Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neurons”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources
PubMed1995

Putative cholinergic neurons of the pedunculopontine tegmental nucleus projecting to the superior colliculus consist of sensory responsive and unresponsive populations which are functionally distinct from other mesopontine neurons.

We examined the sensory properties of putative cholinergic neurons of the pedunculopontine tegmental nucleus projecting to the superior colliculus. Projection neurons were identified by antidromic activation from the contralateral posterior superior colliculus; stimulation of the anterior half was essentially ineffective. Identified neurons fell into two groups, one with a somatosensory input (39%) and one without a sensory input. Somatosensory responsive projection neurons were low threshold and rapidly adapting. Receptive fields were contralateral (94%) and predominantly orofacial (57%). Sensory responsive and unresponsive projection neurons were intermingled within the pedunculopontine tegmental nucleus as identified histologically by reduced nicotinamide adenine dinucleotide phosphate diaphorase or acetylcholinesterase. The properties of neurons outside the nucleus differed significantly. They could not be activated antidromically from the superior colliculus; many had ipsi- or bilateral receptive fields (75%) and wide dynamic range or nociceptive response patterns (52%). The presence of two functionally distinct groups of projection neurons implies a dual or more complex modulation of tectal neurons by the pedunculopontine tegmental nucleus. The pedunculopontine tegmental nucleus has been implicated in a multiplicity of behaviors and, in particular, in rapid eye movement sleep and alerting or arousal functions. By virtue of its many connections with the basal ganglia, limbic system and reticular structures, the projection to the superior colliculus of two distinct groups may provide an important differentiating element of the tectal organization of orienting and spatial cognitive behavior.

Animals↗
PubMed1995

Distribution and synaptic relations of NOS neurons in the dorsal raphe nucleus: a comparison to 5-HT neurons.

Anti-nitric oxide synthase antibody was used to study the distribution, cytoarchitecture, and synaptic relations of nitric oxide synthase-like immunoreactive neurons in the whole rostral-caudal length of the dorsal raphe nucleus of the rat and compared them with serotonergic neurons. Results showed that the distribution of the nitric oxide synthase in the dorsal raphe nucleus was similar to that of the serotonergic neurons at the rostral part of the dorsal raphe nucleus, including the mediodorsal and the medioventral cell groups, and changed at the middle and caudal parts of the dorsal raphe nucleus. The cytoarchitecture of the nitric oxide synthase-like immunoreactive neurons in the medioventral cell group of the dorsal raphe nucleus was similar to that of the serotonergic neurons. Similar to the serotonergic neurons there, nitric oxide synthase-like immunoreactive neurons also received synapses from axon terminals that contained round, or flattened vesicles, or both kinds. Different to the serotonergic neurons, the few nitric oxide synthase-like immunoreactive axon terminals that were in this area formed synapses.

Amino Acid Oxidoreductases↗
PubMedDate not supplied

Aging of neurons in the mollusc Lymnaea stagnalis small parietal ganglion: a morpho-functional comparison in the same neuron.

The aim of this study was to compare the functional and structural changes in similarly identified neurons of the small parietal ganglion in 56 molluscs (Lymnaea stagnalis) of two age groups: adult (10-12 months) and old (20-22 months). No age changes were found in the values of membrane potential, resistance of the neuronal membrane, amplitude, duration, or rate of increase of the anterior action potential front. With aging, the thresholds of direct stimulation were significantly increased, the rate of action potential repolarization decreased, and the amplitude of trace hyperpolarization decreased. The most marked age-dependent changes were observed in the frequency of neuronal spontaneous activity. A clear relationship was established between the frequency of action potentials of the neuron and its structure in adult and old individuals alike. In the molluscs of both age groups, the neurons with a high frequency of action potential displayed ultrastructural features of high activity in the organelles involved in protein biosynthesis. The cytoplasm of these neurons was filled with numerous ribosomes and had a well-developed rough endoplasmic reticulum. The structure of cells with low spontaneous activity in old molluscs differed considerably from that of the corresponding neurons of the adult individuals. The former had significantly marked morphological signs of reduction of the protein-synthesizing processes, as well as of destructive and dystrophic changes. A decrease in the lability of neurons may be an important mechanism of aging.

