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PubMed1990

Ultrastructural organization of receptor cell axons in frog olfactory nerve.

Repeated odorant or electrical stimulation of the frog olfactory nerve leads to long-lasting reduction of excitability of the receptor neurons. In the turtle olfactory nerve electrical stimulation causes an increase in extracellular potassium concentration due to the efflux of potassium from active axons. Elevated potassium concentration depolarizes an axon membrane and inactivates it. If axons travel parallel to each other in the nerve for extended distances, changes in ionic concentration due to activity in one axon will reduce excitability of its neighbors. This phenomenon may have effects like those of lateral inhibition among neighbors first described in Limulus and may act as a filter with a long time constant, for the nervous message. The amphibian olfactory nerve consists of densely packed, small-diameter, unmyelinated fibers. In this study we have examined the ultrastructure of the frog (Rana pipiens) olfactory nerve in longitudinal and cross-sections to determine whether axons follow a sinuous course and change neighbors often along the length of the olfactory nerve, or whether they follow parallel trajectories and thus tend to stay close to the same neighbors. We have found that axons have a very straight course within the nerve and that axons tend to remain adjacent to the same individual axons over long distances. We think that the anatomical substrate of the olfactory nerve favors strong inhibitory axon-axon interaction.

Animals↗
PubMed1994

Axon branching of medullary expiratory neurons in the lumbar and the sacral spinal cord of the cat.

Intraspinal axon collaterals of expiratory (E) neurons in the caudal nucleus retroambigualis extending their desending spinal axons to the lower lumbar (L6-L7) and the sacral (S1-S3) segments were investigated in anesthetized cats. To search for axon collaterals of single E neurons in the lumbar segments, the spinal gray matter was microstimulated from the dorsal to the ventral sites at 100 microns intervals with an intensity of 150-250 microA at 1 mm intervals rostrocaudally along the spinal cord, and effective stimulating sites of antidromic activation in axon collaterals were systematically mapped. In addition, the detailed trajectory of collaterals in the upper lumbar (L1-L3), the middle lumbar (L4-L5), and the sacral (S1-S3) spinal cord was examined by microstimulation at a matrix of points 100-200 microns apart with a maximum stimulus intensity of 50 microA. The trajectory of axon collaterals was reconstructed on the basis of the location of low-threshold foci and the latency of antidromic spikes. Virtually all E neurons examined had 1-7 collaterals at widely separated segments of the lumbar cord. Many axon collaterals were found in the upper lumbar spinal cord as compared to the middle and the lower lumbar spinal cord. The locations of axon collaterals in the upper lumbar spinal cord overlapped with those of abdominal motoneurons. Axon collaterals in the sacral gray matter were found in 3 of 9 E neurons. Axon collaterals were found within the nucleus of Onuf, in the region dorsal to the nucleus of Onuf, and in the intermediate region. The functional significance of the divergent distribution of multiple axon collaterals of single E neurons in different spinal levels of the lumbar and the sacral spinal cord is discussed in relation to the respiratory function of E neurons and other spinal motor activities.

Animals↗
PubMed1996

Estimates of the axonal refractory period of midbrain dopamine neurons: their relevance to brain stimulation reward.

