Distribution Of Nerve Terminals Research Articles

Nuclei-specific differences in nerve terminal distribution, morphology, and development in mouse visual thalamus.

BackgroundMouse visual thalamus has emerged as a powerful model for understanding the mechanisms underlying neural circuit formation and function. Three distinct nuclei within mouse thalamus receive retinal input, the dorsal lateral geniculate nucleus (dLGN), the ventral lateral geniculate nucleus (vLGN), and the intergeniculate nucleus (IGL). However, in each of these nuclei, retinal inputs are vastly outnumbered by nonretinal inputs that arise from cortical and subcortical sources. Although retinal and nonretinal terminals associated within dLGN circuitry have been well characterized, we know little about nerve terminal organization, distribution and development in other nuclei of mouse visual thalamus.ResultsImmunolabeling specific subsets of synapses with antibodies against vesicle-associated neurotransmitter transporters or neurotransmitter synthesizing enzymes revealed significant differences in the composition, distribution and morphology of nonretinal terminals in dLGN, vLGN and IGL. For example, inhibitory terminals are more densely packed in vLGN, and cortical terminals are more densely distributed in dLGN. Overall, synaptic terminal density appears least dense in IGL. Similar nuclei-specific differences were observed for retinal terminals using immunolabeling, genetic labeling, axonal tracing and serial block face scanning electron microscopy: retinal terminals are smaller, less morphologically complex, and more densely distributed in vLGN than in dLGN. Since glutamatergic terminal size often correlates with synaptic function, we used in vitro whole cell recordings and optic tract stimulation in acutely prepared thalamic slices to reveal that excitatory postsynaptic currents (EPSCs) are considerably smaller in vLGN and show distinct responses following paired stimuli. Finally, anterograde labeling of retinal terminals throughout early postnatal development revealed that anatomical differences in retinal nerve terminal structure are not observable as synapses initially formed, but rather developed as retinogeniculate circuits mature.ConclusionsTaken together, these results reveal nuclei-specific differences in nerve terminal composition, distribution, and morphology in mouse visual thalamus. These results raise intriguing questions about the different functions of these nuclei in processing light-derived information, as well as differences in the mechanisms that underlie their unique, nuclei-specific development.

Desmin and nerve terminal expression during embryonic development of the lateral pterygoid muscle in mice

ObjectiveIn adults, the lateral pterygoid muscle (LPM) is usually divided into the upper and lower head, between which the buccal nerve passes. Recent investigations have demonstrated foetal developmental changes in the topographical relationship between the human LPM and buccal nerve. However, as few studies have investigated this issue, we clarified the expression of desmin and nerve terminal distribution during embryonic development of the LPM in mice. MethodsWe utilized immunohistochemical staining and reverse transcription chain reaction (RT-PCR) to clarify the expression of desmin and nerve terminal distribution. ResultsWe observed weak expression of desmin in the LPM at embryonic day (ED) 11, followed by an increase in expression from embryonic days 12–15. In addition, starting at ED 12, we observed preferential accumulation of desmin in the vicinity of the myotendinous junction, a trend that did not change up to ED 15. Nerve terminal first appeared at ED 13 and formed regularly spaced linear arrays at the centre of the muscle fibre by ED 15. The results of immunohistochemical staining agreed with those of RT-PCR analysis. ConclusionWe found that desmin accumulated in the vicinity of the myotendinous junction starting at ED 12, prior to the onset of jaw movement. We speculate that the accumulation of desmin is due to factors other than mechanical stress experienced during early muscle contraction. Meanwhile, the time point at which nerve terminals first appeared roughly coincided with the onset of jaw movement.

Atrial Coronary Arteries: Anatomy And Atrial Perfusion Territories.

