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At least 721 records · Page 40Linked to original sources
PubMed1997

The beta-amyloid precursor protein of Alzheimer's disease enhances neuron viability and modulates neuronal polarity.

beta-Amyloid precursor protein (betaPP) can reside at neuron and glial cell surfaces or undergo proteolytic processing into secreted fragments. Although betaPP has been studied extensively, its precise physiological role is unknown. A line of transgenic knock-out mice selectively deficient in betaPP survive and breed but exhibit motor dysfunction and brain gliosis, consistent with a physiological role for betaPP in neuron development. To elucidate these functions, we cultured hippocampal neurons from wild-type and betaPP-deficient mice and compared their ability to attach, survive, and develop neurites. We found that hippocampal neurons from betaPP-deficient mice had diminished viability and retarded neurite development. We also compared the effects of betaPP secretory products, released from wild-type astrocytes, on process outgrowth from wild-type and betaPP-deficient hippocampal neurons. Outgrowth was enhanced at 1 d in the presence of wild-type astrocytes, as compared with betaPP-deficient astrocytes. However, by 3 d, neurons had shorter axons but more minor processes with more branching when cocultured with wild-type astrocytes, as compared with betaPP-deficient astrocytes. Our data demonstrate that cell-associated neuronal betaPP contributes to neuron viability, axonogenesis, and arborization and that betaPP secretory products modulate axon growth, dendrite branching, and dendrite numbers.

Alzheimer Disease↗
PubMed1998

Two receptor tyrosine phosphatases of the LAR family are expressed in the developing leech by specific central neurons as well as select peripheral neurons, muscles, and other cells.

Receptor protein tyrosine phosphatases (rPTPs) are thought to play a crucial role in neuronal development, particularly in pathfinding by growing processes. We have cloned and sequenced two Hirudo medicinalis rPTPs that are homologous to the Drosophila and vertebrate rPTPs of the Leukocyte common antigen-related (LAR) subfamily. These Hirudo rPTPs, HmLAR1 and HmLAR2, are products of different, homologous genes, both containing two tandem intracellular phosphatase domains and ectodomains with three tandem Ig domains and different numbers of tandem fibronectin type III (FIII) domains. They are expressed in distinct patterns during embryogenesis. HmLAR1 mRNA is expressed by a subset of central and peripheral neurons and by several peripheral muscular structures, whereas HmLAR2 mRNA is expressed by a different subset of central neurons and by the peripheral, neuron-like Comb cells. HmLAR1 and HmLAR2 proteins are located on the neurites of central neurons. In addition, HmLAR2 is expressed on the cell body, processes, and growth cones of the Comb cells. Because of their CAM-like ectodomains and homology to proteins known to be involved in pathfinding and because they are expressed by different subsets of neurons, we hypothesize that HmLAR1 and HmLAR2 participate in navigational decisions that distinguish the sets of neurons that express them. Furthermore, we hypothesize that HmLAR2 is also involved in setting up the highly regular array of parallel processes established by the Comb cells. Lastly, we propose that the HmLAR1 ectodomain on peripheral muscle cells plays a role in target recognition via interactions with neuronal receptors, which might include HmLAR1 or HmLAR2.

Amino Acid Sequence↗
PubMed2003

Dendritic domains of nociceptive-responsive parabrachial neurons match terminal fields of lamina I neurons in the rat.

This study investigates, in the anesthetized rat, the dendritic extent of parabrachial (PB) neurons whose nociceptive response to noxious stimuli has been previously recorded with an extracellular micropipette. The PB neurons were then injected with biocytin through the recording micropipette, via a juxtacellular technique. The dendritic arborization of individual PB neurons was carefully compared with the projections of medullary (trigeminal) and spinal lamina I neurons. The latter projections were labeled in separate animals that received injections of Phaseolus vulgaris-leucoagglutinin restricted to the superficial layers of spinal or medullary dorsal horn. We report here that: 1) PB neurons excited chiefly by noxious stimulation of the face have their dendritic tree located primarily within the field of lamina I trigeminal projections, i.e., in the caudal portion of PB area, around the external medial and the caudal part of the external lateral subnuclei; and 2) PB neurons excited chiefly by noxious stimulation of the paw or the tail have their dendritic tree located primarily within the field of lamina I spinal projections, i.e., in PB mid-extent, around the borderline between the external lateral and both the lateral crescent and the superior lateral subnuclei. Our results suggest the presence of an extensive excitatory axodendritic link between lamina I projections and PB nociceptive neurons around the lateral crescent and the external medial subnuclei. These findings strengthen the possibility of involvement of a subgroup of PB neurons in nociceptive processes.

