摘要:

AbstractCellular properties have been examined in ventrally locatedXenopusspinal cord neurons that are rhythmically active during fictive swimming and presumed to be motoneurons. Resting potentials and input resistances of such neurons are ‐75 ± 2 mV (mean ± standard error) and 118 ± 17 MΩ respectively. Most cells fire a single impulse, 0.5 to 2.0 ms in duration and 48.5 ± 1.8 mV in amplitude, in response to a depolarizing current step. A minority fire several spikes of diminishing amplitude to more strongly depolarizing current. Cells held above spike, threshold fire on rebound from brief hyperpolarizing pulses. Spikes are blocked by 0.1 to 1.0 μM tetrodotoxin (TTX) and are therefore Na+‐dependent. Current/voltage (I/V) plots to injected current are approximately linear near the resting potential but become non‐linear at more depolarized levels. Cells recorded in TTX with CsCl‐filled microelectrodes show a linearized I/V plot at depolarized membrane potentials suggesting the normal presence of a voltage‐dependent K+conductance activated at relatively depolarized levels. Most cells recorded in this way but without TTX fire long trains of spikes of near constant amplitude, pointing to a role of the K+conductance in limiting firing in normal cells. Spike blockage with TTX reveals, in some cells, a transient depolarizing Cd2+‐sensitive and therefore presumably Ca2+‐dependent potential that increases in amplitude with depolarization. Cells in TTX, Cd2+, and strychnine, and recorded with CsCl‐filled microelectrodes to block active conductances respond to hyperpolarizing current steps with a two component exponential response. The cell time constant (τ0) obtained from the longer of these by exponential peeling is relatively long (mean 15.7 ms). These findings contribute to an increased understanding of the cellular properties involved in spinal rhythm generation in

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00376.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

AbstractWe have used computer simulations as one way to test the hypothesis that locomotor rhythm production for swimming in frog embryo spinal cord depends on rebound from inhibition and is sustained by mutual re‐excitation among spinal excitatory interneurons. All simulations were based on physiological and anatomical data on the neurons and circuitry ofXenopusembryo spinal cord.Model ‘neurons’ had resistively coupled axon, soma, and dendrite compartments. Membrane properties were based on Hodgkin‐Huxley equations with resting potential at −75 mV and where soma and dendrite had reduced K+and Na+conductance and slowed K+conductance. These ‘neurons’ fired a single non‐overshooting spike both to depolarizing current and afer hyperpolarizing current given during imposed depolarization. Synapses were made on to the dendrite. Inhibitory and excitatory synaptic channels had Nernst potentials of ‐80 and 0 mV, time constants for opening of 1 ms, and closing of 6 and 75 ms. When the short inhibitory postsynaptic potential occurred on the long (N‐methyl‐D‐aspartate‐type) excitatory postsynaptic potential, it led to rebound firing.A four ‘neuron’ symmetrical network was built with reciprocal inhibition and where excitatory ‘neurons’ re‐excited themselves and the inhibitory ‘neuron’ on their own side. The rhythmic alternating activity with one spike per cycle produced reliably by this network was self‐sustaining, initiated by a brief synaptic input, and closely resembled the spinal cord motor pattern during swimming. The robustness of this activity pattern was investigated by varying cellular and synaptic parameters, initiating inputs, and network connectivity. We conclude that cellular, synaptic, and network properties are all important and that mutual re‐excitation, a form of positive feedback, could sustain motor rhythm

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00377.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