Action Potentials↗
PubMed1986

Presence of TAN (tonically autoactive neuron) and its two analogous neurons, located in the right parietal ganglion of the suboesophageal ganglia of an African giant snail (Achatina fulica Ferussac). Morphological and electrophysiological studies.

Three identifiable giant neurons, which were morphologically and pharmacologically identical, named TAN (tonically autoactive neuron), TAN-2 and TAN-3, were found in line on the dorsal surface of the right parietal ganglion in the suboesophageal ganglia of an African giant snail (Achatina fulica Férussac). The diameters of these neurons were 150-200 microns. They showed regular spontaneous spike discharges at the rate of 30-40 per min. However, the spike discharges of the three neurons were not synchronized. For morphological studies of these neurons, Lucifer Yellow was injected into their somata by pressure. The axonal branches of the three neurons examined extended commonly into the following seven peripheral nerves: left anterior pallial, left posterior pallial, intestinal, anal, right posterior pallial, right anterior pallial and right anterior pallial accessory nerves. The sensitivities of the three neurons examined to the main neurotransmitter candidates and their derivatives were almost identical. These neurons were excited by 5-hydroxytryptamine [the minimum effective concentration (MEC): 10(-5)-10(-4) M] and histamine (MEC: 1-3 X 10(-4) M), and inhibited by dopamine (MEC: 1-3 X 10(-4) M), L-norepinephrine (MEC: 3 X 10(-4)-10(-3) M), L-epinephrine (MEC: 3 X 10(-4) M), GABA (MEC: 10(-5)-10(-4)), acetylcholine (MEC: 1-3 X 10(-4) M) and its derivatives.

Amino Acids↗
PubMedDate not supplied

Astroglia-neuron interactions that promote long-term neuronal survival.

Besides intrinsic determinants of cell growth, epigenetic signals have been proposed to regulate development and maintenance of neurons. Here we provide evidence that cerebral astrocytes contribute significantly to the set of environmental influences that are required for long-term survival of neurons derived from the mammalian central nervous system. Cerebral astrocytes in serum-free culture express diffusible and non-diffusible neuron-supporting signals, including cell-adhesive neurite growth-promoting glycoproteins, diffusible neurotrophic factors as well as membrane-bound molecules that mediate cell contact interactions. The combination and synergistic interaction of these environmental signals markedly enhance the survival of brain neurons. While astroglia-derived cell-adhesive substrates that include a high molecular weight complex consisting of laminin beta-chains and proteoglycan (Matthiessen et al., 1989) stimulate neurite outgrowth, they fail to enhance long-term neuronal survival when additional neurotrophic and cell-contact interactions are lacking. Astrocytes release a diffusible neurotrophic activity that, when permanently applied, maintains long-term survival of central neurons in culture. The soluble neurotrophic activity seems to interact synergistically with cell-bound signals which are also required for long-term survival and which are expressed by astrocytes and neurons, but not by fibroblasts. Among neurons from different brain areas, such as hippocampus, cerebral cortex and septum, regional differences in their responsiveness to the astroglial neurotrophic activity have been observed.

Aging↗
PubMed1995

Histamine-immunoreactive neurons in the brain of the teleost Gasterosteus aculeatus L. Correlation with hypothalamic tyrosine hydroxylase- and serotonin-immunoreactive neurons.