Coronary anatomy has traditionally focused on ventricular circulation. This is largely due to the extent to which coronary artery disease contributes to ischemic heart disease through ventricular myocardial damage. Atrial fibrillation and other tachyarrhythmias that involve the atria, however, remain a major cause of morbidity and mortality. In order to increase mechanistic research and therapeutic interventional procedures for diseases of the atria, an optimal knowledge of atrial anatomy is necessary. While substantial clarity exists regarding the distribution of nerve terminals and the organization of muscle bundles, the anatomy of coronary atrial circulation remains understudied. Historically, the high anatomical variability of atrial coronary branches led to unstandardized nomenclature in the literature. In this review, we delineate the anatomic courses of key atrial coronary branches and their perfusion territories, clarify their nomenclature, and propose unifying anatomical concepts of atrial circulation that we believe to be critical to the success of modern electrophysiologic and surgical procedures.

Nerve terminal distribution in the human tongue intrinsic muscles: An immunohistochemical study using midterm fetuses

Intrinsic tongue muscles, especially the transverse and vertical (T&V) muscles, regulate the shape of the tongue. However, little information is available on the nerve distribution pattern in human T&V muscles. Using S100 protein immunohistochemistry for paraffin-embedded histology, we investigated semiserial sagittal or frontal sections of eight human fetal tongues (180-240 mm crown-rump length: CRL). The height of the T&V muscle bundle showed a threefold difference between specimens with a small and a large CRL. Thus, the T&V muscles were still growing at the stages examined. In the intrinsic longitudinal muscles and all extrinsic tongue muscles, we observed the typical motor endplate band. In lower-magnification views, the T&V muscles also appeared to carry the band in the lateral part of the tongue, where the genioglossus muscle fibers did not cross these muscles. However, in higher magnification views, the nerve terminal distribution in the T&V muscles showed a unique rule: the nerve terminal for the transverse muscle bundle was located distantly from that of the adjacent vertical muscle bundle. This pattern seemed to be established during the stages examined. To provide such "distantly separated nerve terminals," thin nerve twigs took a highly curved course oblique to the T&V muscle bundles. We hypothesize that the unique nerve course and terminal distribution in the T&V muscles are a result of sorting to provide a good functional match between the nerve fiber and the muscle bundle. After sorting, the T&V muscle cells may initiate proliferation to increase the muscle bundle.

Dynamic monitoring of NET activity in mature murine sympathetic terminals using a fluorescent substrate

To validate a fluorescence approach for monitoring norepinephrine transporter (NET) transport rate in mature sympathetic terminals, and to determine how prejunctional muscarinic receptors affect NET rate. Confocal imaging of a fluorescent NET substrate [neurotransmitter transporter uptake assay (NTUA)] as it accumulates in the mature sympathetic nerve terminals of the mouse isolated vas deferens. Fluorescence recovery after photobleaching (FRAP), enhanced green fluorescence protein (EGFP)-transgenic mice and contraction studies were also used. NTUA fluorescence accumulated linearly in nerve terminals, an effect that was prevented with NET inhibition with desipramine (1 microM). Such accumulation was reversed by amphetamine (10 microM), which is known to reverse the direction of transport of NET substrates. NTUA labelling was not present in cholinergic terminals (identified using EGFP fluorescence expressed in transgenic mice under a choline acetyltransferase promoter). FRAP experiments, altered nerve terminal distribution with reserpine pretreatment and co-imaging in terminals filled with a cytoplasmic marker (Alexa 594 dextran) indicated that the NTUA labelling was largely confined to vesicles within varicosities; vesicular exchange between varicosities was rare. The rate of NTUA accumulation was slower in the presence of the muscarinic agonist carbachol (10 microM) demonstrating muscarinic inhibition of NET rate. A straightforward protocol now exists to monitor NET transport rate at the level of the single nerve terminal varicosity, providing a useful tool to understand the physiology of NET regulation, the action of NET inhibitors on mature sympathetic terminals, dynamic vesicular tracking and to identify sympathetic terminals from mixed terminal populations in living organs.