This study examines the distribution of fibre diameter classes at various sites along the retinofugal pathway of adult ferrets. Light microscopic observations were made on semi‐thin sections, and regional fibre diameter spectra were constructed from diameter measurements taken from electron micrographs of thin sections of the intraorbital optic nerve (2.5 mm from the optic disc), the intracranial optic nerve (1 mm rostral to the fusion of the nerves), and the optic tract (just caudal to the optic chiasm).Whereas diameter types are relatively evenly distributed behind the eye in the postoptic nerve, they begin to segregate along its prechiasmatic course. Within this prechiasmatic region, coarse and fine calibre fibres are confined increasingly to more ventral locations in the nerve, leaving a dorsal band populated predominantly by intermediate calibre fibres. In conjunction with this redistribution of axon size classes, the fascicular arrangement of axons which is present distally, changes to a non‐fascicular organization. The prechiasmatic organization of fibre types approximates that found in the optic tract where the coarse and fine calibre fibres lie further ventrally towards the pial surface.The prechiasmatic region can be viewed as a region of transition where the order of fibres in the nerve (retinotopic) starts to change to that present in the optic tract (chronotopic), resulting in the first‐born beta cell axons becoming segregated dorsally, and rostral to the coarse and fine calibre classes which segregate at further caudal locations. Further, since the sorting of fibres according to diameter appears before the fibres reach the optic chiasm, the segregation of diameter classes is not dependent on the chiasmatic sorting of fibres according to their crossed or uncrossed c

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00378.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

AbstractThe present study has examined the transition of fibre order from the optic nerve through the optic chiasm and into the optic tract in the ferret's retinofugal pathway. Semi‐thin sections through the chiasmatic region were examined in normal and in monocularly enucleated ferrets in order to display the segregation of the different axon diameter classes as the fibres pass from the optic nerve into the optic tract, and to determine, for each diameter class, where the crossed and uncrossed components become separated in the chiasmatic region.As demonstrated in the preceding manuscript, fine and coarse optic axons begin to segregate from the medium optic axons rostral to the fusion of the two optic nerves. This segregation continues in the chiasmatic region where the different axon diameter classes decussate at different rostro‐caudal levels: the fine and coarse diameter axons decussate rostrally, accumulating along the ventral, superficial surface of the contralateral half‐chiasm, while the medium diameter axons continue caudally before crossing the midline. These two populations, a ventral, crossed (fine and coarse) population and a dorsal, yet‐to‐cross (medium) population are discriminable not only by their size in the chiasmatic region, but also by a thin invagination of hypothalamic neuropil separating them at their lateral extreme. The population of ipsilaterally projecting fibres is composed of both fine and medium optic axons. No coarse optic axons project ipsilaterally in the ferret: these fibres all decussate rostrally in the optic chiasm, intermingled with many of the decussating fine fibres.The fibre ordering in the adult ferret's optic chiasm is interpreted as reflecting a gradient of axonal arrival during development, with successively later arriving optic axons entering one of the two optic tracts at a progressively more superficial, rostral and ventral, location in the chiasmatic region. A fibre's position and time of arrival may influence its subsequent crossed or uncrossed course during the period of axonal ingrowth in de

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00379.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

AbstractThe autoradiographic localization of radiolabelled taurine taken up in the rat substantia nigrain vivotogether with conditions of release of the [3H]taurine taken up into brain slices were studied to determine whether they are consistent with the hypothesis that taurine may act as a neurotransmitter in the striatonigral pathway.At the light microscopic level the main cellular elements that became radiolabelled following the injection of [3H]taurine into the substantia nigra could be identified as glial cells. Electron microscope autoradiography confirmed that a subpopulation of glial cells including astrocytes, pericytes, and oligodendrocytes were radiolabelled and that neuronal perikarya were not radiolabelled. In addition, axonal elements including both terminal and preterminal boutons were found to have silver grains overlying them and were thus considered to be radiolabelled. This was supported by a quantitative analysis of the distribution of the silver grains; whereas glial elements had a significantly higher number of grains associated with them than with any other structure, axonal elements had a significantly greater number of grains than dendritic structures.Release of the preloaded [3H]taurine from superfused slices of substantia nigra occurred in response to veratridine, was calcium‐dependent and was sensitive to inhibition by high magnesium concentrations or tetrodotoxin. Following the destruction of neurons in the striatum by ibotenic acid injections, although the weight of the ipsilateral substantia nigra was reduced, the uptake of [3H]taurine was not altered. In contrast to this, the veratridine‐stimulated release was markedly attenuated, implying that the destruction of striatal neurons causes the loss of sites in the substantia nigra from which exogenous taurine is released.These results add further support to previous suggestions that taurine might act as a neurotransmitter or neuromodulator in the striatonigral path