The distribution of putative histaminergic neurons in the brain of a teleost, the three-spined stickleback, was investigated by means of immunocytochemistry using specific antibodies against histamine (HA), and conventional microscopy as well as confocal laser scanning microscopy. Histamine-immunoreactive (HAir) neurons form discrete populations ventral to the nucleus of the posterior recess (NRP) and in the nucleus saccus vasculosus (NSV), which belong to the periventricular hypothalamic nuclei. The neuronal somata are subependymally located, and do not possess apical neurites contacting the cerebrospinal fluid. They give rise to both long-range and local axonal projections. The local projections give rise to a field of dense punctate immunoreaction dorsal to the NRP and lateral to the NSV. Long-range projections are comprised of ascending projections to the thalamus, habenula, preoptic area and dorsal telencephalon; and descending projections via the posterior tuberal nucleus, ventrally to the nucleus interpeduncularis, and dorsally into the central gray. HAir neurons occur together with serotoninergic cerebrospinal fluid-contacting (CSFc) neurons in the NRP, and with tyrosine hydroxylase-immunoreactive (THir) neurons in the NSV. Although HAir elements occur together with THir ones in many brain areas, direct contacts between the two neurotransmitter systems are rare. The putative histaminergic neurons in the brain of the three-spined stickleback constitute a very discrete neuronal system, with a major projection area in the dorsal telencephalon in a region which is considered homologous with the dorsal pallium of land vertebrates.

Animals↗
PubMed2005

Stimulation of cardiac sympathetic afferents activates glutamatergic neurons in the parabrachial nucleus: relation to neurons containing nNOS.

Our previous studies have demonstrated that stimulation of cardiac sympathetic afferents activates neurons in the parabrachial nucleus (PBN), a region known to play a role in central integration of cardiovascular autonomic reflexes. However, phenotypes of these activated neurons have not been well identified. Glutamate, an important excitatory neurotransmitter in the brain, is involved in PBN-mediated cardiovascular responses. Recent identification of vesicular glutamate transporter 3 (VGLUT3) has provided a novel and unique marker to locate distinctive perikarya of neurons that use glutamate as a neurotransmitter. The action of glutamate in the brain is influenced by nitric oxide. Thus, using triple immunofluorescent labeling, the present study examined expression of c-Fos, an immediate early gene, in the neurons containing VGLUT3 and neuronal nitric oxide synthase (nNOS) in the PBN following stimulation of cardiac sympathetic afferents. In anesthetized cats with bilateral barodenervation and cervical vagotomy, topical application of bradykinin (BK, 1-10 microg/ml, 50 microl, n = 6) on the left ventricle was performed six times, every 20 min. Repeated administration of BK elicited consistent increases in blood pressure over a 100 min period while no changes were noted in the animals treated with the vehicle for BK (0.9% saline, n=5). Compared to control cats, c-Fos expression was increased significantly in the cell bodies containing VGLUT3 as well as both VGLUT3 and nNOS in the external lateral PBN (elPBN) in BK-treated animals (all P < 0.01). In addition, using similar triple-staining method, we noted that fibers of activated neurons containing nNOS in the elPBN co-localized with vesicular glutamate transporter 2 following BK stimulation. These data suggest that glutamatergic neurons represent a cell type in the PBN that is activated by stimulation of cardiac sympathetic afferents. Nitric oxide has the potential to influence the action of glutamatergic neurons in regulation of excitatory cardiovascular responses induced by activation of cardiac sympathetic afferents.

Afferent Pathways↗
PubMed2006

Glutamatergic innervation of growth hormone-releasing hormone-containing neurons in the hypothalamic arcuate nucleus and somatostatin-containing neurons in the anterior periventricular nucleus of the rat.

Growth hormone-releasing hormone (GHRH) and somatostatin are the two main hypothalamic neurohormones, which stimulate or inhibit directly hypophysial growth hormone (GH) release. Majority of the GHRH neurons projecting to the median eminence is situated in the arcuate nucleus and the somatostatin neurons in the anterior periventricular nucleus. Data suggest that the excitatory amino acid glutamate may play an important role in the control of hypothalamic neuroendocrine neurons and processes including the control of GH. There is a dense plexus of glutamatergic fibres in the hypothalamic arcuate and anterior periventricular nucleus. The aim of the present studies was to examine the relationship of these fibres to the GHRH neurons in the arcuate nucleus and to somatostatin neurons in the anterior periventricular nucleus. Double-labelling immuno-electron microscopy was used. Glutamatergic structures were identified by the presence of vesicular glutamate transporter 2 (VGluT2) (a selective marker of glutamatergic elements) immunoreactivity. A significant number of VGluT2-immunoreactive boutons was observed to make asymmetric type of synapses with GHRH-immunostained nerve cells in the arcuate and with somatostatin neurons in the anterior periventricular nucleus. A subpopulation of somatostatin-immunoreactive neurons displayed also VGluT2 immunoreactivity. Our findings provide direct neuromorphological evidence for the view that the action of glutamate on GH release is exerted, at least partly, directly on GHRH and somatostatin neurons releasing these neurohormones into the hypophysial portal blood.