Animals↗
PubMed1988

Neuronal death in vitro: parallelism between survivability of hippocampal neurones and sustained elevation of cytosolic Ca2+ after exposure to glutamate receptor agonist.

Hippocampal neurones isolated from rat embryos were maintained on glial monolayers in a medium containing no L-glutamate (Glu). The administration of Glu for a limited period induced a massive death (loss) of neurones. The degree of neuronal loss increased with time after exposure to Glu. The extent of neuronal loss assessed 24 h after exposure to Glu was dependent upon the concentration Glu and on the duration of the exposure. An increase in concentration of external Ca2+ during the exposure to Glu enhanced the extent of loss. By contrast, an increment in concentration of environmental Mg2+ reduced the loss. The inhibitor of spike firing, tetrodotoxin (TTX) and the suppressor of Ca2+ entry, nitrendipine, both decreased the extent of loss, when delivered prior to Glu. The toxicity of Glu became progressively more apparent with further days of culture. The cytosolic concentration of Ca2+ ([Ca2+]i) in single hippocampal neurones was monitored by microscopic fluorometry under conditions equivalent to those in the death assay. The time required for the recovery of [Ca2+]i from the level elevated by exposure to Glu to pre-stimulus levels closely paralleled the degree of neuronal loss; i.e. high doses of Glu, long periods of exposure, high concentrations of external Ca2+, low concentrations of external Mg2+, and extended days of culture all retarded [Ca2+]i recovery, while TTX and nitrendipine accelerated it. These findings show that neuronal death resulting from an extraneous excitation (excitotoxicity) can be analyzed in vitro. Furthermore, substantial support has been provided to the hypothesis that excitotoxicity has an underlying mechanism, an excess loading of Ca2+ in neuronal cytoplasm.

Animals↗
PubMed1994

A model for the neuronal implementation of selective visual attention based on temporal correlation among neurons.

We propose a model for the neuronal implementation of selective visual attention based on temporal correlation among groups of neurons. Neurons in primary visual cortex respond to visual stimuli with a Poisson distributed spike train with an appropriate, stimulus-dependent mean firing rate. The spike trains of neurons whose receptive fields do not overlap with the "focus of attention" are distributed according to homogeneous (time-independent) Poisson process with no correlation between action potentials of different neurons. In contrast, spike trains of neurons with receptive fields within the focus of attention are distributed according to non-homogeneous (time-dependent) Poisson processes. Since the short-term average spike rates of all neurons with receptive fields in the focus of attention covary, correlations between these spike trains are introduced which are detected by inhibitory interneurons in V4. These cells, modeled as modified integrate-and-fire neurons, function as coincidence detectors and suppress the response of V4 cells associated with non-attended visual stimuli. The model reproduces quantitatively experimental data obtained in cortical area V4 of monkey by Moran and Desimone (1985).

Animals↗
PubMed1976

Metabolic regulations of the rhythmic activity in pacemaker neurons. II. Metabolically induced conversions of beating to bursting pacemaker activity in isolated Aplysia neurons.

In pacemaker neurons of the sea hare Aplysia californica, isolated from their synaptic, ephaptic and humoral inputs, conversion of the regular beating to a bursting discharge pattern can be induced by certain cell metabolites. Administration of the phosphofructokinase (PFK) activator fructose-6-phosphate (F-6-P), or its nonmetabolizable analogue 1-deoxy-F-6-P, induced bursting discharges in R3, R5, R6 and R11 neurons, with spike doublets and triplets appearing transiently in the time pattern. With another PFK activitor, adenosine-5-monophosphate, only double spikes have been noted in R7, R8 and R14 neurons. Burst activity was induced also in the presence of the fructose-1,6-diphosphatase activators, citrate and 3-phosphoglycerate, in R9, R10 and R12 neurons. Cyclic 3',5'-AMP, which also activates the PFK (beside other effects on cellular metabolism), induced bursting discharges in all R3-R14 neurons. In contrast, the inhibitors of the PFK, citrate and ATP, decreased the spike activity of the bursting L3 and L6 neurons, even changing L3 neurons to the regular beating type. Among a variety of cell metabolites tested only pyruvate was able to induce a burst-like tendency in R9 neurons. The characteristic bursting patterns which appeared in the presence of the described metabolic effectors could not be duplicated by low Ca2+ and/or high K+ media nor by artificial shifts in membrane potential triggered by depolarizing and hyperpolarizing currents.

