelinated vagal fibers is responsible for a reflex increase in heart rate mediated only by sympathetic nerves and for an increase in urinary flow. The efferent pathway of the diuretic response is shown to be nervous and hormonal. Stimulation of atrial receptors causes (1) a reduction of activity in nerves to the kidney, causing an increase in both urinary volume and sodium excretion, and (2) the release of a blood-borne agent, possibly diuretic, that increases urinary volume but does not affect sodium excretion.