Animals↗
PubMed2006

The development and characterisation of complex ovine neuron cultures from fresh and frozen foetal neurons.

Cultures of ovine cerebral and cerebellar neurons from mid-term sheep foetal brains, 9-15 weeks old, have been established for the first time. These foetal brains are relatively mature, being at similar stages of development as peri and post-natal rodent brains. Cultures were routinely maintained for 3-4 weeks, and longer. Nearly all the cells from the younger foetuses adhered as neurons. The proportion of glial cells increased with age, as did the risk of cultures being overtaken by glial cells. Cultured neurons were bipolar, tripolar and multipolar, similar to the morphologies of neurons in vivo. Older foetuses also yield more complex neurons, notably giant cells. Other properties of the cultured neurons also mimic in vivo observations, including neurite beading, complexity in neurotransmitter class (GABAergic and glutamatergic) and calcium binding protein (calbindin and calretinin) content. Single cell divisions of neurons were observed in younger cultures by time-lapse photography and the occurrence of telophase nuclei. The advantage of the high yield of genetically identical cells obtained from a single sheep foetus, 150 million, was extended by cryopreservation of neurons after snap freezing, and later culture. These cultures showed the same characteristics as cultures from the freshly plated cells.

Age Factors↗
PubMed2003

Nitric-oxide-induced depolarization of neuronal mitochondria: implications for neuronal cell death.

Nitric oxide (NO(*)) has known toxic effects on central nervous system neurons. This study characterized the effect of NO(*) on mitochondrial membrane changes by exploring the relationship among NO(*), excitatory receptor activation, and the induction of peroxynitrite, a highly toxic NO(*) reactant, to neuronal injury. Cultured rat cortical neurons were exposed to the NO(*) generator, diethylenetriamine/nitric oxide adduct, and were examined for signs of cell death, mitochondrial membrane potential changes (Deltapsi(m)), and the induction of a mitochondrial permeability transition (MPT). Neurons were also examined for nitrotyrosine (NT) immunoreactivity, a marker of reactive nitrogen species (RNS) formation. Neurons exposed to NO(*) or to N-methyl-D-aspartate (NMDA) exhibited similar rapid depolarization of mitochondria, which was prevented by an NMDA receptor antagonist. Electrophysiological studies demonstrated NO(*) potentiation of NMDA-induced NMDA receptor currents. NO(*) and NMDA-treated neurons had evidence of mitochondrial-specific NT immunoreactivity that was prevented by a SOD/catalase mimetic (EUK-134). EUK-134 treatment reduced both NO(*) and NMDA-induced NT formation and neuronal cell death. EUK-134 did not prevent NO-induced Deltapsi(m) but partially prevented NMDA-induced Deltapsi(m) loss. Although NO(*) and NMDA both induced MPT and MPT inhibitors prevented NO-induced Deltapsi(m), they did not result in significant neuroprotection, in contrast to treatment designed to decrease peroxynitrite formation. These data suggest that NO-induced NMDA receptor activation is closely linked to intramitochondrial NO-peroxynitrite/RNS formation and thereby acts as a major mediator of neuronal cell death.

Animals↗
PubMed2003

Inhibition of staurosporine-induced neuronal cell death by bisphenol A and nonylphenol in primary cultured rat hippocampal and cortical neurons.