Psychophysical studies have shown that the directly activated neurons subserving the rewarding effect produced by electrical stimulation of the medial forebrain bundle (MFB) have refractory periods (RPs) shorter than those of dopaminergic (DA) neurons: this suggests that the directly stimulated substrate for the rewarding effect does not include DA neurons. Comparison of RP estimates. however, is difficult since those of DA neurons were obtained with the standard electrophysiological technique that characterizes cell body/initial segment rather than the directly stimulated axonal segment. Using electrophysiological recording techniques in urethane anesthetized rats, we re-estimated and compared the RP of DA neurons that project to the MFB and the ventral striatum (VST) with two stimulation procedures: one that characterizes the axonal segment near the stimulation electrode and the standard one that characterizes the cell body/initial segment near the recording electrode. Results showed that DA axonal RPs range from 1.0 to 2.2 ms, whereas cell body/initial segment RPs range from 1.0 to 3.0 ms. The axonal RP was equal to or shorter (mean difference = 0.22 ms, n = 15) than the cell body/initial segment RP. Axonal RP estimates for MFB sites range from 1.3 to 2.1 ms. values that slightly overlap with the late recovery from refractoriness reported in psychophysical studies for reward-relevant neurons. Axonal RP estimates obtained for VST sites were very similar (mean = 1.66, LH and 1.62 ms, VST) suggesting that the excitability of DA axons does not differ along their path. These results further support the hypothesis that DA axons are unlikely to constitute a major component of the directly-stimulated reward-relevant axons in the MFB. They also suggest that the direct contribution of DA axons to reward produced by VST stimulation is more important than by the MFB.

Action Potentials↗
PubMed1984

Stereotyped and variable growth of redirected Mauthner axons.

To assay the axon tract organizing capabilities of different regions of the vertebrate CNS, Mauthner axons were redirected by grafting supernumerary hindbrains in Xenopus embryos. The 63 redirected Mauthner axons thus produced included donor axons projecting into the host CNS and host axons that grew through the graft or that were redirected in the host CNS. Two major phenomena were observed. Caudal to the optic chiasm, the Mauthner axons followed a single ipsilateral stereotyped route--the basal substrate pathway--extending in the ventral and ventrolateral marginal zone from the diencephalon to the caudal spinal cord. In contrast, rostral to the optic chiasm, these same Mauthner axons followed variable ipsilateral and contralateral routes. Even pairs of Mauthner axons entering the optic chiasm side-by-side eventually followed different routes in normal forebrains. The contrasting behaviors of the Mauthner axons growing in the rostral diencephalon and telencephalon and of the same Mauthner axons growing elsewhere suggest that there are differences in the effective guidance cues between these two regions of the developing brain. This is consistent with other types of neuroanatomical and neuroembryological evidence indicating a fundamental division between the rostral and the caudal diencephalon.

Animals↗
PubMed1985

Early axon patterns of the spinal cord: experiments with a computer.

In the vertebrate central nervous system, most axons appear in one of two elemental patterns--sheets or bundles. Many developmental mechanisms are involved in the formation of the elemental axon patterns, and these mechanisms often act simultaneously. The major axon-patterning mechanisms include differential adhesivity, internal growth constraints on axons, and initial orientation of axonal outgrowth. To evaluate the effects of these mechanisms on the formation of axon patterns, a computer was used to model axonal growth. Experiments with the computer model suggest that axon sheets are produced by the cooperative action of more than one mechanism. Furthermore, in the appropriate combination, these mechanisms produce orderly axon sheets even on patternless substrates. On the other hand, to transform the sheets into axon bundles, the substrate must be patterned.

Animals↗
PubMed1986

Axonal pathfinding in organ-cultured embryonic avian retinae.

