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PubMed2000

Evidence that Wallerian degeneration and localized axon degeneration induced by local neurotrophin deprivation do not involve caspases.

The selective degeneration of an axon, without the death of the parent neuron, can occur in response to injury, in a variety of metabolic, toxic, and inflammatory disorders, and during normal development. Recent evidence suggests that some forms of axon degeneration involve an active and regulated program of self-destruction rather than a passive "wasting away" and in this respect and others resemble apoptosis. Here we investigate whether selective axon degeneration depends on some of the molecular machinery that mediates apoptosis, namely, the caspase family of cysteine proteases. We focus on two models of selective axon degeneration: Wallerian degeneration of transected axons and localized axon degeneration induced by local deprivation of neurotrophin. We show that caspase-3 is not activated in the axon during either form of degeneration, although it is activated in the dying cell body of the same neurons. Moreover, caspase inhibitors do not inhibit or retard either form of axon degeneration, although they inhibit apoptosis of the same neurons. Finally, we cannot detect cleaved substrates of caspase-3 and its close relatives immunocytochemically or caspase activity biochemically in axons undergoing Wallerian degeneration. Our results suggest that a neuron contains at least two molecularly distinct self-destruction programs, one for caspase-dependent apoptosis and another for selective axon degeneration.

Animals↗

PubMed2000

Growth cones are not required for initial establishment of polarity or differential axon branch growth in cultured hippocampal neurons.

Hippocampal neurons developing in culture exhibit two types of differential, seemingly competitive, process outgrowth in the absence of external cues. During the initial acquisition of polarity, one of several equivalent undifferentiated minor neurites preferentially grows to become the axon. Once the axon has formed, it typically branches, and the branches grow differentially rather than concurrently. In axons with only two branches, growth alternates between branches. In both axon establishment and branch growth alternation, growth among sibling processes or branches must be differentially regulated. We found that elaborate and dynamic growth cones were associated with growth, whereas diminished growth cones were associated with nongrowing processes or branches. To test whether growth cones were necessary for differential growth, growth cone motility was eliminated by application of cytochalasin E. Although cytochalasin treatment before axon formation yielded longer processes overall, a similar percentage of both treated and untreated neurons had one process that grew more rapidly and became much longer than its sibling processes. Immunostaining to visualize dephospho-tau, an axonal marker, demonstrated that these single dominant processes were axons. Axons that formed in cytochalasin were thicker and showed more intense anti-tubulin staining than their sibling processes. Branched axons deprived of growth cones retained a pattern of differential growth and often included alternation. These results indicate that neither formation of a single axon nor differential growth of branches are dependent on growth cone motility and suggest that the neuron can regulate neurite elongation at sites other than at the growth cone.

Animals↗

PubMed2001

Neurotrophins BDNF and NT-3 promote axonal re-entry into the distal host spinal cord through Schwann cell-seeded mini-channels.

To promote axonal regeneration in the injured adult spinal cord, a two-phase repair strategy was employed to (i) bridge a spinal cord hemilesion cavity with a grafted Schwann cell (SC)-seeded mini-channel, and (ii) promote axonal re-entry into the distal cord by infusing two neurotrophins, BDNF and/or NT-3, directly into the distal cord parenchyma. Here we report that infusion of two neurotrophins, delivered alone or in combination, effectively promotes axonal outgrowth from SC-seeded mini-channels into the distal host spinal cord. When an anterogradely transported marker, PHA-L or BDA, was injected into the spinal cord 3 mm rostral to the graft, a large number of axons was observed to regenerate from the SC graft into the distal cord in neurotrophin-treated groups. A subpopulation of these axons was found to grow up to 6 mm within the distal spinal cord. These axons, which were confined mainly within the grey matter, arborized and formed structures which resemble terminal boutons. In channels containing no SCs, the infusion of neurotrophins did not promote axonal ingrowth from the proximal cord stump. In cases which received SC grafts but no neurotrophin infusion, axonal re-entry into the distal cord was limited. Thus, the present study demonstrates that regenerating axons not only cross a lesion site when a permissive cellular bridge is provided but also penetrate into the distal host spinal cord and elongate for a distance of several cord segments after the infusion of two neurotrophins. The latter event is prerequisite for establishment of appropriate connections between regenerating axons and target neurons and thus, functional recovery.

Animals↗

PubMed2001

Evaluation of distal and proximal axonal degeneration in patients with carpal tunnel syndrome.