We examined whether bisphenol A (BPA) and 4-nonylphenol (NP) influenced staurosporine-induced neuronal cell death in primary cultured rat hippocampal and cortical neurons. In hippocampal neurons, 17beta-estradiol (E2) (1 nM and 10 microM) and BPA (10 microM) significantly inhibited the staurosporine-induced release of lactate dehydrogenase (LDH). In cortical neurons, BPA significantly inhibited the LDH release, while E2 did not. In hippocampal neurons, E2 and BPA significantly inhibited the staurosporine-induced increase in caspase-3 activity. In cortical neurons, BPA and NP significantly inhibited the increase in caspase-3 activity, while E2 did not. Furthermore, low-dose BPA (10 nM) also significantly inhibited the increase in caspase-3 activity in both hippocampal and cortical neurons. BPA and NP might impede normal brain development by inhibiting even desirable neuronal cell death, interfering with caspase-3 activation.

Animals↗
PubMed2004

Birth-date dependent alignment of GABAergic neurons occurs in a different pattern from that of non-GABAergic neurons in the developing mouse visual cortex.

In the developing mouse cerebral cortex, gamma-aminobutyric acid (GABA)ergic neurons and non-GABAergic neurons arise in distinct places and migrate into the cortical plate (CP) via different pathways. Although the "inside-out" alignment of projection neurons in the cortex has been thoroughly analyzed, the pattern of interneuron alignment is not well understood. Herein, we show that in the postnatal day (P) 9.5 mouse visual cortex, GABAergic neurons born on embryonic day (E) 12.5 were distributed around two peak locations, mainly around layer V and also around layer II/III, while non-GABAergic neurons born on E12.5 were distributed around only one peak in layer VI. Both cell populations born on E15.5 exhibited only one common peak distribution in layer II/III. The two peak locations of GABAergic neurons born on E12.5 still existed at P30. When the subtypes of GABAergic neurons were analyzed, calretinin-positive cells born on E12.5 were distributed in the cortex around one peak location near layer II/III, whereas somatostatin-positive E12.5 cells were distributed in the cortex around one peak location near layer V. These results suggest that the alignment of interneurons is regulated differently according to subtypes and from that of projection neurons having the same embryonic day of origin.

Animals↗
PubMed2005

Block of voltage-gated potassium channels by Pacific ciguatoxin-1 contributes to increased neuronal excitability in rat sensory neurons.

The present study investigated the actions of the polyether marine toxin Pacific ciguatoxin-1 (P-CTX-1) on neuronal excitability in rat dorsal root ganglion (DRG) neurons using patch-clamp recording techniques. Under current-clamp conditions, bath application of 2-20 nM P-CTX-1 caused a rapid, concentration-dependent depolarization of the resting membrane potential in neurons expressing tetrodotoxin (TTX)-sensitive voltage-gated sodium (Nav) channels. This action was completely suppressed by the addition of 200 nM TTX to the external solution, indicating that this effect was mediated through TTX-sensitive Nav channels. In addition, P-CTX-1 also prolonged action potential and afterhyperpolarization (AHP) duration. In a subpopulation of neurons, P-CTX-1 also produced tonic action potential firing, an effect that was not accompanied by significant oscillation of the resting membrane potential. Conversely, in neurons expressing TTX-resistant Nav currents, P-CTX-1 failed to alter any parameter of neuronal excitability examined in this study. Under voltage-clamp conditions in rat DRG neurons, P-CTX-1 inhibited both delayed-rectifier and 'A-type' potassium currents in a dose-dependent manner, actions that occurred in the absence of alterations to the voltage dependence of activation. These actions appear to underlie the prolongation of the action potential and AHP, and contribute to repetitive firing. These data indicate that a block of potassium channels contributes to the increase in neuronal excitability, associated with a modulation of Nav channel gating, observed clinically in response to ciguatera poisoning.

Action Potentials↗
PubMed2004

Differential regulation of X-chromosome-linked inhibitor of apoptosis protein (XIAP) and caspase-3 by NMDA in developing hippocampal neurons; involvement of the mitochondrial pathway in NMDA-mediated neuronal survival.

