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Neuronal migration on laminin involves neuronal contact formation followed by nuclear movement inside a preformed process.

Neuronal migration was investigated in rodent cerebellum in vitro and in vivo. Time-lapse video recording showed that cultured neurons migrated on laminin by first extending neurites that formed contacts with other neurons. This was followed by movement of the cell nucleus inside the preformed process. No guidance cues other than laminin were required. When the rodent premigratory (E18-P0) cerebellum was examined by immunocytochemistry, the radial glial cells were found to have extracellular punctate deposits of laminin along their fibers. Such punctate deposits of laminin were more numerous in the premigratory cerebellum than during the peak of neuronal migration (e.g., at 7-10 days postnatally). At the same time (E18-P0) L1 antigen- and neurofilament-positive, presumably granule cell processes extend radially from the external granule cell layer (EGL). These results imply that neuronal migration on laminin in vitro involves neuronal contact formation followed by nuclear movement inside a preformed process. That this mode of neuronal migration may occur in vivo is indicated by the fact that L1 antigen- and neurofilament-positive "pioneer neurites" colocalize with the punctate deposits of laminin deposited along the radial glial processes in the premigratory EGL. Taken together these results imply that the established glial dependency of the granule cell migration may in fact be dependency of the granule cells and their pioneer neurites on the punctate deposits of laminin produced and laid down by the glial cells.

Animals↗

Cytophotometric analysis of T-2 toxin induced alterations in chromatin condensation and neuronal nuclear volume of rat supraoptic-magnocellular neurons.

Quantitative cytophotometry and ocular filar micrometry were used to monitor T-2 toxin induced alterations in chromatin and neuronal nuclear volume in supraoptic-magnocellular neurons of rat hypo-thalami. Thirty male Sprague-Dawley rats (200-220g) were given a single i.p. injection of T-2 toxin (0.5, 0.75, 1.0 and 1.5 X LD50), a trichothecene mycotoxin; rats were decapitated 8 hours post-dosing. After stoichiometric Feulgen-DNA staining of brain sections, scanning-integrating microdensitometry was used to quantify changes in the susceptibility of chromatin to Feulgen acid hydrolysis. Changes in neuronal nuclear volumes were also determined histometrically. Within the magnocellular neurons of the supraoptic nuclei, significant reductions in F-DNA reactivity were observed in the 0.5, 0.75, and 1.0 X LD50 groups (i.e. 3.7%, 4.4% and 2.5%, respectively); however, rats receiving 1.5 X LD50 T-2 toxin showed no difference in F-DNA reactivity compared to controls. In addition, ocular filar micrometry demonstrated increased neuronal nuclear volumes in all groups receiving T-2 toxin, and following an inverse trend to that seen with F-DNA stainability. Additional observations included pronounced polydipsia, polyphagia and horripilation in the experimental groups, independent of the dosages employed; these changes were evident within 1 hour post-injection. It is postulated that the T-2 toxin induced reduction in the susceptibility of chromatin to Feulgen acid hydrolysis and concomitant increases in neuronal nuclear volumes represent an early indication of impaired metabolic activity. Since these neurons are important sites of vasopressin (antidiuretic hormone) synthesis, these data suggest an impaired osmoregulatory ability. The pronounced polydipsia which occurred shortly after intoxication is further evidence of this impairment. Although these findings do not provide insight relating to the mechanism of osmoregulatory disruption, it is evident that an impaired ability to osmoregulate is among the earliest indications of acute T-2 toxin mycotoxicosis.

Animals↗

Local circuit neurons of the prefrontal cortex in schizophrenia: selective increase in the density of calbindin-immunoreactive neurons.

Schizophrenia has been reported to be associated with alterations in GABAergic local circuit neurons of the prefrontal cortex. In this study, immunocytochemical techniques and antibodies against the calcium-binding proteins calbindin (CB) and calretinin (CR) were used to determine the laminar distribution and relative density of separate subpopulations of local circuit neurons in prefrontal cortical areas 9 and 46 from five pairs of schizophrenic and control subjects, matched for age, sex, and post-mortem interval. The laminar distribution pattern of CB-immunoreactive local circuit neurons was similar in both schizophrenic and control subjects. In both prefrontal regions, however, the density of CB-labeled neurons was 50-70% greater in schizophrenic subjects compared with control subjects, with cortical layers III and V/VI being preferentially affected. In contrast, the density of CR-IR neurons did not differ significantly between schizophrenic and control subjects. These findings reveal a selective increase in the density of a subpopulation of GABAergic local circuit neurons in the prefrontal cortex. Although other explanations for these observations must be considered, they may be consistent with the hypothesis that gene expression in GABAergic neurons is altered in schizophrenia.