Eye cups from stage 14-28 (E2 to E5) chick and quail embryos consisting of neural retina, lens, and vitreous body were cultured for 1 or 2 days. These eyes expanded by proliferation of the retinal cells and the surface areas of the retinae increased several-fold. The area covered by ganglion cells and axons also expanded in vitro. [3H]Thymidine labeling showed extensive proliferation of the neuroepithelial cells including the formation of new ganglion cells. Culturing eyes from embryos before stage 17 results, as in vivo, in the generation of the first ganglion cells of the retina, but unlike in the in vivo situation, the outgrowing axons always formed a random fiber net in the central portion of the retina. A defined axonal pattern identical to the in vivo developed only in specimens from embryos of stage 17 and older. Some aberrant axons, however, were also observed at the retinal periphery in specimens from embryos of more advanced stages (20-24), but only during the second day of culturing. Axons in retinae from embryos of stages 23 to 26 heading toward the optic fissure often crossed the fissure and, in contrast to the situation in vivo, invaded the opposite retinal side. These axons of wrong polarity followed the pathways of axons growing centripetally but in reverse direction. This suggests that the polarity of growing nerve fibers and their course are determined by different factors. Culturing the eyes of embryos from stages 20 to 25 in the presence of antibodies showed that the antibodies penetrated the entire retina with 6 hr. Neither anti-N-CAM nor the T-61 antibody--both recognizing membrane proteins of retinal cells--affected the growth of the eyes in vitro. The development of the axonal pattern in vitro was not affected by incubation with N-CAM-antibodies at concentrations up to 500 micron/ml, whereas the T-61 antibody which is known to block neurite extention in vitro (S. Henke-Fahle, W. Reckhaus, and R. Babiel (l984). "Developmental Neuroscience: Physiological, Pharmacological, and Clinical Aspects," pp. 393-398. Elsevier, Amsterdam/New York) showed inhibition of axonal growth in retina cultures at 50 micron/ml. These results indicate that the eye cultures can be used as a test system for antibodies against antigens which could be involved in axon extension and neurite pathfinding in situ.

Animals↗
PubMed1986

Molecular structure of the axolemma of developing axons following altered gliogenesis in rat optic nerve.

Axonal and axolemmal development of fibers from rat optic nerves in which gliogenesis was severely delayed by systemic injection of 5-azacytidine (5-AZ) was examined by freeze-fracture electron microscopy. In neonatal (0-2 days) rat optic nerves, all fibers lack myelin, whereas in the adult, virtually all axons are myelinated. The axolemma of neonatal premyelinated fibers is relatively undifferentiated. The P-fracture face (P-face) displays a moderate (approximately 550/micron 2) density of intramembranous particles (IMPs), whereas the E-fracture face (E-face) has few IMPs (approximately 125/micron 2) present. By 14 days of age, approximately 25% of the axons within control optic nerves are ensheathed or myelinated, with the remaining axons premyelinated. The ensheathed and myelinated fibers display increased axonal diameter compared to premyelinated axons, and these larger caliber fibers exhibit marked axonal membrane differentiation. Notably, the P-face IMP density of ensheathed and myelinated fibers is substantially increased compared to premyelinated axolemma, and, at nodes of Ranvier, the density of E-face particles is moderately high (approximately 1300/micron 2), in comparison to internodal or premyelinated E-face axolemma. In optic nerves from 14-day-old 5-AZ-treated rats, few oligodendrocytes are present, and the percentage of myelinated fibers is markedly reduced. Despite delayed gliogenesis, some unensheathed axons within 5-AZ-treated optic nerves display an increased axonal diameter compared to premyelinated fibers. Most of these large caliber fibers also exhibit a substantial increase in P-face IMP density. Small (less than 0.4 micron) diameter unensheathed axons within treated optic nerves maintain a P-face IMP density similar to that of control premyelinated fibers. Regions of increased E-face particle density were not observed. The results demonstrate that some aspects of axolemma differentiation continue despite delayed gliogenesis and the absence of glial ensheathment, and suggest that axolemmal ultrastructure is, at least in part, independent of glial cell association.

Animals↗
PubMed1985

Microtubule density and size of axons in early diabetes: implications for nerve cell homeostasis.

The density of microtubules and the axonal caliber were studied in myelinated axons from sural nerves of young male alloxan-diabetic and age-matched rats, at 0, 15, 30, and 60 days after diabetes induction. The longitudinal growth of axons was normal in diabetic rats, but in contrast, the radial growth of axons was impaired. The axonal area was 20% less than normal in diabetic rats at the 60th day. Microtubule density was assessed in 3-micron-diameter axons. No differences in microtubule density (range: 25.0 to 28.0 microtubules/micron2) were found between or within diabetic and control groups. However, the subnormal axonal size in diabetic rats entailed a reduced content of microtubules in a nerve trunk because the relation between axonal size and microtubule density remained normal. The results showed that microtubule density was independent of axonal length, and of age, weight, or diabetic conditions of the rats, and was related only to the axonal size. These findings have implications in nerve cell homeostasis.