Adenosine Monophosphate↗
PubMed1988

Co-localization of substance P and Met-enkephalin-Arg6-Gly7-Leu8 in the intraspinal neurons of the rat, with special reference to the neurons in the substantia gelatinosa.

A double-labeling immunofluorescence technique was employed to investigate the co-localization of the functionally antagonistic neuropeptides, substance P and enkephalins, within intraspinal neurons of the rat. Anti-Met-enkephalin-Arg6-Gly7-Leu8 (Enk-8) antiserum was used as a marker of the preproenkephalin A neuron system. The observations were focused on the lumbar spinal cord. Co-localization was most prominent within neurons in the substantia gelatinosa, in which more than 95% of substance P-like immunoreactivity neurons showed Enk-8-like immunoreactivity. These double-labeled cells corresponded to 45% of Enk-8-like immunoreactive neurons in the same area. This suggests that SP/Enk-8 interaction occurs at the axon terminals of the substantia gelatinosa neurons. In deeper layers of the dorsal horn (laminae III, IV), only 14% and 6% of SP-like immunoreactive and Enk-8-like immunoreactive neurons were double labeled, respectively. Co-localization was also observed in neurons located in the laminae I, V, VII and X, suggesting concomitant involvement of these peptides in a variety of spinal cord functions.

Animals↗
PubMed1990

Neurotrophic factor for serotonergic neurons prevents degeneration of grafted raphe neurons in the cerebellum.

Earlier studies in this laboratory have shown that partial serotonergic (5-HT) deafferentation from the hippocampus induced a homotypic sprouting. The 5-HT-denervated hippocampus was further found to be a favorable environment for the growth of grafted 5-HT, but not for norepinephrinergic neurons. In the current study, we have extracted a trophic factor in the denervated hippocampus with hypotonic solution in high-speed supernatant fraction. The trophic extract was assayed in a unique experimental paradigm--test the growth of grafted 5-HT neurons in the cerebellum, which receives the least 5-HT innervation, and where grafted 5-HT neurons have seldom survived. The diluted trophic extract (1:200) produced a dramatic increase in (a) the survival rate, (b) the 5-HT fiber-density, and (c) the 5-HT and 5-hydroxyindoleacetic acid levels of grafted 5-HT neurons in the cerebellum. In addition, Nissl-counterstaining showed that the size of the grafted raphe also apparently increased. The concentrated trophic extract (1:1) did not increase the survival rate of the grafted raphe neurons. These results indicate that (a) the supernatant in the 5-HT-denervated hippocampus contains a potent neurotrophic factor to 5-HT neurons (b) which can either directly or indirectly also support non-5-HT raphe neurons, and (c) possibly an inhibitory factor is present which is detrimental to 5-HT neurons in high concentration.

Animals↗
PubMed1992

Interneurons in the rat striatum: relationships between parvalbumin neurons and cholinergic neurons.

A pre-embedding double-labeling immunocytochemical method was used to examine the synaptic relationships between cholinergic neurons and the parvalbumin immunoreactive (PV+) neurons. The PV+ neurons were labeled by silver-intensified colloidal gold particles, and the cholinergic neurons by immunoperoxidase reaction products. Cholinergic and PV+ axon terminals form synapses with both the somata and dendrites of PV+ neurons, as well as unlabeled medium-sized somata with round un-indented nuclei, a typical characteristic of the medium spiny projection neurons. These observations suggest that the PV+ and the cholinergic neurons have converging influences on both the projection neurons and the PV+ interneurons in the striatum.

Acetylcholine↗
PubMed1988

Quantitative analysis of fetal rat brain neurons developing in primary cultures. I. Stereological study of the neuronal differentiation.

An ultrastructural stereological analysis was performed to analyze the morphological differentiation of primary cultures of fetal rat brain neurons, growing for two weeks in a serum-free medium. The number of neurons and of gliofibrillary acidic protein (GFAP)-positive glial cells was estimated by light microscopy counting in the culture wells. These cultures provided a quasi-pure neuronal population, since the number of GFAP-positive glial cells was found to be 1% (day 7) and 2% (day 14) respectively of the total number of cultured cells. Cell counts and the stereological measurements were related to the surface area of the culture well. The neuronal differentiation was characterized by an increase in the plasma membrane surface area (x9) and volume (x8) of neurites, contrasting with the decrease in the perikarya surface area and volume. These primary stereological data were combined with the number of neurons to obtain parameters characterizing an average neuron. The increase in membrane surface area of an average neuron was found to be a linear function of time, 29 micron 2 and 445 micron 2 of new membrane being added per day of culture to perikarya and neurites respectively. The number of chemical synapses was also counted and compared to the changes in the plasma membrane surface area. After 7 days in vitro they increased in number more rapidly than the increase in the plasma membrane surface area of neurons.

Animals↗
PubMed1986

1-Methyl-4-phenylpyridinium (MPP+) but not 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) selectively destroys dopaminergic neurons in cultures of dissociated rat mesencephalic neurons.

Dopaminergic neurons were studied in cultures of dissociated cells from the ventral mesencephalon of fetal rat embryos (gestational day E15-16). After a week of growth, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or 1-methyl-4-phenylpyridinium (MPP+) was added to the growth medium for 24 h. Dopaminergic neurons were then visualized with tyrosine hydroxylase (TH) immunocytochemistry or catecholamine (CA) cytofluorescence. Concentrations of MPTP in the range of 10 to 100 microM obliterated CA fluorescence without affecting the number of TH-positive neurons. At concentrations greater than 100 microM, MPTP decreased the number of TH-positive neurons as well as the number of all other cell types. MPP+ (0.1-10.0 microM) produced a decrease in the number of TH-positive neurons without decreasing the total number of all cell types. The findings indicate that MPP+ but not MPTP is able to selectively destroy rat dopaminergic neurons in our cultures. The selective toxicity of MPP+ for dopaminergic neurons was partially prevented by pretreatment and co-incubation with mazindol (a selective inhibitor of dopamine uptake) but not by desipramine or deprenil, in confirmation of the notion that MPP+ enters dopaminergic neurons by the specific uptake mechanism for dopamine.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1988

Noradrenergic neurons with divergent projections to the motor trigeminal nucleus and the spinal cord: a double retrograde neuronal labeling study.

Double retrograde axonal tracing was combined with the indirect immunofluorescence antibody method to determine whether noradrenergic neurons have divergent projections to the motor nucleus of the trigeminal nerve and the spinal cord. Rhodamine-labeled microspheres were injected into the motor trigeminal nucleus and True Blue was deposited into lumbar segments of the spinal cord. After a 10-18-day survival period, brainstem sections were processed for immunofluorescence staining of noradrenergic neurons using antibodies to rat dopamine-beta-hydroxylase. Rhodamine-labeled noradrenergic neurons were observed ipsilaterally throughout the A5 and A7 groups; the contralateral A5 and A7 groups contained few rhodamine-labeled cells. A few rhodamine-labeled noradrenergic neurons were observed in the locus coeruleus and subcoeruleus. True Blue-labeled noradrenergic neurons were identified in the A5 and A7 groups, in the ventral part of the locus coeruleus and in the subcoeruleus. Double retrogradely labeled noradrenergic neurons were observed in the A5 and A7 groups but not in the locus coeruleus and subcoeruleus. Of the total number of rhodamine-labeled noradrenergic cells, a large percentage also contained True Blue: 54% in the caudal A5 group, 59% in the rostral A5 group, and 72% in the A7 group. Of the total number of True Blue-labeled noradrenergic neurons, the percentage of double retrogradely labeled cells was 33% in the caudal A5 group, 46% in the rostral A5 group, and 56% in the A7 group. The findings of this study provide the first anatomic evidence for the existence of a prominent population of noradrenergic cells in the A5 and A7 groups with divergent projections to the motor trigeminal nucleus and the spinal cord. We propose that this subpopulation of noradrenergic neurons in the A5 and A7 groups influences motoneurons at multiple levels of the neuraxis.

Adrenergic Fibers↗
PubMed1995

Synchronous development of pyramidal neuron dendritic spines and parvalbumin-immunoreactive chandelier neuron axon terminals in layer III of monkey prefrontal cortex.

Postnatal development of the primate cerebral cortex involves an initial proliferation and the subsequent attrition of cortical synapses. Although these maturational changes in synaptic density have been observed across the cortical mantle, little is known about the precise time course of developmental refinements in synaptic inputs to specific populations of cortical neurons. We examined the postnatal development of two markers of excitatory and inhibitory inputs to a subpopulation of layer III pyramidal neurons in area 9 and 46 of rhesus monkey prefrontal cortex. These neurons are of particular interest because they play a major role in the flow of information both within and between cortical regions. Quantitative reconstructions of Golgi-impregnated mid-layer III pyramidal neurons revealed substantial developmental changes in the relative density of dendritic spines, the major site of excitatory inputs to these neurons. Relative spine density on both the apical and basilar dendritic trees increased by 50% during the first two postnatal months, remained at a plateau through 1.5 years of age, and then decreased over the peripubertal age range until stable adult levels were achieved. As a measure of the postnatal changes in inhibitory input to the axon initial segment of these pyramidal neurons, we determined the density of parvalbumin-immunoreactive axon terminals belonging to the chandelier class of local circuit neurons. The density of these distinctive axon terminals (cartridges) exhibited a temporal pattern of change that exactly paralleled the changes in dendritic spine density. These results suggest that subpopulations of cortical neurons may be regulated by dynamic interactions between excitatory and inhibitory inputs during development and, in concert with other data, they emphasize the cellular specificity of postnatal refinements in cortical circuitry.

Aging↗
PubMed1997

Ultrastructural study of nitric oxide synthase-containing striatal neurons and their relationship with parvalbumin-containing neurons in rats.

Single- and double-label electron microscopic immunocytochemistry was used to examine the ultrastructure of striatal neurons containing nitric oxide synthase (NOS+) and evaluate the synaptic relationship of NOS+ striatal neurons with those containing parvalbumin (PV+). In both the single-label and double-label studies, NOS+ perikarya were observed to possess polylobulated nuclei. In the single-label studies, NOS+ terminals were seen forming synaptic contacts with dendritic shafts and dendritic spines that did not contain NOS, but not with NOS+ perikarya or dendrites. In the double-label studies (using diaminobenzidine and silver intensified immunogold as markers), nitric oxide synthase and parvalbumin immunoreactions were found in two different populations of medium-sized aspiny striatal neurons. The PV+ axon terminals were seen forming symmetric synapses on the dendritic spines of neurons devoid of PV or NOS labeling, on PV+ dendrites, and on NOS+ soma and dendrites. In contrast, NOS+ terminals were not observed to form synaptic contacts with the dendrites or soma of either PV+ or NOS+ neurons. These findings suggest that NOS+ striatal interneurons form synaptic contact with the spines and presumably the dendrites of striatal projection neurons, but not with the dendrites or soma of PV+ or NOS+ striatal interneurons. NOS+ neurons do, however, receive synaptic input from PV+ neurons.

Animals↗
PubMed1989

The connections from botzinger expiratory neurons to upper cervical inspiratory neurons in the cat.

These experiments examined possible inhibitory inputs to upper cervical inspiratory neurons from the expiratory neurons of the Botzinger complex. Eighty-one Botzinger neurons were tested with antidromic mapping for a projection to the C1 segment of the spinal cord; 44/81 (54%) were found to project, 27/79 (34%) contralaterally, 17/68 (25%) ipsilaterally, and 1/66 (2%) both contralaterally and ipsilaterally. Antidromic mapping in contralateral C1 demonstrated the presence of a collateral in 3/15 (20%) of the Botzinger neurons tested, while 3/9 (33%) had collateral arborizations in ipsilateral C1. The collaterals mapped were not localized to the region of the upper cervical inspiratory neurons. Microstimulation in C3 (12-17 microA, 0.2-ms duration) at locations which produced short-latency (2.7-3.5 ms) inhibition of phrenic nerve discharge resulted in the short latency (3.0 ms) inhibition of 1/27 (3.7%) upper cervical inspiratory neurons as demonstrated by cross-correlation. It was concluded that while some upper cervical inspiratory neurons may be inhibited during expiration by the Botzinger expiratory neurons, this connection is not a strong one.

Animals↗
PubMed1997

Selective loss of neuronal Na+-dependent phosphate cotransporter mRNA in CA1 pyramidal neuron following global ischemia.

A recently identified neuronal Na+-dependent phosphate cotransporter (rBNPI) has been shown to import inorganic phosphate (P(i)) required for the production of high-energy phosphates which are vital to neuronal energy metabolism. In the present study, we have examined the expression of rBNPI mRNA in the hippocampus of rats subjected to 30 min of global ischemia by four-vessel occlusion. In situ hybridization reveals that transient forebrain ischemia results in a selective reduction in rBNPI mRNA expression in CA1 pyramidal neurons of the hippocampus. Expression of rBNPI is significantly reduced by 24 h and completely absent at 72 h following global ischemia when CA1 pyramidal neurons begin to show cell damage. By contrast, there is no change in the expression of Nedd2 mRNA, a developmentally regulated cell death gene, in CA1 pyramidal neurons at these same time points. The loss of rBNPI transcripts appears to be selective for CA1 pyramidal neurons since rBNPI mRNA expression is unchanged in neurons of the CA2-CA4 pyramidal cell layers following global ischemia. Our data indicate that an early reduction of rBNPI transcripts may contribute to a reduction in P(i)-dependent energy metabolism or signal transduction which has been reported in CA1 hippocampal neurons following global ischemia.

Animals↗
PubMed2000

Neuronal organization of the utricular macula concerned with innervation of single vestibular neurons in the cat.

We investigated whether cross-striolar inhibition, which may increase sensitivity to linear acceleration, contributed to utricular (UT) afferent innervation of single vestibular neurons (VNs). Excitatory and inhibitory postsynaptic potentials (EPSPs, IPSPs, respectively) were recorded from VNs after focal stimulation of the UT macula (M). From a total of 83 VNs, 25 (30%) neurons received inputs from both sides of the UTM, and the response patterns were opposite, i.e. cross-striolar inhibition was observed. In roughly 2/3 of these neurons, stimulation of the medial side of the UTM evoked EPSPs, while stimulation of the lateral side evoked IPSPs. In the remaining 1/3 neurons, the response patterns were opposite. Thirty-two (39%) of the 83 neurons received the identical pattern of inputs from both sides of the UTM: EPSPs in 26 neurons and IPSPs in six neurons. Twenty-six (31%) of the 83 neurons received inputs from either the medial or the lateral side of the UTM. These findings suggest that cross-striolar inhibition existed in the UT system, although it was not a dominant circuit that increased the sensitivity as in the saccular system [15].

Acoustic Maculae↗
PubMed2000

Neuronal structure of microvascular transplants with and without neuronal anastomosis.

OBJECTIVE: Latissimus dorsi transplants have little neuronal regenerative capacity without neuronal anastomosis. Histologic differences between transplants with and without neuronal anastomosis and 2 distinct types of neurosurgical reanastomosis are highlighted in this study. PATIENTS AND METHODS: Fifty-four patients with squamous cell carcinomas of the oral cavity (T4) were treated by tumor resection and homolateral neck dissection. The defect was covered with a microvascular latissimus dorsi transplant. In 15 patients, no neuronal anastomoses were performed. In 21 patients, the thoracodorsal nerves were used for microneurosurgical reanastomosis, whereas in 18 patients, the cutaneous branches of the intercostal nerves were used for microneurosurgical reanastomosis. The transplant was examined during surgery and 9 months after surgery by means of a histologic examination of a biopsy specimen. The number of fascicles, the degree of fibrosis, and the myelination were examined. Furthermore, a neurosensory examination was performed 9 months after surgery. RESULTS: Overall, our patients had an average of 12.1 fascicles during surgery. After surgery, patients without neuronal anastomosis showed an average of 4.9 fascicles, patients with nerve anastomosis to the cutaneous branches of the intercostal nerve showed an average of 6.2 fascicles, and patients with anastomosis to the thoracodorsal nerve showed an average of 9.6 fascicles. In cases of nerve anastomosis, a lesser degree of fibrosis was found, together with good myelinization. The clinical examination showed the best neurosensory function in the transplants with anastomosis to the thoracodorsal nerve and the worst function in those without neuronal anastomosis. CONCLUSION: Neuronal reanastomosis led to more surviving neuronal structures in the postoperative histologic specimen. The highest density of fascicles was found in the well vascularized thoracodorsal nerve. The neurosensory function agrees with the histologic result.

Adult↗