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00380.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

AbstractThe effects of brief anoxic episodes on intracellularly recorded CA3 pyramidal neurons have been studied in the hippocampal slice preparation. Anoxia induced a depolarization occasionally preceded by a transient hyperpolarization associated with a fall in input resistance. The anoxic depolarization was due to the release of glutamate from presynaptic terminals since it was blocked by tetrodotoxin (TTX) (1 μM) or by the broad spectrum excitatory amino acid antagonist kynurenate (1 mM). In the presence of TTX (1 μM) or kynurenate (1 mM), anoxia only induced ahyperpolarizationwhich was due to activation of a K+ conductance. The anoxicdepolarizationwas blocked by galanin, a hormone which activates ATP sensitive K+ (K + ATP) channels. Anoxic depolarization was increased by the potent sulfonylurea agent glibenclamide (GLIB) which blocks K + ATP channels. Bath applications of these agents had little effect when applied in oxygenated Krebs solution suggesting that their action may be mediated by K + ATP channels. Since excessive release of glutamate during anoxia is neurotoxic, agents such as galanin which activate K + ATP channels may provide tissue specific protection against anoxic damag

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00381.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

AbstractIn order to obtain information on the physiological regulation of NGF‐synthesis in the central nervous system (CNS) we investigated the effects of a series of growth factors (known to be present in the CNS) in cultures of purified rat astrocytes and compared these effects with those observed after intraventricular injection of the same molecules. After preliminary experiments had shown that 10% fetal calf serum (FCS) produced a marked increase in NGF‐mRNA levels in astrocytes (but neither in microglia nor oligodendrocytes) as demonstrated by Northern blot analysis andin situhybridization the experiments were performed at low (0.5%) FCS concentrations. Supramaximal concentrations of IL‐1 and various growth factors caused a 5‐ to 7‐fold increase in NGF‐mRNA after 6 h. By 24 h the NGF‐mRNA levels approached control values again, most probably due to inactivation of the added factors since after readdition after 24 h the response was about the same as the initial one. Norepinephrine and 8‐bromo‐cAMP did not change NGF‐mRNA levels. The growth factor‐mediated changes in NGF‐mRNA levels in astrocyte cultures were not consistently reflected by the changes observed after intraventricular injection. IL‐1 produced by far the largest increase in hippocampal NGF‐mRNA after intraventricular injection. This large response to IL‐1 could result from a positive feedback mechanism, since IL‐1β injection not only increases NGF‐mRNA but also IL‐1β‐mRNA in the hippocampus. The understanding of the physiological regulation of NGF synthesis in the CNS is the basis for a rational approach to its pharmacological modification. This, in turn, is an attractive alternative to the (long‐term) infusion of NGF or the transplantation of NGF‐secreting cells with the goal of providing trophic support to the cholinergic neurons of the basal forebrain nuclei. These neurons are consistently affected in the early stages of Alzheimer's disease, their impaired function being essenti

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00382.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

