Peripheral Nerve Trunks Research Articles

Comparison of the acetylcholine response potentials with the synaptic potentials in molluscan central nerve cells

1. Synaptic potentials following stimulation of the main peripheral nerve trunks have been investigated in central nerve cells of suboesophageal ganglia of the snail Heobania vermiculata (Helicidae). 2. The somatic response potentials to ionophoretic application of acetylcholine were compared with PSPs also in presence of cholinolytics. 3. IPSP reversed at −50/−58 mV, whereas the extrapolated values for EPSP reverse level were ranged between −35/+18 mV. 4. A presumable decrease of receptor sensitivity to ACh/neurotransmitter action with the membrane hyperpolarization is described. 5. Differences between equilibrium potentials for PSP and for cholinergic extrasynaptic response were analysed and discussed in terms of a possible neurotransmitter role of ACh in the ganglia.

Axonal GABA-receptors in mammalian peripheral nerve trunks

Axonal GABA-receptors in mammalian peripheral nerve trunks

Vascular permeability and neurotoxicity.

Neurotoxic substances affect the nervous system in a selective manner. One possible basis for this selectivity is blood vessel permeability. In general, the central nervous system and the peripheral nerve trunks have impermeable blood vessels, but in certain parts the capillaries are "leaky," allowing the passage of a plasma filtrate. Intravenously injected protein tracers rapidly reach nerve cells in these regions, with the implication that these nerve cells are also readily accessible to circulating neurotoxic substances. Some examples of neurotoxicity in the central nervous system show a selectivity that could be due to capillary permeability. In experimental methylmercury poisoning, cranial nerve V and sensory dorsal root ganglia, which lie in regions of vascular permeability, are particularly susceptible. A number of drug and chemically induced neuropathies are predominantly sensory, and may be due, directly or indirectly, to the accessibility of neurotoxic substances to sensory neurons. Examination of areas of potential vulnerability to circulating toxic substances may be of value in the experimental testing of substances for neurotoxicity, where pharmacological tests may be negative and clinical symptoms difficult to assess.

Osteosclerotic myeloma with polyneuropathy and ectopic secretion of calcitonin

The authors report the clinical observation of a patient with radiological features of an IgA with light chains type lambda osteosclerotic myeloma, associated with progressive sensorimotor polyneuropathy. Attention is drawn to these rare sclerotic forms of myeloma and the high frequency of associated neuropathies. In this case, marked hypercalcitoninemia was discovered with no other abnormality of the phosphocalcic balance. The authors advance the hypothesis of an ectopic secretion of calcitonin by tumoral plasma cells and discuss the potential role of this hormone in the pathogenesis of myeloma osteosclerosis. In addition, the fixation of the M-Component on the peripheral nerve trunks is demonstrated by means of immunofluorescence techniques, thus directly supporting the immunological conception of dysglobulinemic neuropathies.

The effect of extraction of the intrafascicular contents of peripheral nerve trunks on perineurial structure.

The intrafascicular contents have been extracted from the tibial nerve of the rabbit through perineurial incisions. Within 6--8 days following this procedure, the perineurial cells separate from one another, become dissociated from their basement membranes and assume a fibroblast-like appearance. The intrafascicular space becomes populated with endoneurial fibroblasts. With the ingrowth of regenerating axons, bundles of axons and associated Schwann cells become surrounded by cells of fibroblastic appearance which undergo perineurial transformation resulting in the development of multiple small fascicles. The cells of the surrounding perineurium appear to reassume a lamellar organization and to reestablish contacts with each other with the formation of junctional complexes. It is therefore suggested that neural structures may be responsible for the development and maintenance of the structural organization of the perineurium.

Uptake and retrograde transport of HRP by axons of intact and damaged peripheral nerve trunks

A light microscope study has been made of the uptake and transport of horseradish peroxidase (HRP) by axons of intact and damaged peripheral nerve trunks. Topically applied HRP entered axons of guinea pig cervical vagi and hypoglossal nerves whether or not these were damaged by crushing or local freezing at the site of application of HRP. If damaged, the corresponding cell bodies contained HRP, but little was detected in the cell bodies of undamaged axons. If the damage was distal to the site of HRP application, there was no significant retrograde transport. The presence of HRP within axons appears to be insufficient for its transport; traffic is initiated only from axon terminals and regions which have been damaged.