Acute and chronic sectioning of fifth lumbar spinal nerve has equivalent effects on the primary afferents of sciatic nerve in rat spinal cord

The mechanism of neuropathic pain may be associated with sprouting of uninjured primary afferents of peripheral nerves into regions of the spinal cord denervated through peripheral injury. However, this remains controversial. Therefore, the purpose of the present investigation was, first, to determine in detail the central distributions of the unmyelinated primary afferents of each of the L4, L5, and L6 components of sciatic nerve, then to assess the distribution of afferent sciatic terminals following acute and chronic injury to (L5) nerve. First, we injected isolectin B4 (IB4), into the sciatic nerves in three groups of rats, each of which had two of the three L4, L5, or L6 components ligated and cut, and the one remaining, uninjured. Although the terminal labelling found in the L5 segment of the spinal cord originated from the L5 component, some terminal labelling remained in cases when either the L4 or L6 component was intact. Second, tracers transported in predominantly unmyelinated (IB4 and WGA-HRP) or myelinated (cholera toxin subunit B) nerves were injected into the sciatic nerve following acute or chronic (21-day) injury restricted to the L5 component. In each case, the central distribution of nerve terminals in the spinal dorsal horn was equivalent following either acute or chronic injury to the L5 component. Consequently, these data provide no support for the suggestion that neuropathic pain in spinal ligation model results from uninjured L4 and L6 components sprouting to occupy sites vacated by the injured L5 component of the sciatic nerve.

Enhanced neuropeptide Y immunoreactivity and vasoconstriction in mesenteric small arteries from the early non-obese diabetic mouse

The present study investigated whether sympathetic neurotransmission is altered at an early stage of diabetes in mesenteric small arteries isolated from female non-obese diabetic (NOD) and control animals without diabetes from the same mouse strain. The NOD diabetic mice had increased plasma glucose and hypertension. Confocal microscopy showed distribution of nerve terminals was similar, but immunoreaction intensity for neuropeptide Y (NPY) and tyrosine hydroxylase was higher in small arteries from NOD diabetic compared with NOD control mice. In the presence of prazosin and activated with vasopressin, electrical field stimulation evoked contractions which were more pronounced in mesenteric arteries from NOD diabetic versus NOD control mice and inhibited by the NPY Y 1 receptor antagonist, BIBP 3226. NPY concentration–response curves were leftward shifted in arteries from NOD diabetic versus NOD control both in arteries with and without endothelium, but not in the presence of the BIBP 3226. The present findings suggest that enhanced NPY content and vasoconstriction to NPY by activation of NPY Y 1 receptors in arteries from diabetic mice may contribute to the enhanced sympathetic nerve activity and vascular resistance in female non-obese early diabetic animals.

Acetylcholine receptors and nerve terminal distribution at the neuromuscular junction of long-term regenerated muscle fibers

Mdx mice are deficient in dystrophin and show muscle fiber regeneration. Changes in the distribution of acetylcholine receptors have been reported at the neuromuscular junction of mdx mice and may be a consequence of muscle fiber regeneration. In this study, we examined whether the distribution of receptors was still altered in long-term, regenerated muscle fibers from C57Bl/10 mice. The left sternomastoid muscle of adult mice was injected with 60 microl of lidocaine hydrochloride to induce muscle degeneration-regeneration. In some mice, the sternomastoid muscle was denervated at the time of lidocaine injection. After 90 and 150 days, the nicotinic acetylcholine receptors were labeled with rhodamine-alpha-bungarotoxin for confocal microscopy. At both intervals studied, the receptors were distributed in spots. In denervated-regenerated fibers, the receptors were distributed as regular branches similar to denervated muscles without lidocaine treatment. These findings suggested that nerve-dependent mechanisms were involved in the changes in receptor distribution seen in regenerated muscle fibers after lidocaine treatment, and that a similar phenomenon could explain the changes in receptor distribution seen in dystrophic muscle fibers.

Ultrastructural evidence for a preferential elimination of glutamate‐immunoreactive synaptic terminals from spinal motoneurons after intramedullary axotomy

After axotomy in the ventral funiculus of the cat spinal cord, about half of the population of lesioned motoneurons die at 1-3 weeks postoperatively, whereas the other half survives and generates new axons through the lesion area. To identify conditions that may promote survival and regeneration of motoneurons subjected to this kind of injury, the authors examined ultrastructurally lesion-induced changes in the number and distribution of nerve terminals on the somata and proximal dendrites of alpha-motoneurons in the 7th lumbar spinal segment (L7) of the cat spinal cord. Intramedullary axotomy resulted in a profound reduction in the number of nerve terminals impinging on the somata and proximal dendrites, with the maximal effect seen at 3 weeks postlesion. At that time, only 12-25% of the normal number of terminals remained on the cell somata, and 22-33% remained on proximal dendrites. Thereafter, a gradual increase in terminal numbers occurred, reaching normal levels at 34 weeks after the lesion. Already at 2 days postoperatively and, most obviously, at 3 weeks postoperatively, type S nerve terminals were eliminated to a larger degree than type F terminals. Postembedding immunohistochemistry confirmed that the largest reduction at 3 weeks was seen for excitatory glutamate-immunopositive type S nerve terminals (90%), whereas inhibitory glycine-immunoreactive and gamma-aminobutyric acid (GABA)-immunoreactive type F terminals were affected less (70% reduction). This led to a distinct shift in the ratio between the numbers of terminals that were immunopositive for glycine and GABA and the numbers of terminals that were labeled for glutamate. For the cell body, this ratio increased from 3.7 in normal material to 14.5 in lesioned motoneurons, whereas the corresponding values for proximal dendrites were 3.8 and 7.5. The preferential elimination of glutamatergic inputs to lesioned motoneurons may reflect an active reorganization of the synaptic input to diminish the excitotoxic influence on these neurons, thereby promoting the survival of motoneurons after intramedullary axotomy.

Confocal imaging of N-methyl- d-aspartate receptors in living cortical neurons

The fluorescence-conjugated N-methyl- d-aspartate receptor-selective antagonist, BODIPY-conantokin-G, was employed to label N-methyl- d-aspartate receptors in living neurons derived from the visual cortex of embryonic rats. The fluorescent labeling was visualized and analysed using confocal microscopy and digital imaging techniques. BODIPY-conantokin-G binding sites were homogeneously distributed across somata four days after neurons (E17–20) were placed in culture. In five-day-old cultures, BODIPY-conantokin-G binding sites became clusters of fluorescently labeled spots which were arranged irregularly on somata and proximal neurites. Distal neurites displayed fluorescent labeling after 10–15 days in culture. Displacement experiments showed that spermine and unlabeled conantokin-G compete with BODIPY-conantokin-G labeling at the N-methyl- d-aspartate receptor-associated polyamine site. The N-methyl- d-aspartate receptor antagonist 2-amino-5-phosphonovaleric acid also depressed the labeling but with a weaker effect, probably due to interactions occurring between the N-methyl- d-aspartate receptor agonist binding site and the polyamine modulatory site. The fluorescent dyes FM 1-43 and FM 4-64 were used in double-labeling studies to compare the distribution of nerve terminals with that of BODIPY-conantokin-G binding sites. BODIPY-conantokin-G binding clusters were associated with presynaptic nerve terminals while isolated BODIPY-conantokin-G binding sites were not always opposed to terminals. The aggregation of receptors to form clusters may lead to the functional formation of excitatory synapses. To investigate whether modulation of membrane potentials affected the formation of N-methyl- d-aspartate receptor clusters, cultured neurons were chronically treated for a week with either tetrodotoxin (to block membrane action potentials) or a high concentration of potassium to depolarize the membrane. While neurons in the tetrodotoxin-treated group showed a similar number of fluorescently labeled clusters compared with the control group, neurons in the high potassium group exhibited a higher number of fluorescently labeled receptor clusters. These results suggest that more active neurons may tend to form more N-methyl- d-aspartate synapses during early development.

Effects of Glial Cell Line-Derived Neurotrophic Factor on Developing and Mature Ventral Mesencephalic Grafts in Oculo

The search for trophic factors that can support injured dopaminergic neurons and can enhance dopaminergic graft survival and outgrowth for therapeutic uses in Parkinson's disease has lately focused on members of the transforming growth factor (TGF) β superfamily. In this paper we have studied the effects of a member of the TGBβ family, glial cell line-derived neurotrophic factor (GDNF), on immature and mature ventral mesencephalic tissue grafted to the anterior chamber of the eye. The results confirm that GDNF increases survival of TH-positive neurons and enhances TH-immunoreactive nerve fiber formation when the grafts are treated during their development. The distribution of nerve terminals is densest within the area of TH-immunoreactive neurons and at the surface of the grafts. However, there is no change in the number of calcium-binding protein (CaBP)-positive neurons, suggesting that the subpopulation of TH-positive neurons that is increased are the CaBP-negative neurons of the ventral tier of pars compacta. Terminals from those neurons form the striatal patches during normal development. When the grafts are treated with GDNF after maturation, no change in TH-positive cell survival is seen but an increase of nerve terminals is still found within the cell dense area of the graft. Potassium-evoked dopamine release, measured using in vivo chronoamperometry, revealed significantly increased extracellular overflow in transplants treated with GDNF during development. The dopamine uptake blocker nomifensine significantly increased the time for clearance of the released dopamine. These data suggest that GDNF treatment of immature grafts enhances survival of TH-positive neurons, which would have innervated the striatal patches, and also increases TH-immunoreactive nerve fiber formation and dopamine release. Furthermore, GDNF treatment of mature grafts also increases dopamine fiber formation within the TH-positive neuronal area, indicating that adult dopaminergic neurons are also responsive to this agent.

Abnormal distribution of nerve terminals in the normoganglionic bowel of Hirschsprung's disease: A causative factor of failed pull-through operations? : A. Yamataka, T. Miyano, T. Okazaki, et al. Pediatr Surg Int 9:264–267, (April), 1994

Abnormal distribution of nerve terminals in the normoganglionic bowel of Hirschsprung's disease: A causative factor of failed pull-through operations? : A. Yamataka, T. Miyano, T. Okazaki, et al. Pediatr Surg Int 9:264–267, (April), 1994

Abnormal distribution of nerve terminals in infantile hypertrophic pyloric stenosis

Smooth muscle biopsy specimens obtained from nine infants with infantile hypertrophic pyloric stenosis (IHPS) and from three controls were studied immunohistochemically with respect to the distribution of nerve terminals and neurofilaments. To label nerve terminals and neurofilaments, monoclonal antibodies (MAb) 171B5 and 2F11 were used, respectively. In all specimens of the control group, nerve terminals were numerous in both the myenteric plexus and the muscle layer. There were abundant neurofilaments in the myenteric plexus and a moderate number in the muscle layer. In all specimens of the IHPS group, the density of nerve terminals and neurofilaments was reduced in the muscle layer. In the myenteric plexus, there was no such reduction. The results indicate poor neuronal innervation of the muscle layer in the pylorus of infants with IHPS. This poor innervation may be related to the pathogenesis of pyloric stenosis and hypertrophy.

Abnormal distribution of nerve terminals in the normoganglionic bowel of Hirschsprung's disease: a causative factor of failed pull-through operations?

The aim of this study was to examine the innervation pattern of the muscle layers of normoganglionic pulled-through bowel in patients with Hirschsprung's disease (HD) by observing the distribution of nerve terminals comprising neuromuscular junctions and synapses. As a marker for nerve terminals, monoclonal antibody (MAb) 171B5 was used. Pulled-through normoganglionic bowel from 12 patients with HD that was either biopsied or resected at operation and normal bowel specimens from 7 age-matched controls were labelled using an immuno-histochemical technique with MAb 171B5. In all specimens of the control group and 9 patients of the HD group, numerous neuromuscular junctions were demonstrated in the muscle layers of the normoganglionic bowel and numerous synapses in the myenteric plexuses. However, in the specimens of 3 patients of the HD group abnormal distribution of nerve terminals was seen in the normoganglionic bowel. Two of these 3 patients had abnormal postoperative defecation. Based on our study, there appears to be a small number of HD patients who have an innervation disorder of the muscle layers in the proximal, normoganglionic bowel pulled through at surgery, which hitherto have been thought to be normal.

Glutamate-like immunoreactivity revealed in rat olfactory bulb, hippocampus and cerebellum by monoclonal antibody and sensitive staining method

Although there is good evidence favoring L-glutamate as a major excitatory amino acid transmitter, relatively little is known about the distribution of nerve terminals using this substance. A method visualizing glutamate-like immunoreactivity at the light microscopic level by means of a monoclonal antibody, mAb 2D7, is described. --The antigen used for immunization was a glutaraldehyde-linked glutamate-BSA conjugate, and hybridomas were differentially screened by ELISA for production of antibodies recognizing glutamate- but not aspartate-BSA. The crossreactivity of 'anti-glutamate' mAb 2D7 as estimated in absorption tests was low even with conjugates closely related to glutamate-BSA.--Semithin sections from rapidly perfusion-fixed, plastic-embedded rat brain tissues were etched and stained by a combination of the peroxidase-antiperoxidase method and silver enhancement of the diaminobenzidine reaction product. Only this amongst several other immunohistochemical methods tried produced labeling patterns which showed terminal-like elements in brain regions such as olfactory bulb, hippocampus and cerebellum, and which were mostly consistent with already available information on systems using glutamate as neurotransmitter. Particularly striking was the staining of elements reminiscent of mossy fiber terminals in hippocampus and cerebellum as well as of cerebellar parallel fiber terminals.

Somatostatin-like immunoreactivity in neurons, nerve terminals, and fibers of the cat spinal cord.

The distribution of somatostatin-like immunoreactivity (SS) was studied in the spinal cord of untreated cats and of cats that had received colchicine at all levels of the cord. In the dorsal horn small (less than 15 microns in diameter), round neurons were found in Rexed laminae II and III at all levels. At all levels laminae IV-VI contained smaller numbers of immunoreactive neurons that were medium (between 15 and 25 microns in diameter) to large (greater than 25 microns in diameter) in size. In addition, small numbers of medium-sized neurons were observed at the dorsal and dorsomedial borders of the gray and white matter in segments C1-5. In the sacral cord (S1-3), a group of medium-sized bipolar neurons was found in the dorsolateral funiculus. In transverse sections the processes of the neurons in these two latter groups travelled in a direction parallel to the border of the gray and white matter. In the intermediate and central gray matter, in addition to the immunoreactive neurons found in the region of the intermediolateral nucleus and nucleus intercalatus of lamina VII in segments C8 to L4 (Krukoff et al., '85a), lamina VII contained immunoreactive neurons at all levels with the largest number occurring in the thoracic cord. These neurons were medium to large in size and were generally multipolar with processes travelling in all directions. Multipolar small immunoreactive neurons were also found in the central gray region (lamina X) in the thoracic and upper lumbar cord. Finally, small numbers of neurons containing SS were found in the ventral horn of the cervical and upper thoracic cord. These multipolar neurons were medium to large in size. The distribution of nerve terminals and fibers containing SS was similar to that previously described in mice, rats, guinea pigs, and primates. Although the function of somatostatin in the spinal cord is not known, its presence in neurons with short processes suggests that it may act to modify local activity in the regions where it is found, including areas involved in sensory, visceromotor, and motor functions.

Morphology of physiologically identified slowly adapting lung stretch receptor afferents stained with intra-axonal horseradish peroxidase in the nucleus of the tractus solitarius of the cat. I. A light microscopic analysis.

The present series of experiments was designed to study the organization of preterminal processes and synaptic boutons of single physiologically identified slowly adapting receptor (SAR) pulmonary stretch afferent fibers. Intra-axonally injected horseradish peroxidase-wheat germ agglutinin (HRP-WGA) conjugate was used as the label. In the first paper, we describe the pattern of arborization of axon collaterals from single physiologically identified SAR afferent fibers evident in the various subnuclei of the nucleus of the tractus solitarius (nTS). In the second paper, details are presented regarding the ultrastructure of these synaptic boutons and axon collaterals. A number of significant findings resulted from this study: (1) A single lung stretch SAR afferent fiber arborized over a considerable distance rostrocaudally in the brain stem (1,700-2,100 microns). (2) A single lung stretch SAR afferent fiber terminated as hundreds of bouton terminals (650-1,180). (3) There was a remarkable consistency in the subnuclei of the nTS that received these terminal arborizations of SAR afferents. (4) The ventral (vnTS), intermediate (nI), ventrolateral (vlnTS), and interstitial (ni) subnuclei of the nTS were the only regions of the nTS receiving bouton terminals of SAR afferent fibers. (5) Under the light microscope the pattern of termination of SAR afferents was similar in all the axons studied in this series. (6) The injected parent axon in each case could be followed in the TS at all levels and remained consistent with regard to position and orientation and could be traced rostrally to levels as far as 3.5 mm rostral to the obex whereas the region of terminal arborization was located around 1.7-2.1 mm rostral to the obex. This pattern indicates that a single lung stretch SAR afferent fiber descends caudally upon entering the nTS. In the cat vagal afferent fibers are known to enter the medulla at levels between 0.5 mm and 3.2 mm rostral to the obex (Kalia and Mesulam, '80a). The results of the light microscopic analysis presented in this article indicate that lung stretch (SAR) afferents from the lungs and tracheobronchial tree have distinctly localized patterns of distribution in the nTS. In addition, these findings support the concept that representation of pulmonary afferents in the medulla is constituted by a differentiated distribution of nerve terminals in the various subnuclei of the nTS. Modality-specific localization (SAR afferents in this case) appears to be predominant in the nTS. The widespread rostrocaudal distribution of the terminal field of a single lung stretch SAR afferent is remarkable.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of alcohol on functional development of the auditory pathway in the brainstem of infants and chick embryos.

The effects of alcohol on the development of neural function in the auditory pathway of the brainstem have been examined in human neonates and chick embryos. Auditory brainstem evoked responses were recorded in six infants of mothers for whom there was evidence of alcohol abuse during pregnancy. In four of the infants, evoked responses were abnormal, with poorly defined, inconsistent peaks. Neurophysiological and histological studies were done on chick embryos which received a single dose of alcohol early incubation. In most surviving embryos the neuroanatomical arrangement of the auditory nuclei in the brainstem was normal. However, Golgi impregnation revealed abnormalities in the length and structure of the dendrites in nucleus laminaris. Electrically evoked neuronal activity revealed abnormalities of synaptic function and the distribution of nerve terminals. The results indicate that in infants and chick embryos the functional development of the auditory pathway in the brainstem is disrupted by exposure to alcohol. Such early changes in this sensory pathway may contribute to the behavioural and intellectual handicaps associated with the fetal alcohol syndrome.

Quantitative analysis for innervation of smooth muscle cells in the wall of the urinary bladder

The distribution of nerve terminals to different parts of the urinary bladder was studied by electron microscopy with the aid of 6-hydroxydopamine treatment. A quantitative analysis was made for each region. In the sphincter and trigone areas nerve terminals were found to be much more numerous (3 times more) than in sections from the body and the apex of the bladder. In much of the bladder there were 6–7 smooth muscle cells for each nerve fiber, however in the trigone area 1–2 muscle cells were supplied by terminal nerve fiber. The narrowest gap between nerve terminals and smooth muscle cells was found to be 150–250 nm. It was commonly seen that Desmosome-like attachments, called nexuses, connected adjacent smooth muscle cells. After 6-hydroxydopamine treatment degenerated terminals could be found mostly in the fine periarterial plexuses but some were also observed that were not related to blood vessels, especially in the trigone area. Summation of our figures and results for terminal density suggests to us that contractions of the urinary bladder are initiated or controlled in the trigone region and that other parts of the wall are activated by local nerve processes and the numerous nexal contacts.

Spatial distribution of excitatory innervation on a muscle fiber of the lobster (Homarus americanus).

The distribution of nerve terminals from a single excitatory motor axon has been followed along a fiber from the proximal accessory flexor muscle of the lobster by thin serial sectioning at periodic intervals. The excitatory motor axon provides small axonal branches (diameter 5--12 micron) of varying lengths that travel along the surface of the muscle fiber. Each of these branches gives rise to discrete synaptic terminals which are not uniformly distributed. Individual terminals vary in length from 10--60 micron and the majority possess neuromuscular synapses. The greatest distance between synapses is slightly over 1 mm which is well within the length constant (2.6 mm) of this muscle fiber. Thus the spatail distribution of synapses is such as to ensure adequate depolarization along the entire length of the muscle fiber.