AbstractCarotid body glomus cells produce and release acetylcholine (ACh), catecholamines, and neuropeptides, and there is biochemical evidence that these cells possess receptors for these substances. Thus, we studied the effects of cholinergics [ACh, nicotine (Nic), bethanechol (BN)] and peptides [met‐enkephalin (ME), substance P (SP)]on the membrane potential (Em), voltage noise (Erms), and input resistance (R0) of glomus cells. Sliced carotid bodies (for cell visualization) of cats, rabbits, and mice were used.The mean Emand R0of rabbit glomus cells were lower than those of cat and mouse. R0of mouse cells was the largest, whereas Ermswas similar in all species. The various agents had qualitatively similar effects on the cells of the three species although some quantitative differences were sometimes observed. But, for simplicity, results were pooled.ACh depolarized most cells (effect depressed by zero [Ca2+]0and Mn2+), reduced their resistance, and induced variable changes in Erms. Different ACh doses produced non‐linear effects on ΔEm. Nic and BN also depolarized most cells, reducing R0and Erms. Atropine depressed the cell responses to BN; α‐bungarotoxin the depolarizing response to Nic. ME and SP depolarized most cells, but only ME significantly reduced R0. Neither peptide significantly changed voltage noise.Comparing the effects of all drugs showed that BN was the most effective depolarizing agent, producing the largest reductions in R0. There were negative correlations between ΔEmand ΔR0with the cholinergics and SP; correlations between ΔErmsand ΔR0were significant and positive only with the cholinergics.These results confirm the presence of nicotinic, muscarinic, and peptidergic receptors in glomus cells. The similar effects of cholinergics and peptides and those of flow interruption and anoxia suggest that the latter may partly act via autoreceptors for the released t

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00383.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

AbstractThe structure and function of C‐ and A‐fibres have been studied 3–12 months following a single 30 min exposure of the saphenous nerve of adult rats to 1% capsaicin. Examination of nerve cross‐sections showed that the number of C‐fibres was reduced by 36%, but A‐fibres were unaffected. The remaining C‐fibres included many that were unusually small in size. The changes were not restricted to the treatment site but were found over at least a further 10 mm proximal and distal to it. In treated nerves, the C‐fibre component of the compound action potential was reduced in size relative to the Aαβ component. Single unit studies revealed that an unusually high proportion of C‐fibres had no cutaneous receptive field (54%, compared with 28% in controls). There was no such change for A‐fibres. The conduction velocity range for C‐fibre units in treated nerves was almost normal, but this sample contained an unusually low proportion of polymodal nociceptors. Allowing for the fall in total numbers and the reduction in units with cutaneous receptive fields, it was calculated that overall the numbers of C‐polymodal nociceptor units had fallen by 74%. No significant changes in number had occurred in the other classes of C‐afferents. The reduction in the numbers of nociceptive C‐fibres is likely to be the direct cause of the reduction in pain responses and in neurogenic inflammation that several groups have reported following treatment of adult rats with capsaicin. Reduction in the numbers of C‐fibre is also likely to be the reason for reduced neuropeptide levels seen in tissu

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00384.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

AbstractLevels of several neuropeptides were measured in the frontal cortex, dorsal hippocampus, striatum, and amygdala/pyriform cortex in rats kindled for 5 weeks by daily injection of pentylenetetrazol (30 mg/kg, i.p.). Significantly increased concentrations (by 30–140%) were found in all examined brain areas for neuropeptide Y, somatostatin (except hippocampus) and neurokinin‐like immunoreactivity 10 days after the last kindling session. Similar but less pronounced changes were also found 24 h after the last seizure. The increase in total neurokinin‐like immunoreactivity was due to a marked increase in neurokinin B as revealed by HPLC analysis. Increases in peptide levels, however, were restricted to fully kindled animals. At the same time no changes in levels of substance P, vasoactive intestinal polypeptide and calcitonin gene‐regulated peptide were observed. Cholecystokinin octapeptide was enhanced only in the hippocampus (by 46%). The increases in neuropeptide Y, somatostatin, and neurokinin‐like immunoreactivity subsided after 3 months. A markedly decreased seizure threshold was observed 10 days and 2 months after the final kindling session.No nerve cell degeneration was observed in kindled rats 24 h or 10 days after the last pentylenetetrazol injection. Some animals (2 of 4), however, exhibited signs of blood‐brain barrier damage when examined 24 h after the last kindling session which may reflect the preceding convulsions. No such changes were detected after 10 days.The increases in peptide levels may suggest increased activity of respective neurons which, at least to some degree, may be associated with γ‐aminobutyric acid. The changes in peptide levels may be more closely related to the kindling procedure itself than to the decreased seizure threshold

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1990.tb00385.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY