Catecholamine varicosities in cat dorsal root ganglion and spinal ventral roots

Convergence upon reticulospinal neurons which mediate disynaptic, contralateral pyramidal EPSPs to neck motoneurons has been examined in cats with contralateral pyramidal transection at the obex. Conditioning stimuli in the contralateral tectum and ipsilateral mesencephalic tegmentum produced monosynaptic facilitation of the disynaptic pyramidal EPSP, whereas facilitation evoked from the ipsilateral pyramid showed a disynaptic time course. These results show that contralateral pyramidal, tectal and ipsilateral tegmental fibers converge onto common reticulospinal neurons which have direct excitatory connections with neck motoneurons.     

Opioid regulation of intracellular free calcium in cultured mouse dorsal root ganglion neurons

Opioid agonists induced an increase in the intracellular free calcium concentration ([Ca²⁺]_i) or an inhibition of K⁺ (25 mM)-stimulated increase in [Ca²⁺]_i in different subsets of mouse dorsal root ganglion (DRG) neurons. The total neuronal population was grouped into three classes according to somatic diameter and defined as small (<16 μm), intermediate (16–25 μm), or large (>25 μm) neurons. Substance P-like immunoreactivity was detected mainly in the small and intermediate neurons. The δ, κ, and μ opioid receptor agonists [D-Ser², Leu⁵]enkephalin-Thr (DSLET), U69593, and [D-Ala², MePhe⁴, Gly-ol⁵]enkephalin (DAMGO) each induced a transient increase in [Ca²⁺]_i in a small fraction (<30%) of neurons. The increases in [Ca²⁺]_i were blocked by the opioid antagonist naloxone. The dihydropyridine-sensitive calcium channel blocker nifedipine also blocked the increase in [Ca²⁺]_i induced by 1 μM DSLET. The rank order of potency (percentage of cells responding to each opioid agonist) was DSLET > U69593 > DAMGO. The opioid-induced increase in [Ca²⁺]_i was observed mainly in large neurons, with a low incidence in small and intermediate neurons. Opioid agonists also caused inhibition of K⁺-stimulated increases in [Ca²⁺]_i, which were blocked by naloxone (1 μM). Inhibition of the K⁺-stimulated increase by 1 μM DSLET or U69593 was greater in small and intermediate neurons than in large neurons. © 1996 Wiley-Liss, Inc.     

Rhythmic antidromic discharges of single primary afferents recorded in cut dorsal root filaments during locomotion in the cat

Extracellular recordings were made from 52 units in perifused 300 microns thick slices of rat hypothalamus taken parallel to the ventricular surface of the arcuate nucleus and kept at 37 degrees C in an organ bath. Addition of 8 nM adrenocorticotrophic hormone (ACTH) to the perfusate reversibly and rapidly inhibited 15 of the 38 units found within 300 microns of the ventricular surface (in the arcuate nucleus), and there were no comparable excitations. A prompt and reversible excitation of 6/14 units by ACTH was found when records were made from units found 300-600 microns lateral to the ventricle in the lateral arcuate region. It is suggested that ACTH may be an inhibitory transmitter in the arcuate nucleus and that this action may be an inhibition of ACTH-containing neurons.     

育亨宾对慢性压迫背根节神经元自发放电的兴奋作用

采用离体灌流背根节 (dorsalrootganglion ,DRG)和单纤维记录神经元自发放电的方法 ,观察到育亨宾对受损DRG神经元的自发放电呈现兴奋作用 ,并初步研究了其发生机制。用外源性育亨宾 (10 μmol/L)灌流损伤的DRG时 ,在 2 2个有自发放电的DRG神经元中 ,有 18个神经元产生明显反应。育亨宾对损伤神经元自发放电的兴奋作用 ,可被α1 肾上腺素能受体拮抗剂哌唑嗪 (5 μmol/L)明显阻断。用 6 羟多巴胺化学性交感神经切断和胍乙啶耗竭交感末梢后 ,育亨宾的兴奋作用均明显减小。结果表明 :育亨宾阻断交感节后神经末梢上的α2 肾上腺素能受体 ,引起去甲肾上腺素 (norepinephrine,NE)的释放 ;释放的NE作用于损伤DRG神经元上的α1 肾上腺素能受体 ,而对受损神经元自发放电呈现兴奋作用。提示交感节后神经末梢可能存在一种持续性抑制NE释放的新机制 ,这种抑制作用不依赖交感节后神经节和动作电位的存在     