Absence of autoregulation in peripheral nerve blood flow

Blood flow was measured in the sciatic nerve of cats utilizing the method of hydrogen polarography. The mean baseline blood flow for all animals was found to be 47.1 ml 100 g min ± 14.9 SD . The flow changes produced by lowering the blood pressure by exsanguination and elevation by the use of angiotensin were then evaluated. The highest (normal) levels of blood flow were observed between the mean blood pressures of 80–110 mm Hg. At mean systemic arterial pressures of less than 85, there was a marked decrease in peripheral nerve blood flow with no detectable flow being measured below mean systemic pressures of 50 mm Hg. Above 105 mm Hg mean arterial pressure, there was a very gradual and progressive decline in blood flow to the levels measured at 200 mm Hg. These findings indicate a complete absence of vascular autoregulation in the peripheral nerve trunks.

Ultrastructural Studies of the Dying-Back Process

The spatio-temporal evolution of peripheral giant axonal degeneration has been studied in rats during the development of concurrent peripheral (PNS) and central (CNS) nervous system dying-back disease after chronic intoxication with the neurotoxic hexacarbons n-hexane (CH3CH2CH2CH2CH2CH3), methyl n-butyl ketone (MBK) (CH3COCH2CH2CH2CH3), or 2,5-hexanedione (CH3COCH2CH2CHOCH3), a neurotoxic metabolite of MBK. Each compound caused animals insidiously to develop identical, symmetrical peripheral neuropathies characterized by eversion and drop of hindfeet, inability to extend hindlimbs and upper extremity weakness. Teased fiber studies demonstrated that giant axonal swellings first developed on the proximal sides of multiple paranodes sited in distal, non-terminal regions of large myelinated fibers. Later, swellings developed at internodal sites. Smaller myelinated and unmyelinated fibers also underwent multifocal, giant axonal swelling. In affected myelinated fibers, swollen nodal and paranodal axons were frequently associated with retracted paranodal myelin sheaths. Adjacent distal internodes were attenuated and corrugated. Demyelinated paranodes apparently underwent local shrinkage and remyelination before complete distal fiber breakdown commenced. The proximal limits of chains of homogeneous myelin ovoids were interfaced with proximal, preserved regions at sites of giant axonal swellings. Regeneration of myelinated axons also occurred during intoxication. Regenerating fibers wre composed of multiple, short, branched internodes which sometimes appeared multifocally swollen. Interfaces between regenerating and preserved portions of fibers were unswollen. Thick section studies showed that pronounced endoneurial edema accompanied fiber degeneration in peripheral nerve trunks. Ultrastructural studies revealed multifocal, giant axonal swellings containing masses of 10 nm neurofilaments and sometimes, clustered mitochondria, neurotubules and smooth endoplasmic reticulum. Enlarged granular mitochondria, interdigitated Schwann cell/axon networks and corrugated myelin sheaths were common findings. Dense granules, vesicles and hexagonal particles were also noted in the axoplasm. These findings provide new insights into the nature of the dying-back process: although there was a retrograde, temporal spread of axonal swelling up affected nerve trunks, axonal degeneration neither began in the nerve terminal nor spread seriatim centripetally along individual nerve fibers. The dying-back process was further examined in a companion study in this issue (32) which analyzed some of the factors determining the differential vulnerability of PNS and CNS fibers in animals intoxicated either with these neurotoxic hexacarbons or with acrylamide.

2990. Occupational exposure to fibreglass: Enterline, P. E. & Henderson, V. (1975). The health of retired fibrous glass workers. Archs envir. Hlth30, 113

A peripheral nerve trunk is composed of nerve fascicles supported in a fibrous collagenous sheath and defined by concentric layers of cells (the perineurium) that separate the contents (the endoneurium) from its fibrous collagen support (the epineurium). In the endoneurium are myelinated and unmyelinated fibers that are axons combined with their supporting Schwann cells to provide physical and electrical connections with end-organs such as muscle fibers and sensory endings. Axons are tubular neuronal extensions with a cytoskeleton of neurotubules and tubulin along which organelles and proteins can travel between the neuronal cell body and the axon terminal.During development some axons enlarge and are covered by a chain of Schwann cells each associated with just one axon. As the axons grow in diameter, the Schwann cells wrap round them to produce a myelin sheath. This consists of many layers of compacted Schwann cell membrane plus some additional proteins. Adjacent myelin segments connect at highly specialized structures, the nodes of Ranvier. Myelin insulates the axon so that the nerve impulse can jump from one node to the next.The region adjacent to the node, the paranodal segment, is the site of myelin terminations on the axolemma. There are connections here between the Schwann cell and the axon via a complex chain of proteins. The Schwann cell cytoplasm in the adjacent segment, the juxtaparanode, contains most of the Schwann cell mitochondria.In addition to the node, continuity of myelin lamellae is broken at intervals along the internode by helical regions of decompaction known as Schmidt−Lanterman incisures; these are seen as paler conical segments in suitably stained microscopical preparations and provide a pathway between the adaxonal and abaxonal cytoplasm.Smaller axons without a myelin sheath conduct very much more slowly and have a more complex relationship with their supporting Schwann cells that has important implications for repair.

Experimental immunohistochemical studies on the localization and distribution of substance P in cat primary sensory neurons

With the indirect immunofluorescence technique of Coons and collaborators the occurrence of substance P (SP)-like immunoreactivity was studied in spinal ganglia (L6-S1), the spinal cord (L6-S1) and the pad skin of the hind paw of the cat. In untreated cats a very dense network of SP-positive fibers was found in the spinal cord in Lissauer's fasciculus, in laminae I–III and a rather dense plexus was seen in the ventral horns, in the area around the central canal (laminae X) and in the medial parts of laminae VI and VII. SP-positive fibers were also observed in the connective tissue under the epithelium of the skin. However, in untreated cats no specific immunofluorescence was observed in the spinal ganglia, dorsal roots or certain large peripheral nerve trunks. After certain experimental procedures such as local application of colchicine or compression of the dorsal root close to the spinal ganglion, SP-positive fluorescence was observed in a rather small number of neuronal cell bodies and in fibers. The fluorescent material was observed in the peripheral parts of the cytoplasm and the cell bodies were exclusively of the small type. Ten days after transection of the dorsal roots a marked decrease in the number of SP-positive fibers was observed in the substantia gelatinosa but not in the ventral horns. The present results give strong evidence for the occurrence of SP in a certain population of primary sensory neurons and support earlier findings that SP may act as a transmitter or modulator in these neurons.

Degeneration of muscle in association with carcinoma of the bronchus.

The clinical features and necropsy findings are described in three cases in which severe and rapidly progressive muscle weakness developed in association with carcinoma of the bronchus. In all three cases, muscular weakness was directly responsible for death. Histological and ultramicroscopical examination in all cases showed an unusual type of degeneration of muscle fibres accompanied by degeneration of intramuscular nerve fibres, but without involvement of the central nervous system, or of the peripheral nerve trunks. The findings are compared with those of previously reported cases, and possible mechanisms for the muscle degeneration are discussed.

Nerve impulse-enhanced release of amino acids from non-synaptic regions of peripheral and central nerve trunks of bullfrog

Nerve impulse-enhanced release of amino acids from non-synaptic regions of peripheral and central nerve trunks of bullfrog

Mapping of nerve cells in the suboesophageal ganglia of Helix aspersa

Abstract o 1. More than 100 different neurones have been investigated in three suboesophageal ganglia (left parietal, visceral and right parietal ganglia) of the snail Helix aspersa . 2. Diagrams and photographs of the ganglia are presented so that the cells may be identified and localized. 3. The responses following stimulation of the main peripheral nerve trunks are analysed and described, in terms of EPSP, IPSP and antidromic potentials. 4. The cells' responses to iontophoretic application of acetylcholine, dopamine, 5-HT and glutamate are described. The majority of responses to the drugs are as follows: H to ACh; H to dopamine; H to 5-HT and D to glutamate. 5. The anatomical position, spontaneous electrical activity and responses to stimulation of the main peripheral nerves and drug application make it possible to identify specific nerve cells from preparation to preparation. 6. The axons from some cells have been traced following intracellular injections of CoCl 2 and precipitation of CoS. This supported the electrophysiological method of tracing axons by recording antidromic spikes in the cell body following stimulation of a peripheral nerve. 7. It is suggested that some of the nerve cells will be homologous with other nerve cells throughout the Gastropod Molluscs.

Functional micro-anatomy of the peripheral nerve trunks

Functional micro-anatomy of the peripheral nerve trunks

Functional micro-anatomy of the peripheral nerve trunks

Functional micro-anatomy of the peripheral nerve trunks

Distribution of tetanus toxin in rat peripheral nerve trunks during the development of local tetanus.

Mouse bioassay studies were made on the tetanus toxin content of three different segments of both sciatic nerve trunks after unilateral gastrocnemius muscle injections. Multiple toxin dosages, sampling times, nerve transections, and nerve dissections to produce three samples per segment (undissected nerve, epineurium, and perineurium plus endoneurium) were used.

Electrically excitable nerve cell bodies in the central ganglia of two insect species Periplaneta americana and Schistocerca gregaria. Investigation of cell geometry and morphology by intracellular dye injection

1. 1. Intrasomatic recordings were made from nerve cell bodies in the central ganglia of the cockroach and locust and the electrical excitability of the cell bodies was tested. 2. 2. Dorsally situated cell bodies from the ganglia of both animals were electrically excitable, giving overshooting action potentials of up to 110 mV. 3. 3. Ventrally situated cell bodies were electrically inexcitable but gave small action potentials of up to 40 mV. 4. 4. Electrically excitable cockroach cell bodies were filled with Procion Yellow and their axon branches were mapped out. 5. 5. All the cells had bifurcating axons which innervated both sides of the ganglion. 6. 6. Some cells sent axons out of the ganglion in peripheral nerve trunks.

Pathology of ther peripheral nerves in leprosy: report of a case.

Peripheral nerve trunks were examined from a case of lepromatous leprosy. M. leprae was seen in the nerves in several types of cells. Isolated nerve fibre preparations showed demyelinating lesions due to Schwann cell damage and complete nerve fibre degeneration. The causes of this mixed pattern of damage may involve both a direct effect of the bacilli on nerve fibres and various epiphenomena.

Identification of neuronal connections in the central nervous system of Onchidium verruculatum.

1. Investigations were made on the nervous system of Onchidium verruculatum, pulmonate mollusc. A microelectrode was inserted into the soma of the giant neuron on the dorsal surface of the perioesophageal ganglion complex in order to record the change in membrane potential.2. Peripheral nerve trunks were stimulated electrically through bipolar electrodes. Each peripheral stimulus evoked the change in the membrane potential which were averaged by the digital computer, LINC-8.3. The analysis of the averaged responses could disclose the modes of synaptic connections, including a direct connection; i. e. an axon or an axonal branch.4. On the basis of the averaged responses, neuronal connections were deduced between peripheral nerve trunks and ganglion cells which could be always identified under a binocular microscope.5. The possibility and the limitation of the averaging technique are discussed.

Ischemic mononeuropathy and mononeuropathy multiplex in diabetes mellitus.

Abstract Seven cases of mononeuropathy multiplex occurring in association with diabetes are described, including a case previously reported in which numerous small infarcts in the peripheral nerve trunks proved to be the basis for the neuropathy. It is suggested that all the asymmetric types of diabetic neuropathy, including the cranial-nerve palsies, mononeuropathies and mononeuropathy multiplex, are caused by infarcts within nerve. Diabetic amyotrophy is a proximal mononeuropathy multiplex and should not be separated from the other asymmetric neuropathies. Because these asymmetrical neuropathic syndromes do not seem to be unique to diabetes and the role of diabetes in their pathogenesis is still uncertain, the term ischeic mononeuropathy or mononeuropathy multiplex associated with diabetes mellitus is recommended.