In patients with carpal tunnel syndrome, varying degrees of demyelination and axonal degeneration occur in the median nerve. Only a few studies have examined axonal degeneration produced at proximal to the lesion. In this study proximal axonal degeneration was evaluated and compared with other parameters. In 40 consecutive CTS patient hands, distal latency (DL), compound muscle action potential amplitude (CMAP) and motor conduction velocity (MCV) were analyzed by conventional motor nerve conduction studies. Intrafascicular compound nerve action potential amplitude (N-CNAP) at the elbow after wrist simulation and its nerve conduction velocity (NCV) between wrist and elbow were also analyzed. The negative correlation of DL with CMAP was statistically significant (r = 0.577, p < 0.001). CMAP was correlated with either MCV (r = 0.537, p < 0.001) or N-CMAP (r = 0.710, p < 0.001). A significant correlation of MCV with NCV (r = 0.517, p < 0.001) was also indicated. There were no any other significant correlation among the parameters. In CTS the degree of demyelination and axonal degeneration influence the prognosis for nerve recovery after decompressive surgery. DL is mainly influenced by demyelination that results in conduction block and slowing at the carpal tunnel. CMAP and N-CNAP indicate the degree of axonal degeneration at distal and proximal to the compression site. As in electrophysiologic evaluation of mononeuropathies, proximal axonal degeneration is best assessed by both stimulation and recording electrode locationing proximal to the lesion. Recording of intrafascicular nerve action potential was a little invasive method, but it provided important informations. The negative correlation between DL and CMAP implies that distal axonal degeneration can occur in proportion to the conduction disturbance. Moreover, N-CNAP had a higher correlation with CMAP. The greater the distal axonal degeneration, the more the proximal axonal degeneration. Conduction velocity represents the velocity of the fastest conduction fiber, not the degree of axonal degeneration.

Action Potentials↗

PubMed2001

Axon branching requires interactions between dynamic microtubules and actin filaments.

Cortical neurons innervate many of their targets by collateral axon branching, which requires local reorganization of the cytoskeleton. We coinjected cortical neurons with fluorescently labeled tubulin and phalloidin and used fluorescence time-lapse imaging to analyze interactions between microtubules and actin filaments (F-actin) in cortical growth cones and axons undergoing branching. In growth cones and at axon branch points, splaying of looped or bundled microtubules is accompanied by focal accumulation of F-actin. Dynamic microtubules colocalize with F-actin in transition regions of growth cones and at axon branch points. In contrast, F-actin is excluded from the central region of the growth cone and the axon shaft, which contains stable microtubules. Interactions between dynamic microtubules and dynamic actin filaments involve their coordinated polymerization and depolymerization. Application of drugs that attenuate either microtubule or F-actin dynamics also inhibits polymerization of the other cytoskeletal element. Importantly, inhibition of microtubule or F-actin dynamics prevents axon branching but not axon elongation. However, these treatments do cause undirected axon outgrowth. These results suggest that interactions between dynamic microtubules and actin filaments are required for axon branching and directed axon outgrowth.

Actin Cytoskeleton↗

PubMed2003

The L1 cell adhesion molecule is essential for topographic mapping of retinal axons.

The retinocollicular projection is a preferred axon guidance pathway for investigating molecular mechanisms of synaptic targeting in the mammalian CNS. Here we identify a previously unrecognized role of the L1 cell adhesion molecule in topographic mapping of retinal ganglion cell (RGC) axons to their targets in the mouse superior colliculus (SC). L1 was transiently expressed on RGC axons during axon growth and targeting. DiI labeling of retinal axons revealed that temporal axons of L1-minus mice bypassed correct target locations in the anterior SC, forming termination zones at incorrect posterior sites, which were often skewed along the mediolateral axis. During development of the retinotopic map L1-minus temporal axons extended across the anteroposterior axis of the SC like wild-type axons but failed to arborize at normal anterior target sites. L1-minus RGC axons exhibited normal crossing at the optic chiasm and fasciculation of the optic nerve. Results suggest that retinal axons require the function of L1 in addition to repellent EphA guidance receptors to achieve proper topographic mapping.

Animals↗

PubMed2003

GABAergic control of action potential propagation along axonal branches of mammalian sensory neurons.

The main axons of mammalian sensory neurons are usually viewed as passive transmitters of sensory information. However, the spindle afferents of jaw-closing muscles behave as if action potential traffic along their central axons is phasically regulated during rhythmic jaw movements. In this paper, we used brainstem slices containing the cell bodies, stem axons, and central axons of these sensory afferents to show that GABA applied to the descending central (caudal) axon often abolished antidromic action potentials that were elicited by electrical stimulation of the tract containing the caudal axons of the recorded cells. This effect of GABA was most often not associated with a change in membrane potential of the soma and was still present in a calcium-free medium. It was mimicked by local applications of muscimol on the axons and was blocked by bath applications of picrotoxin, suggesting activation of GABA(A) receptors located on the descending axon. Antidromic action potentials could also be blocked by electrical stimulation of local interneurons, and this effect was prevented by bath application of picrotoxin, suggesting that it results from the activation of GABA(A) receptors after the release of endogenous GABA. We suggest that blockage is caused mainly by shunting within the caudal axon and that motor command circuits use this mechanism to disconnect the rostral and caudal compartments of the central axon, which allows the two parts of the neuron to perform different functions during movement.

Action Potentials↗

PubMed2002

Morphometry of axons in optic nerves of Siamese's twins.

PURPOSE: To observe the development of optic nerve, we examined four optic nerves from Siameses Twins by absolute counts of axons. METHODS: Mean axon diameter, mean axon density, totally axonal population and optic nerve area were noted for each optic nerve. The mean axon diameter and the mean axon density were compared between paraxial (inner sectors) and cortical(outer sectors) areas of the nerves. RESULTS: More myelinated axons were seen in the inner sectors as compared to the outer sectors (average 11 axons/1000 microm2 in inner sectors and 34 axons/1000 microm2 in outer sectors (P = 0.036). The myelinated fibers were also smaller (63 microns) in the outer sectors as compared to the inner sectors (72 microns) (P = 0.001). The average cross sectors area for the four 40 week stage optical nerves of Siamese Twins was 3.32 x 103 as compared to 1 million axons for 32-week-old normals. CONCLUSION: Our finding of fewer axonal number and small myelinated fibers in the Siamese Twins suggests hypoplasia. Myelination was more abnormal in the paraxial optic nerve than that in the peripheral sectors, suggesting anomalous development of optic nerve peripherally and delayed developnent centrally. Axonal density is higher in inner sectors than that in outer sectors, suggesting delayed development of the outer nerve sector.

Anthropometry↗

PubMed2005

Microscale surgery on single axons.

OBJECTIVE: The lack of meaningful axon regeneration after central nervous system damage and poor functional recovery after serious peripheral nervous system nerve injuries have been long-standing problems of substantial interest to both neurosurgeons and neurobiologists. As an alternative to strategies that seek to promote the regeneration of adult axons, our research group has taken advantage of advances in microtechnology to develop a paradigm of direct axon repair involving the substitution of damaged axon regions with healthy segments from donor axons. METHODS: This repair methodology uses a novel combination of microtechnology, electrokinetic axon manipulation, and the well-established biological principle of cell fusion. These three fields of research have been integrated in a multidisciplinary approach to develop a solution for a significant clinical problem that currently has no specific treatment. RESULTS: The findings reported here provide some initial proof of principle for the core technologies we intend to use for axon repair. Functional recovery from nerve damage of course is clinically challenging, and many obstacles would need to be overcome before such axon repair procedures can be contemplated for therapeutic use. We identify some of the clinical issues that must be addressed for microtechnology-assisted axon repair to transition from the realm of research into actual surgical settings. CONCLUSION: It is hoped that each advance in axon repair technology will spur additional research to provide us with a comprehensive understanding on how best to pursue neurosurgical intervention at the microscale.

Animals↗

PubMed1991

Effects of axotomy on the cholinesterase and carbonic anhydrase activities of axons in the proximal and distal stumps of rabbit sciatic nerves: a temporal study.

The temporal changes in transected sciatic nerves of rabbits were studied using recently developed histochemical techniques for discriminating between sensory and motor axons. A segment of the nerve was removed to inhibit spontaneous regeneration across the gap. Staining characteristics of the proximal and distal nerve stumps were studied at 1, 2, 3, 4, 9, and 35 days following axotomy and compared with control sciatic nerves. In the control and test nerves, subpopulations of myelinated sensory axons were identified histochemically by carbonic anhydrase (CA) staining, and a subset of alpha motor axons were visualized by cholinesterase (CE) staining. Axon staining patterns were reciprocal; i.e., sensory axons were CA-positive and CE-negative, whereas motor axons were CE-positive and CA-negative. Histochemical activities persisted at day 35 after axotomy in the proximal stump and until day 9 after axotomy in the distal stump. This implies that these techniques may aid in both immediate and delayed primary nerve repair. With time, there is buildup of scar tissue adding to the proximal and distal stumps. Therefore, sections for demonstrating sensory and motor axons must be taken progressively further back from the nerve stump ends. Histochemical axon typing indicated that sensory axons regenerated earlier and to a greater degree than motor axons in the developing neuroma. Use of both the carbonic anhydrase and cholinesterase staining methods is more accurate than either technique alone as an adjunct for examining normal and injured peripheral nerves.

Animals↗

PubMed1991

The monoclonal antibody E587 recognizes growing (new and regenerating) retinal axons in the goldfish retinotectal pathway.

E587 is a new monoclonal antibody against a 200 kDa cell-surface glycoprotein in the fish retinotectal pathway. The E587 antigen probably belongs to the class of cell adhesion molecules, and more specifically, to the family of L1-like molecules. The immunopurified protein is recognized by the antibody against the HNK1/L2 sugar epitope (associated with most cell adhesion molecules) and by a polyclonal antiserum against chick G4, which is related to the cell adhesion molecule L1 in mouse. Moreover the NH2-terminal sequence of E587 shows similarity with L1 and Ng-CAM. The E587 immunostaining pattern in the fish retinotectal pathway suggests that the E587 antigen is a growth-associated molecule on fish retinal axons. In fish embryos, all retinal axons are labeled. In adult fish, however, only the young axons from newly added ganglion cells carry E587 staining. After optic nerve transection (ONS) and retinal axonal regeneration, all axons reexpress the E587 antigen into their terminal processes in the tectal retinorecipient layers. The reexpression of the E587 antigen is temporally regulated, and E587 immunoreactivity declines by 7 months and disappears at 12 months after ONS. We hypothesize that the E587 antigen may mediate axon-axon associations. In its restricted appearance on young axons in normal adult fish, it may contribute to the selective fasciculation of the newest axons with young axons and thus participate in the creation of the age-related fiber organization in the fish optic nerve.

Animals↗

PubMed1991

Ribosomes in myelinated axons of the rabbit spinal ganglion neurons.

To clarify whether, in the mature pseudounipolar neurons of mammalian spinal ganglia, a small number of ribosomes are dispersed in many or possibly all axons beyond their initial segments or if a large number of ribosomes is confined to a few axons only, three series of consecutive sections (of 449, 702 and 865 sections respectively) were cut from the sensory portion of rabbit spinal nerves very close to the ganglion. In these series of sections, portions (from 4.5 to 69.2 microns long) of 198 myelinated axons were examined. Clusters of ribosomes were detected only in three of the 198 axons examined, where they were present in 73-99% of the sections. In the nerves we studied ribosomes are not sparsely dispersed in many or possibly all axons, but are confined to a few axons only, where they are present in a high percentage of sections. Both size and density of axonal ribosomes were identical to those of adjacent Schwann cell ribosomes and clearly different from those of glycogen particles. The great majority of axonal ribosomes were localized within the subaxolemmal band of axoplasm whereas their frequency was lowest within the axonal core. The possible origin of the ribosomes found within the three axons is briefly discussed.

Animals↗

PubMedDate not supplied

The response of noradrenergic axons to systemically administered DSP-4 in the rat: an immunohistochemical study using antibodies to noradrenaline and dopamine-beta-hydroxylase.

The response of noradrenaline (NA) axons to the effects of systemic injections of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) was studied in the rat brain. Antibodies to NA and to dopamine-beta-hydroxylase (DBH) were employed to assess by immunohistochemistry the effects of DSP-4 on NA axons between 6 h and 2 weeks after drug administration. The changes in NA and DBH staining after DSP-4 treatment were restricted to brain regions innervated by the locus coeruleus. In these areas, DSP-4 induced profound loss of both NA and DBH from NA axons, but with a distinctly different time-course. While NA disappeared within hours after drug treatment, DBH staining of NA axons remained unchanged during the first 4 days after DSP-4 treatment. Thereafter, there was an abrupt loss of DBH staining which coincided with the appearance of numerous brightly stained, thick and swollen NA axons. The distribution of these fibres suggests that they represent the distal ends of preterminal NA axons. Two weeks after drug treatment, NA axons could no longer be visualized by either NA or DBH immunohistochemistry in regions affected by DSP-4. During this 2-week time-period, the staining of cell bodies in the locus coeruleus and of ascending NA axons in the dorsal bundle was unaffected. The results suggest two phases in the response of NA axons to DSP-4: an acute phase, marked by loss of transmitter, and a neurodegenerative phase, characterized by loss of DBH and structural disintegration of NA axons.

Animals↗

PubMed1989

[Ischemic axonal injury and its recovery after focal cerebral ischemia].

After focal cerebral infarction by occluding the middle cerebral artery (MCA) of the rat, the neuronal death occurred in the ipsilateral thalamic neurons, because axons of the thalamic neurons were injured by infarction and retrograde degeneration occurred in the thalamic neurons. However, cortical neurons adjacent to the infarction survived despite their axons injured by ischemia. We employed immunohistochemical staining for 200 kilodalton (kD) neurofilament (NF), in order to study those responses of cortical and thalamic neurons against axonal injury caused by focal cerebral infarction. In the sham operated rats the immunoreactivity to the anti-200 kD NF antibody was only detected in the axon but not in the cell bodies and dendrites. At 3 days after MCA occlusion, axonal swelling proximal to the site of ischemic injury was found in the caudoputamen and internal capsule of the ipsilateral side. At 7 days after occlusion, cell bodies and dendrites of the neurons in the ipsilateral cortex and thalamus were strongly stained with anti-NF antibodies. At 2 weeks after occlusion these responses disappeared in the cortex, but lasted in the thalamus. These phenomena are caused by stasis of the slow axonal transport, because the NF is transported by slow axonal transport. In the cortical neurons impairment of slow axonal transport recovered in the early phase after injury, but in the thalamic neurons the impairment prolonged up to 3 weeks after occlusion. The early recovery of axonal transport from ischemia seemed to be essential for survival of neurons after ischemic axonal injury.

Animals↗

PubMed1989

Axonal dystrophy as a consequence of long-term demyelination.

Central nervous system lesions in guinea pigs sensitized for chronic relapsing experimental allergic encephalomyelitis for between 18 and 36 months have been found to possess a small but probably significant degree of axonal involvement. Axonal identity was established by light and electron microscopy and immunocytochemistry. The axonal changes were restricted to white matter and consisted of massive (up to 95 microns) scattered axonal spheroids which displayed lateral branches and vacuoles; small groups of spheroids filled with a wide assortment of axoplasmic organelles; and deeper, more extensive collections of affected demyelinated axons and spheroids which frequently displayed abortive axonal regeneration into the Virchow-Robin space. Although accumulations of most axoplasmic organelles occurred in the spheroids and reactive axons, microtubules were relatively rare. These formations were never seen in adjacent unaffected white matter and spinal cord tissue from normal aged animals contained only the occasional spheroid. It is hypothesized that the disease process in experimental allergic encephalomyelitis may be more dynamic than previously described and that prolonged interruption in normal axon-glial relationships in chronically demyelinated (sometimes remyelinated) gliotic lesions might lead to a block in axoplasmic transport and a disruption of the axonal cytoskeleton. Although most affected axons appeared intact, some of the spheroids probably represented proximal stumps from which sprouting occurred, leading to neuroma-like formations. The implications of the findings are discussed in reference to long-term demyelination and multiple sclerosis where almost identical profiles have been documented.

Animals↗

PubMed1985

Development of the rat superior cervical ganglion: ingrowth of preganglionic axons.

The growth of sympathetic preganglionic axons has been studied in the fetal rat. Preganglionic axons first emerge from the spinal cord and enter the paravertebral chain of ganglia between days 12 and 13 of gestation (E12 to E13). By E14, hundreds of preganglionic neurons have sent axons into the sympathetic chain. Even at this age, the arrangement of the preganglionic axons conforms to the adult organization in a number of ways. As in maturity, these axons leave the spinal cord only through the ventral root of the segment in which their cell bodies reside. Furthermore, axons grow into the superior cervical ganglion only from the same set of spinal segments as supply this ganglion in maturity, and in correct segmental proportions, although there is a slight rostral-to-caudal lag along the spinal cord in the full establishment of the projection. The development of appropriate projections in this system owes little to the growth of axons along stereotyped pathways. Rather, preganglionic organization apparently reflects a more general instruction that governs the relative number of axons from each spinal segment which course rostrally or caudally within the sympathetic chain. The appropriate distribution of preganglionic axons early in development suggests that a fiber's segmental level of origin biases the axon to grow in a particular direction.

Animals↗

PubMed1987

Organization of individual afferent axons in layer IV of striate cortex in a primate.

Evidence from a number of anatomical and physiological studies shows that information is transmitted from the retina to visual cortex via physiologically and anatomically distinct populations of neurons in the lateral geniculate nucleus (LGN). In order to gain a better understanding of the functional roles of these parallel channels from the LGN to cortex in primates, individual afferent axons to layer IV of striate cortex of galagos were filled with HRP by bulk injection into the white matter underlying striate cortex. A total of 55 axons and their terminal arbors, from zones representing both the central and peripheral visual fields, were completely reconstructed through serial sections. Based upon the sublaminar distribution and the morphology of these axons, they have been categorized into 2 groups, designated type I and II axons. Evidence from both past work and the present study suggests that type I axons represent the projections from physiologically defined Y-like cells in the magnocellular layers of the LGN, while type II axons represent the projections from X-like cells in the parvocellular LGN layers. Our results show that type I (presumed Y-like) arbors occupy relatively more cortical space within their main terminal sublayer (IV alpha) than is the case for the type II (presumed X-like) arbors which ramify primarily in layer IV beta. In addition, type I arbors have larger parent axons, fewer boutons along a restricted length of axon, and a greater tendency to branch in layer VI than type II arbors. Finally, both axon types are larger in the area of cortex representing central vision than in the area representing peripheral vision. These morphological characteristics suggest that the physiological differences between magnocellular and parvocellular geniculate cells may be amplified in cortex by differences in the organization of their terminal arbors. Further, within each afferent population, the terminal organization of axons reflects their visuotopic relationships in striate cortex. Comparison of these findings with data from cats and monkeys supports the idea that the relationship between the size of the terminal arbors of LGN X-like or parvocellular cells and the size of the cortical spatial subunit varies with differences in visual acuity across species; for LGN Y-like (or magnocellular) cells this relationship remains constant.

Afferent Pathways↗

PubMed1987

Comparison of electrical responses of terminals, axons, and somata of a peptidergic neurosecretory system.

Spontaneous and evoked electrical activity was recorded intracellularly from somata, axons, and terminal dilatations of an isolated peptidergic neurosecretory system, the X-organ-sinus gland, of the crabs Cardisoma carnifex and Podophthalmus vigil in order to compare their electrical characteristics. Spontaneous impulse activity was present in most penetrations and included irregular and pacemaker-like firing, as well as patterned activity (bursting). Extracellular recording showed that spontaneous impulses and bursting originate in a proximal region of the axon tract. Somata vary from being electrically nonresponsive to having overshooting impulses with a relatively slow rate of rise. Overshooting impulses were consistently recorded from axons and terminals. Regional differences include (1) a longer action potential duration in terminals, (2) ability of axons and terminals but not somata to sustain repetitive firing, (3) presence of depolarizing afterpotentials in axons but of hyperpolarizing afterpotentials in somata and terminals, and (4) occurrence of impulse broadening during repetitive firing in some terminals but not in axons or somata. Somata and terminals sustained reduced and slowed, but regenerative impulses in nominally Na-free saline and showed alterations of waveform in nominally Ca-free salines, while axons showed no regenerative responses in Na-free saline and no change of impulse form in Ca-free saline. Terminal responses in the presence of tetraethylammonium chloride (TEA) (50 mM) or Ba (50 mM) exhibited long depolarized plateaus, while impulses of somata were much less prolonged. Bursts often took the form of impulses superimposed on a depolarized plateau. Bursts could be evoked by single stimuli applied to the axon tract but not by current passed intracellularly. After addition of TTX, axon tract stimulation evoked plateaus without superimposed impulses. Terminals exhibit specialization of their electrical responses by comparison to axons and somata in having long-duration action potentials attributable to participation of Ca, capability of sustained firing, impulse broadening, and channels supporting sustained inward currents, all of which might enhance the admission of Ca for initiation of peptide secretion.

Action Potentials↗