The effects of convulsant doses of penicillin on primary afferents, dorsal root ganglion cells, and on ‘presynaptic’ inhibition in the spinal cord

Intracellular recordings were made from neurons in dorsal root ganglia (DRG) of rats, isolated in vitro. The depolarization of DRG cells caused by the application of gamma-aminobutyric acid (GABA) diminished reversibly when penicillin (0.08–2.0 mM) was added to the bathing fluid. The decrease of the input resistance of DRG cells measured during GABA perfusion was also depressed in the presence of penicillin, but no evidence of a shift of the reversal potential of the GABA-induced depolarization was found. Nor did penicillin (up to 10 mM) cause a change in the voltage-current function, in electrical excitability, in the inclination to repetitive firing, bursting discharge, or after discharge. In decapitate cat preparation the amplitude of the negative dorsal root potential (DRP or DR V) diminished by 0–50% after the i.v. administration of 0.5–1.0 × 10⁶I.U./kg (the convulsant dose) of penicillin. Post-tetanic depression of the DRP was aggravated by penicillin. The degree of depression of the DRP bore no relationship to the promptness of the eruption, and to the intensity, of the seizure activity induced by penicillin. The rates of rise and fall of the negative DRP (DR V) were consistently slowed, the positive DRP (DR V) reduced, and the dorsal root reflex (DRR) blocked by penicillin. Inhibitory reflex effects presumed to be presynaptic were either enhanced or unchanged, never depressed by penicillin. This was seen when inhibitory function was gauged by monosynaptic reflex amplitude, and also from the inhibition of ventral root electronic excitatory postsynaptic potentials (VR EPSPs). Possible explanations of these seemingly paradoxical findings are discussed, with arguments in favor and against each.     

Somatic and visceral primary afferents in the lower thoracic dorsal root ganglia of the cat

Anterograde transport of horseradish peroxidase (HRP) through somatic and visceral nerves was used to estimate the proportions of somatic and visceral dorsal root ganglion (DRG) cells of the lower thoracic ganglia of the cat. A concentrated solution of HRP was applied for at least 5 hours to the central end of the right greater splanchnic nerve and of the left T9-intercostal nerve of adult cats. Some animals remained under chloralose anaesthesia for the duration of the HRP transport time (up to 53 hours) whereas longer HRP application and transport times (4-5 days) were allowed in animals that recovered from barbiturate anaesthesia. Visceral DRG cells were found in approximately equal numbers in all ganglia examined (T7-T11). Population estimates were obtained for the T8 and T9 ganglia where visceral DRG cells were found to be 6.2% (T8) and 5.2% (T9) of the total cell population. In contrast, somatic DRG cells were found in large numbers in the ganglia examined (T8 and T9) where they amounted to over 90% of the cell population. Measurement of cross-sectional areas and estimates of cell diameters of the DRG cells showed greater proportions of large somatic cells (diameter greater than 40 micron) than of large visceral cells. Similar distributions of cell size were found for both somatic and visceral DRG cells with diameters less than 40 micron. These results show that the proportion of visceral afferent fibres in the dorsal roots that mediate the spinal cord projection of the splanchnic nerve is very small. Since viscerosomatic convergence in the thoracic spinal cord is very extensive, the present results suggest considerable divergence of the visceral afferent input to the central nervous system.     

The contribution of increases in extracellular potassium to primary afferent depolarization in the bullfrog spinal cord

To assess the extent to which depolarization by accumulated K+ contributes to the generation of primary afferent depolarization (PAD), the isolated bullfrog spinal cord was superfused with K+-rich Ringer solutions and the resultant dorsal root depolarizations were recorded extracellularly. Action potential blockade (with tetrodotoxin) did not reduce the K+-induced depolarization of primary afferents, indicating that the depolarization was generated locally in the region around the afferents. In this respect superfusion with K+-rich solutions adequately models the localized K+ accumulation which occurs physiologically during afferent activity. K+-induced depolarizations were decreased in the presence of 20 mM Mg2+; this effect was due to a direct decrease in the membrane response to K+ and not to blockade of K+-induced transmitter release onto primary afferents. The depolarization caused by a K+ concentration comparable to a maximum estimate of the K+ accumulating around afferent terminals following a single afferent volley was found to account for no more than about one-third of the DRP height. However, higher K+ levels, comparable to those resulting from high frequency afferent stimulation, caused large depolarizations of primary afferents, sometimes greater than the DRP amplitude. Therefore, K+-induced depolarization may contribute more significantly to PAD evoked by high frequency afferent activity.     

Patterned assembly and neurogenesis in the chick dorsal root ganglion

The birth of small‐diameter TrkA+ neurons that mediate pain and thermoreception begins ≈24 hours after the cessation of neural crest cell migration from progenitors residing in the nascent dorsal root ganglion. Although multiple geographically distinct progenitor pools have been proposed, this study is the first to comprehensively characterize the derivation of small‐diameter neurons. In the developing chick embryo we identify novel patterns in neural crest cell migration and colonization that sculpt the incipient ganglion into a postmitotic neuronal core encapsulated by a layer of proliferative progenitor cells. Furthermore, we show that this outer progenitor layer is composed of three spatially, temporally, and molecularly distinct progenitor zones, two of which give rise to distinct populations of TrkA+ neurons. J. Comp. Neurol. 518:405–422, 2010. © 2009 Wiley‐Liss, Inc.     

The development of the relationship between dorsal root afferents and motoneurons in the larval bullfrog spinal cord

The relationship of dorsal root afferents to motoneuron somata and dendrites was studied by labelling dorsal and ventral roots of the tadpole lumbar enlargement with HRP at different stages of hindlimb development. Procedures were used which allowed for sequential light and electron microscopic analysis to determine whether close appositions between labelled elements represented synaptic contacts. Lateral motor column (LMC) motoneuron dendrites grow first into the lateral funiculus, and later begin arborizing within the spinal gray, concurrent with the arrival of developing dorsal root afferent fibers. Mature-appearing synaptic contacts between dorsal root afferents and motoneuron dendrites are established first on distal dendrites, and are observed on progressively more proximal dendrites as hindlimb development proceeds. Migrating motoneurons were also labelled in some animals. Distinct dorsal and ventral migratory pathways were noted; cells migrating dorsally were contacted by developing dorsal root afferents. Migrating motoneurons were associated with radially oriented processes, and were often closely apposed to other cells. The coincident development of dorsal root projections and the motoneuron dendrites which these fibers innervate in the adult, as well as the interaction between these two systems during cell migration, suggest that these two systems may be interdependent in establishing their normal relationship during development.     

去甲肾上腺素对背根神经节神经元P物质释放的调节作用(英文)

目的观察激活或抑制α-肾上腺素受体是否影响体外培养的背根神经节(dorsal root ganglion,DRG)神经元P物质(substance P,SP)的释放。方法胎龄15天的Wistar大鼠DRG神经元培养2天后,分别用去甲肾上腺素(nora-drenaline,NA)(1×10-4mol/L)、α1-受体拮抗剂哌唑嗪(1×10-6mol/L)+NA(1×10-4mol/L)、α2-受体拮抗剂育亨宾(1×10-5mol/L)+NA(1×10-4mol/L)孵育4天。用RT-PCR法检测DRG神经元编码SP蛋白的PPTmRNA表达水平,用Western blot法检测DRG神经元SP蛋白的表达水平,用酶联免疫吸附测定法检测SP的基础释放量和辣椒素刺激后的释放量。结果 NA单独孵育显著增加了DRG神经元辣椒素刺激后的SP释放量,α1-受体拮抗剂哌唑嗪预处理可阻断NA的效应,而α2-受体拮抗剂育亨宾不产生此作用。在各种实验条件下,PPT mRNA水平、SP蛋白表达水平和SP的基础释放量没有显著性差异。结论 NA通过激活α1-受体增加了DRG神经元辣椒素刺激后的SP释放量,这一作用可能与去甲肾上腺素能的疼痛调...     

Expression and effect of sodium-potassium-chloride cotransporter on dorsal root ganglion neurons in a rat model of chronic constriction injury

Sodium-potassium-chloride cotransporter 1 (NKCC1) and potassium-chloride cotransporter 2 (KCC2) are associated with the transmission of peripheral pain.We investigated whether the increase of NKCC1 and KCC2 is associated with peripheral pain transmission in dorsal root ganglion neurons.To this aim,rats with persistent hyperalgesia were randomly divided into four groups.Rats in the control group received no treatment,and the rat sciatic nerve was only exposed in the sham group.Rats in the chronic constriction injury group were established into chronic constriction injury models by ligating sciatic nerve and rats were given bumetanide,an inhibitor of NKCC1,based on chronic constriction injury modeling in the chronic constriction injury + bumetanide group.In the experiment measuring thermal withdrawal latency,bumetanide (15 mg/kg) was intravenously administered.In the patch clamp experiment,bumetanide (10 μg/μL) and acutely isolated dorsal root ganglion neurons (on day 14) were incubated for 1 hour,or bumetanide (5 μg/μL) was intrathecally injected.The Hargreaves test was conducted to detect changes in thermal hyperalgesia in rats.We found that the thermal withdrawal latency of rats was significantly decreased on days 7,14,and 21 after model establishment.After intravenous injection of bumetanide,the reduction in thermal retraction latency caused by model establishment was significantly inhibited.Immunohistochemistry and western blot assay results revealed that the immune response and protein expression of NKCC1 in dorsal root ganglion neurons of the chronic constriction injury group increased significantly on days 7,14,and 21 after model establishment.No immune response or protein expression of KCC2 was observed in dorsal root ganglion neurons before and after model establishment.The Cl^– (chloride ion) fluorescent probe technique was used to evaluate the change of Cl^– concentration in dorsal root ganglion neurons of chronic constriction injury model rats.We found that the relative optical density of N-(ethoxycarbonylmethyl)-6-methoxyquinolinium bromide (a Cl^– fluorescent probe whose fluorescence Cenintensity decreases as Cl– concentration increases) in the dorsal root ganglion neurons of the chronic constriction injury group was significantly decreased on days 7 and 14 after model establishment.The whole-cell patch clamp technique revealed that the resting potential and action potential frequency of dorsal root ganglion neurons increased,and the threshold and rheobase of action potentials decreased in the chronic constriction injury group on day 14 after model establishment.After bumetanide administration,the above indicators were significantly suppressed.These results confirm that CCI can induce abnormal overexpression of NKCC1,thereby increasing the Cl^– concentration in dorsal root ganglion neurons;this then enhances the excitability of dorsal root ganglion neurons and ultimately promotes hyperalgesia and allodynia.In addition,bumetanide can achieve analgesic effects.All experiments were approved by the Institutional Ethics Review Board at the First Affiliated Hospital,College of Medicine,Shihezi University,China on February 22,2017 (approval No.A2017-169-01).     

Spontaneous voltage and current fluctuations in tissue cultured mouse dorsal root ganglion cells

Fetal mouse dorsal root ganglion (DRG) neurons were maintained in primary dissociated cell culture for periods of 7 days to 3 months. Intracellular recordings from these cells revealed the presence of spontaneous subthreshold potentials in 101/177 neurons studied. When measured at the resting membrane potential, these spontaneous voltage events took two forms: (a) high frequency potential fluctuations several millivolts in peak-to-peak amplitude and (b) small, discrete hyperpolarizations. Neurons exhibiting either type of event were designated as 'active' DRG cells. No spontaneous potentials were seen in DRG cells hyperpolarized to membrane voltages more negative than -64 +/- 11.5 mV (n = 5 cells). Under voltage-clamp conditions, the subthreshold potentials of active DRG cells were replaced by fluctuations in outward current. The power spectral density, S(f) of these current fluctuations was approximated by an equation of the form S(f) = (S(o)/[1 + (f/fc) alpha] where 2 less than or equal to a less than or equal to 3 and the half-power frequency fc = 11.3 +/- 3.1 Hz at 23 degrees C (n = 17 cells). The spontaneous voltage fluctuations of active DRG cells were abolished in Ca2+-free saline, and of the divalent metal cations Sr2+, Mg2+, Ba2+, Co2+ and Mn2+, only Sr2+ could substitute for Ca2+ in the maintenance of this activity. Tetraethylammonium ions (1-10 mM) reversibly blocked the spontaneous potentials, while caffeine (10 mM) increased the frequency of these events. The spontaneous voltage fluctuations were not dependent on the presence of spinal cord neurons in the culture plate, and they were also observed in cultured DRG cells derived from adult mice.     

Spontaneous dorsal root potentials arise from interneuronal activity in the isolated frog spinal cord

Spontaneous dorsal root potentials (sDRPs) were recorded from the dorsal roots of the isolated frog spinal cord using sucrose gap techniques. sDRPs were always negative (depolarizing) in sign and ranged in size from about 100 μV to 6.0 mV. The largest sDRPs were 25–40% of the amplitude of DRPs evoked by stimulation of adjacent dorsal roots. Hypoxia or accumulation of extracellular K⁺ ions did not appear responsible for the generation of this spontaneous activity since exposing the cord to unoxygenated Ringer's solution decreased sDRPs and K⁺-sensitive microelectrodes indicated that only small changes in extracellular K⁺ (approximately 0.15 mM) were produced coincidently with the largest sDRPs.Chemically-mediated synaptic transmission was found to be necessary for the production of sDRPs because the addition of Mn²⁺ or Mg²⁺ ions or tetrodotoxin to the Ringer's solution or reduction of its Na⁺ concentration blocked sDRPs, whereas application of 4-aminopyridine enhanced them.It did not seem that a direct action of GABA on afferent fiber terminals was responsible for the generation of spontaneous potentials since an increase in sDRPs was seen after: application of the GABA antagonists, bicuculline and picrotoxin; exposure to the glutamic acid decarboxylase inhibitor, semicarbazide (which significantly reduced the concentration of GABA in the cord); and lowering of the external Cl⁻ concentration. Similarly taurine is probably not significant since the taurine antagonist, TAG, increased the amount of spontaneous activity.On the other hand, (−)-baclofen, which is thought to reduce excitatory amino acid release,d,l-α-aminoadipic acid, α,-diaminopimelic acid, and 2-amino-4-phosphonobutyric acid, which are believed to be selective postsynaptic excitatory amino acid antagonists, and [d-Pro²-d-Phe⁷-d-Trp⁹]-substance P, a postsynaptic blocker of the action of substance P, markedly and reversibly reduced sDRPs.Experiments were performed on isolated cords without supraspinal or afferent input; therefore sDRPs must be generated by intraspinal structures. It would seem that interneurons are responsible because addition of mephenesin or pentobarbital — compounds which inhibit polysynaptic reflex transmission involving interneurons — reduced the production of sDRPs.sDRPs may result from the action of excitatory transmitters such asl-glutamate,l-aspartate, or substance P released by interneuronal firing in the spinal cord. Moreover, because sDRPs were increased by application of yohimbine, corynanthine and propanolol and reduced by haloperidol, such interneurons may be under descending control of adrenergic and dopaminergic fibers.     

Depolarization triggers intracellular magnesium surge in cultured dorsal root ganglion neurons

Intracellular magnesium concentration ([Mg²⁺]_i) of cultured dorsal root ganglion (DRG) neurons was measured using the magnesium indicator Mag-Fura-2/AM. [Mg²⁺]_i was 0.48±0.08 mM (mean±SEM, n=23) at rest, and it increased 3-fold by depolarization with a 60-mM K⁺ solution. The [Mg²⁺]_i increase was observed in the absence of extracellular Mg²⁺, but the increase disappeared in the absence of extracellular Ca²⁺. 50 μM cadmium or 100 μM verapamil, a Ca²⁺ channel blocker, also diminished the rise of [Mg²⁺]_i. The additional measurement of an intracellular Ca²⁺ concentration ([Ca²⁺]_i) indicated that the [Mg²⁺]_i rise requires a threshold concentration of [Ca²⁺]_i to be reached; above 60 nM. The present results indicate that depolarization induces a Ca²⁺-influx through voltage dependent Ca channels and this causes the release of Mg²⁺ from intracellular stores into the cytoplasm.     

硬膜外移植自体髓核大鼠背根神经节的非压迫性损伤

背景：最新的研究表明,髓核所致的炎性反应是导致坐骨神经痛的重要原因之一,在此过程中背根神经节可能起重要作用,但是其病理生理变化目前尚不完全清楚。目的：探讨在无机械压迫情况下,腰椎间盘髓核突出引起坐骨神经痛的发病机制。方法：10月龄雄性SD大鼠24只,随机分成实验组和对照组,每组12只。切开大鼠尾椎椎间盘,髓核呈胶冻样,取5个髓核并加入50 µL生理盐水,充分搅拌稀释成混悬液备用。实验组大鼠行硬膜外穿刺,注射混悬液到腰椎硬膜外腔制作动物模型。对照组硬膜外腔注射生理盐水。测定大鼠后肢机械刺激缩爪阈值并对疼痛相关行为和背根神经节组织形态学进行观察。结果与结论：在无机械压迫情况下,硬膜外移植自体髓核能使大鼠后肢产生明显的痛觉过敏,背根神经节会出现节细胞肿胀、核膜不清晰、核仁变淡或消失、胞浆出现空泡、尼氏小体颜色变浅分布不均匀、内膜间质增宽、充血和水肿等形态学改变。结果表明,移植自体髓核所致的炎性反应是引起大鼠背根神经节损伤和坐骨神经痛的重要原因之一。     

Spontaneous hyperpolarizations at the membrane of cultured mouse dorsal root ganglion cells

Intracellular recordings from cultured mouse dorsal root (sensory) ganglion cells revealed the presence of spontaneous hyperpolarizing potentials in over half of the cells. The potentials were resistant to tetrodotoxin and under voltage clamp were replaced by fluctuations in outward current. The power spectral density plots of these current fluctuations were predominantly of the Lorentzian type. These events may play an important role in the functioning of some sensory nerve cells.     

Isolation and age-related characterization of mouse Schwann cells from dorsal root ganglion explants in type I collagen gels

A technique for isolation of adult Schwann cells (ScC) from dorsal root ganglia (DRG) is described. Decapsulated DRG explants embedded into type I collagen gels were cultured for 3 days in serum-free medium during which ScC migrated from the explant. These explants were then grown in serum-supplemented medium to allow ScC proliferation. On day 10 the number of ScC isolated from DRG explants per mouse was about 2.5 × 10⁵, and the purity was greater than 95%. This culture system provided sufficient numbers of highly purified adult ScC in a shorter culture period (2–3 times) than other methods. We used ScC from this method to determine the age-related changes in attachment, growth, and survival of ScC cultured in serum-free medium. The attachment capacity of adult ScC on type I collagen or polylysine was similar to that of newborn ScC. However, the collagen promoted growth and survival of adult ScC but not that of neonatal ScC, indicating age-related differences of ScC properties in vitro. © 1993 Wiley-Liss, Inc.     

Synaptic connections between spinal motoneurons and dorsal root ganglion cells in the cat

Light- and electron-microscopical horseradish peroxidase (HRP) studies have been employed in conjunction with a degeneration study in order to clarify the origin and axonal passage of afferent synaptic terminals in cat dorsal root ganglia. After injection of HRP into ganglia (C3) without involvement of the ventral roots and spinal nerves, a few ipsilateral spinal ventral horn neurons (C3) were retrogradely labeled with HRP. The labeled neurons were localized in the dorsomedial and the ventromedial nuclei. Following ventral rhizotomy of C3, the afferent terminals in the ganglia (C3) anterogradely degenerated and contained accumulated and disintegrated neurofilaments, depleted, aggregated and enlarged synaptic vesicles. Subsequent to an HRP and wheat germ agglutinin (WGA)-HRP-mixture injection into the dorsal neck or suboccipital muscles, many spinal motoneurons (C3) were labeled retrogradely with an HRP mixture. On the other hand, the afferent synaptic terminals in ganglia contained the membrane-bound and electron-dense bodies which were anterogradely labeled with an HRP mixture in addition to the normal synaptic elements. The present findings strongly suggest that some spinal motoneurons send their axon collaterals to the dorsal root ganglia, in which the terminals of the axon collaterals directly synapse with the dorsal root ganglion cells.     

Direct visualization and characterization of stable microtubules from the neurites of cultured dorsal root ganglion cells

We tested the stability of microtubules (MTs) in the neurites of cultured dorsal root ganglion cells by dissolving the cytoplasmic membrane with detergent and exposing them to defined extracellular medium under observation with a video-enhanced differential interference contrast (DIC) microscope. Smooth cytoplasmic filaments visualized after membrane removal were suggested to be MTs by the preservation of all of the filaments in the presence but not in the absence of taxol. They were further confirmed to be MTs by specific immunostaining with anti-tubulin antibody. A significant number of MTs in the established neurites of 6-day-old cultures remained longer than 10 min after membrane removal while MTs in the Schwann cell processes or in the distal regions of the growth cone-bearing neurites of 3-day-old cultures disappeared within 2 min. A population of very stable MTs persisting longer than 30 min was also found specifically in the 6-day-old cultures. Association with other structures or bundling seemed to stabilize the MTs to some degree. The most stable MTs, however, were not associated with some structure along the length but were mainly anchored at points, suggesting that specific point attachments may be another important mechanism operating in MT stabilization. The present method is thus capable of directly demonstrating the unusual stability of neuritic MTs, and provides a new system for further investigation on the mechanism of stabilization. J. Neurosci. Res. 50:81–93, 1997. © 1997 Wiley-Liss, Inc.     

Correlation of cell body size, axon size, and signal conduction velocity for individually labelled dorsal root ganglion cells in the cat

Measurements of cell body and peripheral and central axon sizes were made for primary sensory neurons outlined by the intracellular injection of HRP. Conduction velocities were also measured on the outlined processes. The sensory neurons were then subdivided into A and C cells on the basis of the conduction velocity of the impulses carried by the processes of these cells. Central processes of both A and C cells are smaller than the peripheral processes, but the size differential is greater for the C cells. For A cells there is a linear relation between the size of the peripheral axon and the conduction velocity of the impulses carried by these axons, but the confidence limits are wide. For C cells there is a linear relation between the size of the central process and conduction velocity of the impulses carried by the processes, but for the peripheral processes two aberrant processes resulted in no correlation between process size and conduction velocity. For A cells, the size of the central and peripheral processes and the conduction velocity of the impulses carried by the peripheral processes are linearly correlated with cell body size. By contrast no such correlations can be demonstrated for C cells. This presumably implies an important difference in that the size of the cell body is correlated with axon size and impulse conduction velocity for A cells but not for C cells. A widely accepted generalization is that large sensory cells give rise to myelinated axons and small sensory cells to unmyelinated axons. In this study, myelinated and unmyelinated are defined on the basis of impulse conduction velocity. For those cells that are clearly large (greater than 50 microns in diameter), the conduction velocity of the impulses carried by their processes is always greater than 2.5 m/s, and for those cells that are clearly small (less than 35 microns in diameter), the conduction velocity is always less than 2.5 m/s. Thus for these cells the above generalization holds. For the intermediate-sized cells (35-50 microns), however, the size of the cell body bears no predictable relation to the conduction velocity of the impulses carried by those processes, and thus to whether the axons are myelinated or unmyelinated. Thus the above generalization does not hold for this intermediate group of cells, and since there are many cells in this size range, we feel that the generalization that large cells give rise to myelinated axons and small cells to unmyelinated axons is an oversimplification.