Adult↗

Early postnatal lesions of the substantia nigra produce massive shrinkage of the rat striatum, disruption of patch neuron distribution, but no loss of patch neurons.

Unilateral lesions of the substantia nigra in the first postnatal week cause a massive shrinkage (> 50%) of the ipsilateral rat striatum, due primarily to neuronal cell death. Striatal patch neurons (marked by retrograde labeling from the substantia nigra prior to the lesions) selectively survive the striatal cell death caused by the lesions. However, after the lesions these early retrogradely labeled patch neurons are distributed diffusely through the remaining striatum, in contrast to their normal patchy distribution throughout the postnatal period. Thus, many striatal neurons (but not the patch and matrix neurons with early axonal projections to the substantia nigra) are critically dependent upon interactions with the substantia nigra for their survival during the early postnatal period, and in the absence of these missing striatal and substantia nigra neurons, the remaining striatal patch neurons are no longer distributed in a patchy fashion.

Animals↗

Osmotic stimulation causes structural plasticity of neurone-glia relationships of the oxytocin but not vasopressin secreting neurones in the hypothalamic supraoptic nucleus.

A comparative quantitative analysis was carried out on identified supraoptic neurones of male and female Wistar and Long Evans rats under normal conditions and after chronic osmotic stimulation, and in homozygous Brattleboro rats suffering from diabetes insipidus. The neurones were identified by immunocytochemical or morphological means. Osmotic stimulation resulted in significant increases in the number and extent of direct neuronal appositions and in the number of presynaptic terminals contacting two neurosecretory cells simultaneously ("double" synapses). In the supraoptic nuclei of both sexes these increases were restricted to the oxytocin secreting neurones. In Brattleboro homozygous rats treated with vasopressin, the proportion of oxytocinergic neurones in apposition was not modified, but the number of appositions per soma profile decreased as did the incidence of "double" synapses. In nuclei of osmotically stimulated rats, increase in cell volume affected both types of neurosecretory cell and was accompanied by an increase of the absolute extent of glial coverage. However, the extent of glial coverage of the oxytocinergic neurones did not match the hypertrophy of the cells, resulting in a decrease in their relative glial coverage, compared to normal hydrated animals. The increased neuronal appositions, therefore, cannot result simply from a retraction of glial processes. The structural reorganization of the oxytocinergic system observed during chronic osmotic stimulation was as extensive as that observed at lactation. Moreover, the changes were as extensive in Wistar as in Brattleboro lactating rats, although the latter have an added osmotic stimulus. This implies that lactation and osmotic stimulation do not produce additive effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The nigrotectal projection and tectospinal neurons in the rat. A light and electron microscopic study demonstrating a monosynaptic nigral input to identified tectospinal neurons.

In order to investigate the nigro-tecto-spinal pathway in the rat, the pattern of termination of nigrotectal fibres and the distribution of tectospinal neurons have been investigated in a light and electron microscopic study of the superior colliculus. In addition, the pattern of termination of nigrotectal fibres was compared to the pattern of acetylcholinesterase staining. The light microscopic studies showed that the nigrotectal fibres, which had been identified by anterograde transport of horseradish peroxidase from the substantia nigra, terminated in a distinctive clustered pattern throughout the rostrocaudal extent of the stratum griseum intermedium, stratum album intermedium and adjacent dorsal portion of the stratum griseum profundum of the ipsilateral superior colliculus. The clusters of nigrotectal terminals formed a series of branching, interconnected longitudinal columns which largely corresponded with the pattern of acetylcholinesterase staining. The tectospinal neurons, which had been identified by retrograde transport of horseradish peroxidase from the spinal cord, had mainly large-sized somata, were stellate in shape with multiple long dendrites, and formed variable-sized clusters of 4-15 neurons within lateral regions of the ventral stratum album intermedium and dorsal stratum griseum profundum. In experiments where both the nigrotectal terminals and the tectospinal neurons were labelled by the transport of horseradish peroxidase, the clusters of tectospinal neurons largely corresponded with the regions of densest nigrotectal fibre termination in the lateral regions of the superior colliculus. In addition, a small contralateral nigrotectal projection was localized in the rostrolateral region of the superior colliculus where the crossed fibres terminated in a clustered pattern in alignment with clusters of tectospinal neurons in this region. Electron microscopic examination of the superior colliculus following ibotenic acid lesions in the substantia nigra and horseradish peroxidase injections in the spinal cord showed multiple degenerating nigrotectal boutons in synaptic contact with the soma and the mainstem and secondary dendrites of labelled tectospinal neurons in the lateral regions of the stratum album intermedium and stratum griseum profundum of the superior colliculus. The majority of the degenerating nigrotectal boutons showed electron-lucent degenerative changes and were in axodendritic contact. All of the identified nigrotectal synapses were of the symmetrical type.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗

Topographic distribution of the neurons of the central complex (centre médian-parafascicular complex) and of other thalamic neurons projecting to the striatum in macaques.

The distribution of the neurons of the central complex (or "centre médian-parafascicular complex") and of other thalamic regions projecting to the striatum was studied using a cartographic technique based on ventricular landmarks. The brain of a macaque was used as a reference for the cytoarchitectonic study of the complex. Three parts were isolated: the pars parafascicularis (or medial part), the pars media (or middle part) and the pars paralateralis (or lateral part). Wheat germ agglutinin conjugated to horseradish peroxidase was stereotaxically injected into either the sensorimotor or the associative territory of the striatum (i.e. the striatal space occupied by the axonal endings coming from either the sensorimotor or the associative cortex) of four macaques. Neurons projecting to the sensorimotor territory of the striatum were found to be located within the pars media (middle part) of the central complex while neurons projecting to the associative territory of the striatum were located within the pars parafascicularis. In all experimental cases, labelled neurons were scarce or absent in the pars paralateralis (or lateral part). Outside the central complex, neurons projecting to the sensorimotor territory of the striatum were scattered within the lateral part of the lateral mass, in the intralaminar nuclei and in the posterior part of the internal lamina. Neurons projecting to the associative territory of the striatum were observed mainly in the paraventricular region, dorsal to the rostral part of the lateral mass, and in the dorsolateral part of the nucleus oralis medialis. Our three-dimensional analysis of the clusters of the central complex cells projecting to the two striatal territories justifies the partitioning of the central complex into three parts. The pars media (or middle part), which projects to the sensorimotor territory of the striatum, receives selectively pallidal afferent axons. It belongs to the Nauta-Mehler loop, a closed loop linking the central complex to the basal ganglia. The pars parafascicularis, which projects to the associative territory of the striatum, seems more related to oculomotor neuronal systems. The pars paralateralis (or lateral part) appears to have very little, if any, relation with the striatum.

Afferent Pathways↗

Neuronal subtypes and anatomic asymmetry: changes in neuronal number and cell-packing density.

The combined volume of an asymmetric cytoarchitectonic area is smaller than that of symmetric homologs. Asymmetry reflects fewer numbers of neurons in the smaller of the two sides. In this study we examined two types of neurons to check whether lateral differences in neuronal numbers affect different types of neurons comparably in the neocortex of the rat. As with overall neuronal numbers, both parvalbumin-immunoreactive (mostly long projection) neurons, and vasoactive intestinal peptide-immunoreactive interneurons increase in number in the larger of the two sides. Moreover, the concentration of parvalbumin- but not vasoactive intestinal peptide-immunoreactive neurons also increases on the larger side. Thus, there may be qualitative as well as quantitative differences in the connectivity of the larger side of an asymmetric architectonic region.

Animals↗

Barosensitive neurons in the rostral ventrolateral medulla of the rat in vivo: morphological properties and relationship to C1 adrenergic neurons.

The aim of this study, conducted in anaesthetized rats, was to examine the morphology of barosensitive neurons in the rostral ventrolateral medulla and their immunoreactivity for a catecholamine synthesizing enzyme, tyrosine hydroxylase. Thirty neurons displaying inhibitory postsynaptic potentials following stimulation of the aortic depressor nerve were intracellularly labelled with Lucifer Yellow or Neurobiotin. Some of these neurons could be excited antidromically from the second thoracic segment of the spinal cord, with conduction velocities of spinal axons ranging from 1.9 to 7.2 m/s. The filled somas were found immediately caudal to the facial nucleus and ventral or ventromedial to compact formation of the nucleus ambiguus. Some dendrites reached the ventral medullary surface. Axons usually projected dorsomedially and then made a sharp rostral and/or caudal turn. The caudally projecting axon could, in some cases, be followed to the first cervical segment of the spinal cord. Seven cells issued fine axon collaterals on the ipsilateral side. These were identified mainly in two areas: in the rostral ventrolateral medulla (or immediately dorsomedial to that region), and within the dorsal vagal complex. Seven of 27 examined cells (26%) were tyrosine hydroxylase-immunoreactive and were classified as C1 adrenergic neurons. No clear relationship was found between the presence or absence of adrenergic phenotype and the morphology of filled cells. However, the amplitude of aortic nerve-evoked inhibitory postsynaptic potentials was significantly larger in tyrosine hydroxylase-positive neurons. Possible reasons for the low percentage of barosensitive cells with tyrosine hydroxylase immunoreactivity found in this study, in comparison with previously published estimates, are discussed. This is the first study describing the morphology of neurons in this part of the medulla identified as barosensitive in vivo, and directly demonstrating adrenergic phenotype in a subset of these neurons.

Adrenergic Fibers↗

Excitation of inspiratory neurons by preinspiratory neurons in rat medulla in vitro.

In brain stem-spinal cord preparations isolated from newborn rats, we examined synaptic connections to inspiratory neurons from preinspiratory (Pre-I) neurons, by spike-triggered averaging. Potentials were simultaneously recorded intracellularly from inspiratory neurons, and extracellularly from Pre-I neurons in the ipsilateral ventrolateral medulla. The Pre-I neuron pulses were used to trigger computer averaging of potential changes. A total of 16 pairs were analyzed, and EPSP-like depolarizing potentials locked to the triggering Pre-I spikes were obtained from three pairs. Latency from the Pre-I spikes was 3.4-4.5 ms, and the amplitude was 0.07-0.4 mV. These connections were concluded to be monosynaptic, because the antidromic latency was 3.6 +/- 1.5 ms. The present results suggest the presence of excitatory synaptic connections from Pre-I neurons to inspiratory neurons in the ventrolateral medulla. These excitatory synaptic connections are probably important in the initiation of inspiratory burst activity.

Animals↗

Activation of rat peritoneal mast cells in coculture with sympathetic neurons alters neuronal physiology.

Rat peritoneal mast cells (PMC) were activated with anti-IgE or 48/80 while in coculture with neurons dissociated from mouse superior cervical ganglia. At 18-24 h of coculture, microelectrode recordings from neurons were made 15 min after activation of PMC with anti-IgE antibody or the secretagogue compound 48/80. These recordings showed that PMC activation caused depolarization of the neurons and decreased their membrane resistance. Both methods of activation resulted in similar changes in these neuronal characteristics. The resting potential decreased by an average of 15% from the control value of -36.0 +/- 0.6 mV (SEM) (n = 121). The membrane resistance decreased by an average of 60% from the control value of 34.2 +/- 2.0 M omega (n = 75). Application of PMC secretion products directly onto neuronal somata caused reversible changes similar to those caused by activation of cocultured PMC. A decrease in membrane resistance that was observed in neurons cocultured with PMC for 18-24 h without stimulation was due to a proportion of PMC undergoing spontaneous activation. These changes in neuronal physiology are attributed to the action of substances released from the mast cells. This coculture model offers the means to study the cellular interactions involved in neuroimmune communication.

Action Potentials↗

Distribution of dopamine-immunoreactive neurons and their relationships to transmitter and hypothalamic hormone-immunoreactive neuronal systems in the rat mediobasal hypothalamus. A morphometric and microdensitometric analysis.

A morphometric and microdensitometric characterization of the dopamine neurons of the mediobasal hypothalamus and their relationships with several other chemically identified systems, including putative tyrosine hydroxylase-positive/dopamine-negative neurons, was carried out after visualization of dopamine content by both immunocytochemistry and the Falck-Hillarp technique. Quantitative assessment of co-existence demonstrated that more than 95% of dopamine-immunoreactive neurons also contained tyrosine hydroxylase immunoreactivity and more than 90% of growth hormone-releasing factor-immunoreactive neurons also contained tyrosine hydroxylase immunoreactivity. Morphometric and densitometric analysis of dopamine, tyrosine hydroxylase and growth hormone-releasing factor-immunoreactive neurons in the arcuate nucleus showed that dopamine/tyrosine hydroxylase-containing and growth hormone-releasing factor/tyrosine hydroxylase-containing neuronal populations are two largely segregated cell groups with specific localization in the arcuate region, rostrocaudal extension and tyrosine hydroxylase-immunoreactivity content. Morphometric characteristics of dopamine-immunoreactive neurons were shown to be equivalent to those of catecholamine fluorescent cell bodies in the arcuate region. In addition, a cell group lacking detectable catecholamine fluorescence in normal animals but accumulating L-DOPA after peripheral loading was identified and characterized from a morphometric standpoint in the ventral premammillary nucleus. Quantitative analysis of nerve terminal co-distribution in the median eminence revealed significant correlations between dopamine and other transmitter or neurohormone systems, such as gamma-aminobutyric acid, galanin, luteinizing hormone-releasing hormone, in specific subregions of the palissade zone. These data point to discrete subregions of the median eminence, which have been called 'medianosomes', as main sites of interactions between transmitter-identified nerve terminal systems in the control of hypothalamic hormone release.

Animals↗

NOS-positive preganglionic neurons innervate a subpopulation of postganglionic neurons in superior cervical ganglion in rats.

To determine the postganglionic targets of NOS-containing preganglionic neurons, we studied the association of NADPH-diaphorase positive preganglionic fibers and retrogradely labeled postganglionic neurons in the superior cervical ganglion (SCG) in rats. Wheat germ agglutinin-horseradish peroxidase solution was applied to the anterior chamber of the eye, middle cerebral artery, subcutaneous layer of the facial skin, or submucosal layer of the inside of the lip. Two days after tracer application, the rats were perfused with fixative solution. Serial sections of the SCG were stained histochemically for NADPH-diaphorase followed by diaminobenzidine reaction. More than 80% of the labeled postganglionic neurons innervating the structures in the subcutaneous or submucosal layer showed close association with NADPH-diaphorase positive preganglionic nerve terminals; approximately one-third of these labeled neurons were encircled by dense baskets of pericellular terminals. On the other hand, most of the postganglionic neurons innervating the iris (69%) or the cerebral artery (90%) did not show a distinct association with NADPH-diaphorase positive terminals. These results suggest that one of the principal roles of the NOS-containing preganglionic neurons may be in controlling the postganglionic neurons which innervate the structures in the subcutaneous or submucosal layer.

Animals↗

Neuron-specific and state-specific differences in calcium homeostasis regulate the generation and degeneration of neuronal architecture.

Many stimuli (e.g., neurotransmitters and electrical activity) regulate neuromorphogenesis by changing intracellular calcium. The ionophore A23187 was employed as a receptor-independent method to investigate neuronal calcium homeostasis. Distinctive neuron-specific (B5 versus B19) and state-specific (growing versus non-growing) differences in calcium homeostasis were observed in cultured identified Helisoma neurons. Fura-2 studies revealed that A23187 induced a transient rise in intracellular calcium in growing neurons B5 but a sustained rise in growing neurons B19. In stable-state (non-growing) cells A23187 evoked only a transient calcium rise. Both neuron-specific and state-specific differences in calcium homeostasis were dependent on extracellular sodium. Morphological studies also indicated that such differences in calcium-regulatory capacity can have profound consequences on the generation and degeneration of neuronal architecture.

Animals↗

Differentiation of pluripotent embryonic stem cells into the neuronal lineage in vitro gives rise to mature inhibitory and excitatory neurons.

Embryonic stem (ES) cells represent a suitable model to analyze cell differentiation processes in vitro. Here, we report that pluripotent ES cells of the line BLC 6 differentiate in vitro into neuronal cells possessing the complex electrophysiological and immunocytochemical properties of postmitotic nerve cells. In the course of differentiation BLC 6-derived neurons differentially express voltage-dependent (K+, Na+, Ca2+) and receptor-operated (GABAA, glycine, AMPA, NMDA receptors) ionic channels. They generate fast Na(+)-driven action potentials and are functionally coupled by inhibitory (GABAergic) and excitatory (glutamatergic) synapses as revealed by measurements of postsynaptic currents. Moreover, BLC 6-derived neurons express neuron-specific cytoskeletal, cell adhesion and synaptic vesicle proteins and exhibit a Ca(2+)-dependent GABA secretion. Thus, the ES cell model enables the investigation of cell lineage determination and signaling mechanisms in the developing nervous system from a pluripotential stem cell to a differentiated postmitotic neuron. The in vitro differentiation of neurons from ES cells may be an excellent approach to study by targeted gene disruption a variety of neuronal functions.

Action Potentials↗

Neuronal differentiation and synapse formation of PC12 and embryonic stem cells on interdigitated microelectrode arrays: contact structures for neuron-to-electrode signal transmission (NEST).

The development of neuron-microelectrode interfaces (neurochips) is highly desirable for the non-invasive recording of the cellular response to neuroactive drugs as well as the electrical stimulation of nervous tissue by implantable electrodes. A prerequisite for neuron-to-electrode signal transmission (NEST) is the formation of synapse-like contacts between the neuronal cell and the conductive surface of a microelectrode array. We attempted synapse formation by neuronal differentiation of rat pheochromocytoma cells (PC12) and blastocyst-derived murine embryonic stem cells (ES-J1) on interdigitated microelectrode arrays that were made of gold (Au), platinum (Pt), or indium tin oxide (ITO). PC12 or ES cells were in vitro differentiated by incubation with nerve growth factor (NGF) and forskolin, or by serum deprivation and treatment with basic fibroblast growth factor (FGF-2), respectively. On top of ITO electrodes, the neuronal cells extended extremely long processes that terminated in pili-like contact structures, which is typical for growth cone formation. ES cells differentiated into neurons as verified by immunofluorescence staining of MAP-2 and developed synapse-like junctions with the ITO electrode surface as indicated by synaptophysin staining. Differentiated PC12 and ES cells showed bona fide morphological characteristics of synaptic growth cones that were unprecedented in tissue culture. Cones formed by PC12 cells could be stimulated with KCI and carbachol as shown by uptake of FM1-43, a fluorescent marker for synaptic vesicle formation. In contrast to Electrical Cell Impedance Spectroscopy (ECIS) recordings, AC impedance spectrometry with differentiated PC12 cells settled on interdigitated microelectrode arrays revealed lower AC impedance than that with undifferentiated cells, indicating that the complex impedance is dependent on ion fluxes at the neuron-to-electrode contact surface.

Animals↗

Experimental and theoretical analysis of neuron-transistor hybrid electrical coupling: the relationships between the electro-anatomy of cultured Aplysia neurons and the recorded field potentials.

Understanding the mechanisms that generate field potentials (FPs) by neurons grown on semiconductor chips is essential for implementing neuro-electronic devices. Earlier studies emphasized that FPs are generated by current flow between differentially expressed ion channels on the membranes facing the chip surface, and those facing the culture medium in electrically compact cells. Less is known, however, about the mechanisms that generate FPs by action potentials (APs) that propagate along typical non-isopotential neurons. Using Aplysia neurons cultured on floating gate-transistors, we found that the FPs generated by APs in cultured neurons are produced by current flow along neuronal compartments comprising the axon, cell body, and neurites, rather than by flow between the membrane facing the chip substrate and that facing the culture medium. We demonstrate that the FPs waveform generated by non-isopotential neurons largely depends on the morphology of the neuron.

Action Potentials↗

Neuronal network properties of human teratocarcinoma cell line-derived neurons.

Understanding the structural and functional development of neurons in networks has a high impact to estimate the potentials for restorative therapies. Neurons derived from the human NT2 cell line (hNT) formed networks with a clustered neuritic architecture in vitro, whereas primary dissociated embryonic rat cortical neurons (Cx) displayed a more homogenous cell assembly. Spontaneous spikes of both cell types were recorded on microelectrode arrays within 2 weeks after seeding, but hNT showed a mostly uncorrelated firing pattern in contrast to Cx with highly synchronized bursting. hNT neurons were less sensitive to TTX (IC50 = 5.7 +/- 0.1 nM vs. IC50 = 1.1 +/- 0.2 nM), magnesium (IC50 = 1.83 +/- 0.01 mM vs. IC50 = 0.161 +/- 0.023 mM), and APV (IC50 > 100 microM vs. IC50 = 18 microM). We conclude that embryonic cortical neurons and hNT neurons have different network properties. This should be carefully considered before hNT neurons are used in therapeutic approaches, e g., central nervous system (CNS) grafting.

2-Amino-5-phosphonovalerate↗