Animals↗
PubMed1985

Evolution of axonal swellings in cats intoxicated with beta,beta'-iminodipropionitrile (IDPN). An electrophysiological and morphological study.

beta,beta'-Iminodipropionitrile (IDPN) causes formation of axonal swellings in the proximal internodes of spinal motor axons. The swellings enlarge and demyelinate with the progression of the neuropathy. The correlation between axonal swellings and electrophysiologic function of motoneurons was examined in cats 2 to 35 days after initial administration of IDPN. Morphologic changes in intraspinal motor axons, occasionally observed 2 days after the first injection, became progressively more evident at later times, with enlargement at the first internode in some axons and appearance of fusiform or balloon-like axonal swellings. At 7 days axonal swellings were infrequently observed and the main structural feature was a reduction in myelin thickness in affected nerve fibers. Despite scant histopathologic changes, motoneuron action potential discharge at this time was significantly altered in latency to onset of spike and rate of rise. Abnormal motoneuron firing patterns were observed at this time. As the neuropathy progressed, both the frequency of occurrence and the size of axonal swellings increased markedly but at no time was there morphologic evidence of chromatolysis. At 14 and 35 days, (after two or five IDPN injections) action potential discharge became further altered in latency to spike onset, rate of rise, initial segment conduction time and somal-dendritic threshold. The incidence of repetitive firing increased and axonal conduction block was observed in several motoneuron recordings. The electrophysiologic changes closely resemble those reported in chromatolytic motoneurons after axotomy. The axonal swellings induced by IDPN may produce an axotomy-like condition which becomes more prominent as the neuropathy progresses but without morphologic evidence of chromatolysis.

Action Potentials↗
PubMed1987

Selective reinnervation of distal motor stumps by peripheral motor axons.

Random matching of regenerating axons with Schwann tubes in the distal nerve stump is thought to contribute to the often poor results of peripheral nerve repair. Motor axons would be led to sensory end organs and sensory axons to motor end plates; both would remain functionless. However, the ability of regenerating axons to differentiate between sensory and motor environments has not been adequately examined. The experiments reported here evaluated the behavior of regenerating motor axons when given equal access to distal sensory and motor nerve stumps across an unstructured gap. "Y"-shape silicon chambers were implanted within the rat femoral nerve with the proximal motor branch as axon source in the base of the Y. The distal sensory and motor branches served as targets in the branches of the Y, and were placed 2 or 5 mm from the axon source. After 2 months for axon regeneration, horseradish peroxidase was used to label the motoneurons projecting axons into either the motor or the sensory stump. Equal numbers of motoneurons were labeled from the sensory and motor stumps at 2 mm, but significantly more motoneurons were labeled from the motor stump at 5 mm. (P = 0.016). This finding is consistent with selective reinnervation of the motor stump. Augmentation of this phenomenon to produce specific reunion of individual motor axons could dramatically improve the results of nerve suture.

Animals↗
PubMed1978

Abnormalities of the sciatic nerves of dystrophic mice with reference to the large U-axons.

A statistical study using regression analysis was used to evaluate the density of axonal organelles in dystrophic peripheral nerves. The slope of the density of neurotubules (NT) in myelinated (M-) axons was different from that in small unmyelinated (U-) axons. The slope of the density of NT in large U-axons (larger than 1.5 micron in diameter) was similar to that of the M-axons in both the dystrophic and control mice. There was a higher density of NT in the dystrophic M-axons than in the controls in the anterior, posterior and mixed nerves of the sciatic nerve. There was also a higher density of NT in the dystrophic small U-axons than in the controls. There was a higher density of neurofilaments (NF) of M-axons in the dystrophic mice than in the controls. On the contrary, the NF of small U-axons were lower in density in the dystrophic mice. These results were different from our previous reports, which were observed in the distal part, depending on when the groups of U-axons were divided (Okada, Mizuhira and Nakamura 1976a).

Animals↗
PubMed1992

Increase in diameter of the axonal initial segment is an early change in amyotrophic lateral sclerosis.

We measured the diameter of the most distal portion of the axonal initial segment, the neuronal size of anterior horn cells, and the length of the axon hillock plus the initial segment (AH+IS) in the lumbar spinal cord in motor neuron disease. Three patients with amyotrophic lateral sclerosis (ALS) and one with lower motor neuron disease (LMND) were compared with 11 controls. Serial plastic sections stained with toluidine blue and electron micrographs were studied. A total of 214 axons directly emanating from the somata (n = 207) and the primary dendrites (n = 7) were observed in the patients. Approximately 19% of the proximal myelinated axons (24 axons out of 155 in ALS, and 17 axons out of 59 in LMND) were swollen at the first internode, and most of the swellings extended to the middle portion of the initial segment. Electron microscopy showed that the swellings of the proximal axons (the initial segment and the first internode) directly connected with their somata consisted mainly of accumulations of 10-nm neurofilaments. The average diameter of the most distal initial segment was markedly larger in ALS (n = 155) (P less than 0.0001) and LMND (n = 59) (P less than 0.0001) than in the controls (n = 258). Moreover, the average diameter of the most distal portion of even normal-appearing initial segments of the non-swollen axons was larger in ALS (n = 131) (P less than 0.0001) than in the controls. The perikarya and axon hillocks connected with the normal-appearing and swollen proximal axons and their dendrites almost always appeared normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyotrophic Lateral Sclerosis↗
PubMed1986

The time course of the changes in axon number of both oculomotor nerves in normal and unilaterally enucleated Xenopus laevis.

UNLABELLED: In this paper we analyze long-term changes, extending into adulthood, of the number of axons in the oculomotor nerve of Xenopus laevis. We counted the number of axons in that nerve in normal control (nor) animals, and on the operated (ipsilateral, ip) and contralateral (co) sides of enucleated animals at premetamorphosis, metamorphic climax, juvenile (3 and 7 months) and adult (16.5 months) stages. The experimental animals had had one of their ocular primordia removed at hatching. In the nor-nerves there is a loss of 23% of the axons between premetamorphosis and climax, then a further drop of 35% by the 3-month stage, followed by a gain of 39% on reaching adulthood. At premetamorphosis the ip-nerves already contain less than the normal number of axons, which is reduced a further 73% by 3 months; there is no subsequent increase in adulthood. The co-nerves lose no axons from premetamorphosis to climax; they therefore have 30% more axons than normals; this excess is kept until 7 months; from then to sexual maturity the increase is only 11%. CONCLUSIONS: (1) unilateral target removal affects also the nerve innervating the contralateral target: the increased loss of axons on the operated side is accompanied by reduced loss on the other; (2) the contralateral side displays for some time an excess of axons compared to normal, but this is finally cancelled out by the addition of many axons in the adult nor animals; (3) adjustment of axon number is not restrained to embryonic stages but continues at least until sexual maturation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Transient pattern of exuberant projections of olfactory axons during development in the rat.

The purpose of our study was twofold: (1) to trace the development of the olfactory axons from early embryonic stages until the mature pattern of connectivity and (2) to determine whether a transient penetration of them exists beyond the olfactory glomeruli. Two techniques were employed: DiI applied in the olfactory epithelium after aldehyde fixation, and olfactory marker protein (OMP) immunostaining. At E13 and E14 olfactory axons were observed spreading over the telencephalic vesicle and entering deeply into the prospective olfactory bulb, extending near the ventricular zone. Growth cones were seen at the end of these axons. At E15, the bundles of olfactory axons form a network, in which axons, growth cones and cells were seen. Some of these axons entered the olfactory bulb. Using OMP immunostaining olfactory axons were observed along the external plexiform layer, the mitral cell layer and in the granular layer from E19 to P6. At P9 some OMP immunoreactive axons were observed in the external plexiform layer. No OMP immunostained axons could be observed outside the glomeruli at P10. Our conclusions are that a transient immature pattern of early invasion over the telencephalic vesicle and of the olfactory bulb by olfactory axons occurs in the olfactory system. By the second postnatal week the glomerular layer reaches its mature configuration, and no olfactory fibers are seen outside the glomerular layer.

Animals↗
PubMed1986

Partial depletion of neuropeptide Y from noradrenergic perivascular and cardiac axons by 6-hydroxydopamine and reserpine.

The effects of 6-hydroxydopamine (6-OHDA) and reserpine on the storage of neuropeptide Y (NPY) in noradrenergic cardiovascular nerves were examined with both immunohistochemistry and radioimmunoassay (RIA). Immunohistochemical double-labelling techniques demonstrated that NPY was located only in noradrenergic axons in the guinea-pig carotid artery, mitral valve, thoracic inferior vena cava, thoracic aorta, superior mesenteric artery and small saphenous vein. Treatment with 6-OHDA in vivo eliminated noradrenergic, NPY-containing axon terminals from all tissues, but preterminal axons were still prominent in the superior mesenteric artery. The greatest depletion of NPY detected by RIA after 6-OHDA treatment was found in tissues with a predominance of terminal noradrenergic axons, such as the small saphenous vein, whereas NPY accumulating in preterminal axons masked the loss of NPY from terminal axons in the superior mesenteric artery. After treatment with doses of reserpine that led to a rapid depletion of noradrenaline (NA) from perivascular nerves, NPY was still detected histochemically at all times although levels sometimes appeared to be reduced. RIA demonstrated that the partial depletion of NPY after reserpine consisted of a rapid phase seen in the vena cava and saphenous vein after the highest doses, and a slower phase of NPY depletion from all tissues after all doses of reserpine. The greatest depletion of NPY from terminal axons by reserpine (in small saphenous vein) was 85-90%. These results demonstrate that some NPY can be stored in noradrenergic perivascular axons in the absence of noradrenaline, but that partial depletion of NPY from axon terminals results when NA stores are depleted by reserpine. The variation in extent of NPY depletion between tissues after drug treatments can be explained by variation in the ratio of preterminal to terminal axons.

Animals↗
PubMed1996

Fixed-diameter polyethylene cuffs applied to the rat sciatic nerve induce a painful neuropathy: ultrastructural morphometric analysis of axonal alterations.

Polyethylene cuffs of varying inner diameters were applied to the rat sciatic or sural nerve with the aim of inducing a standardized nerve injury, as assessed by morphometric analyses of fiber-size spectrum alterations, associated with behavioral manifestations of neuropathic pain. The temporal sequence of axonal degeneration and regeneration was examined in parallel with behavioral analyses of pain initiation and recovery over a 6-week postoperative (PO) period. Cuffs of 0.028-0.030" inner diameter loosely enclosed sciatic nerves of young rats and elicited relatively uniform axonal degeneration and 'pain'. Large myelinated axons underwent an early and sustained numerical depletion. Both the thinly myelinated and unmyelinated axon populations were initially diminished, but later rose to levels significantly greater than control values, likely the result of: (1) demyelination, (2) early stages of remyelination, (3) regenerative sprouting, and/or (4) collateral sprouting of undamaged unmyelinated axons. Pathological alterations of the injured nerve included edematous swelling, hypertrophy of the perineurial sheath, infiltration of fibroblasts and collagen into the intraneurial compartment, increasing interaxonal space and decreasing order and density of axonal packing. Animals displayed maximal pain-related behaviors, including gait and postural asymmetries and hypersensitivity to mechanical compression and cold, during the 2nd week PO and had largely recovered by approximately 4 weeks PO. Consistent behavioral manifestations of pain were achieved over a wide range of fiber spectrum alteration; however, with the largest cuffs or 'bracelets' used in this study, a substantial axonal fiber spectrum change was produced without inducing pain-related behavior, suggesting that decrement in the number of myelinated axons was not always sufficient to elicit pain. Similar morphometric and pathological results were achieved with sural neuropathy after 0.010" ID cuffs and 14 days PO survival. Considering the lack of correlation between axonal alterations and pain, modification in the local intraneurial microenvironment at the site of injury may be a key component of peripheral pain mechanisms; these include changes in the biochemical milieu, increased intraneurial pressure, and altered nociceptor sensitivity or impulse propagation in the relatively intact unmyelinated axon population.

Animals↗
PubMed1989

Neurofilament elongation into regenerating facial nerve axons.

Immunocytochemistry was used to show that neurofilaments advance into regenerating facial nerve axons at 2.5 mm/day, which is less than the rate of axonal elongation (4.3 mm/day), measured from the transport of radiolabeled protein into the axons. Thus, the distal region of the newly-regenerated axons is deficient in neurofilaments, and this was confirmed by electron microscopy. These neurofilament-free regenerating axons could also be detected by immunocytochemistry using antibody to protein B50 (GAP43), a component of growth-cones. Immunoblots of nerve segments, incubated with monoclonal antibodies against the three neurofilament proteins, showed that all three proteins were present in the neurofilaments elongating into the regenerating axons, and confirmed the more distal extensions of B50 immunoreactivity. These results show that neurofilament immunocytochemistry underestimates the extent of axonal regeneration, and it is suggested that this technique should be employed with caution in regeneration studies. When the facial nerve received a conditioning lesion 7 days prior to a test lesion, axonal regeneration rate increased to 6.0 mm/day, and there was a proportional increase in neurofilament elongation rate to 4.4 mm/day. This occurred in spite of the reduction in cell body neurofilament protein synthesis induced by the lesions. It is concluded that the rate of neurofilament extension into regenerating axons is not governed by cell body synthesis but by local interactions with other cytoskeletal materials which support the increased regeneration rate of conditioned axons.

Animals↗
PubMed1991

The organization of serotonergic projections to cerebral cortex in primates: regional distribution of axon terminals.

Serotonergic axons are widely distributed in the primate forebrain and represent the most abundant ascending projection from the reticular formation. Immunocytochemical methods have been utilized to examine the density, laminar distribution and morphology of serotonergic axons in both primary projection (motor, somatosensory) and association areas (dorsolateral prefrontal, area 5) as well as in the hippocampus and in cingulate cortex of rhesus and cynomolgus macaques. Serotonergic axons are present in all areas of cortex examined, and all cortical layers receive serotonergic afferents. However, the intracortical distribution of serotonergic axon terminals is not uniform; rather, different regions of cortex exhibit dissimilarities in both the density and laminar distribution of serotonergic axons. Thus, there are local patterns of serotonin innervation that are characteristic of each cortical area. Highly diverse patterns of serotonin innervation are found in heterotypical areas of cortex; more subtle variations are present among homotypical areas. Two morphologic types of serotonergic axon terminals, fine and beaded, are present in all cortical areas, and they typically exhibit different laminar distributions: in most areas of neocortex, beaded axons predominate in layer I while fine axons predominate in layers II-VI. However, exceptions to this pattern were observed in primary visual cortex and in the hippocampal formation. The distinctive local patterns of serotonin innervation observed in this study indicate that raphe-cortical projections are likely to have differential influences on particular cytoarchitectonic areas of cerebral cortex in the primate. Moreover, the discrete laminar distribution of serotonin axons suggests that serotonergic projections selectively innervate particular neuronal elements in cerebral cortex. The present findings suggest that the two classes of serotonergic axons, fine and beaded, which have different patterns of termination, affect different sets of cortical neurons. In addition, these two serotonergic projections may be associated with different sets of serotonergic receptors and thus produce selective effects on cortical function.

Afferent Pathways↗