N-methyl-d-aspartate (NMDA) subtype of glutamate receptors plays an important role during brain development and receptor activation has been shown to promote neuronal survival. The mechanisms by which NMDA increases neuronal survival are not fully understood. Here, we show that treatment with low concentrations of NMDA upregulates the neuroprotective molecule, X-chromosome-linked inhibitor of apoptosis protein (XIAP) in cultured hippocampal neurons at the post-transcriptional level. In contrast, NMDA treatment decreased mRNA and protein levels of caspase-3 in these neurons. The activation of the caspase-3 was also inhibited by NMDA, and the neurons were more resistant towards death caused by high concentrations of glutamate and staurosporine. Data on cytochrome c release in hippocampal neurons showed that NMDA pretreatment inhibits the mitochondrial pathway of cell death. The results demonstrate that the activation of NMDA receptors induces an anti-apoptotic program in hippocampal neurons that involves mitochondria and alterations of the levels of caspase-3 and XIAP. These findings are of importance for understanding the function of NMDA receptors in the control of neuronal survival during development and in other conditions.

Animals↗
PubMed2001

Hypothalamic dorsomedial nucleus neurons innervate thyrotropin-releasing hormone-synthesizing neurons in the paraventricular nucleus.

To determine whether the hypothalamic dorsomedial nucleus (DMN) may serve as a relay center for the central actions of leptin on thyrotropin-releasing hormone (TRH)-synthesizing neurons in the paraventricular nucleus (PVN), axonal projections from the DMN to TRH-containing neurons in the PVN were studied using the anterogradely transported marker substance, Phaseolus vulgaris-leucoagglutinin (PHA-L). Stereotaxic injections of PHA-L were targeted to the mid-dorsal and mid-ventral portions of the DMN. After 10-14-day survival, the brains were prepared for immunohistochemistry and immunostained with an antibody directed against PHA-L. Focal injections confined to the DMN were identified in 14 animals and gave rise to a fiber bundle that entered the PVN at the caudal pole of the nucleus, densely innervating all parvocellular subdivisions of the PVN. In double-labeled preparations using antisera to PHA-L and preproTRH 178-199, the latter as a marker for TRH-containing neurons in the PVN, proTRH-IR neurons were observed to be enmeshed in a network of PHA-L-containing fibers. When the injection site covered the entire DMN or the mid-dorsal part of the DMN, PHA-L-containing axon varicosities were juxtaposed to approximately 97 and 90% of proTRH neurons, respectively, in all parvocellular subdivisions of the PVN, and by ultrastructural analysis were shown to be synaptic. In contrast, when the injection site was centered primarily in the mid-ventral part of the DMN, only approximately 52% of proTRH-synthesizing neurons appeared to be innervated by PHA-L-containing axons. These data demonstrate that a major projection pathway exists from the DMN, specifically to TRH-producing neurons in the PVN, and suggest that the DMN is anatomically situated to exert a regulatory effect on TRH-synthesizing neurons in the PVN.

Animals↗
PubMed1996

Existence of multiple receptors in single neurons: responses of single bullfrog olfactory neurons to many cAMP-dependent and independent odorants.

The responses of single bullfrog olfactory neurons to various odorants were measured with the whole-cell patch clamp which offers direct information on cellular events and with the ciliary recording technique to obtain stable quantitative data from many neurons. A large portion of single olfactory neurons (about 64% and 79% in the whole-cell recording and in the ciliary recording, respectively) responded to many odorants with quite diverse molecular structures, including both odorants previously indicated to be cAMP-dependent (increasing) and independent odorants. One odorant elicited a response in many cells; e.g. hedione and citralva elicited the response in 100% and 92% of total neurons examined with the ciliary recording technique. To confirm that a single neuron carries different receptors or transduction pathways, the cross-adaptation technique was applied to single neurons. Application of hedione to a single neuron after desensitization of the current in response to lyral or citralva induced an inward current with a similar magnitude to that applied alone. It was suggested that most single olfactory neurons carry multiple receptors and at least dual transduction pathways.

Adaptation, Physiological↗
PubMed1996

In vitro hypoxia of cortical and hippocampal CA1 neurons: glutamate, nitric oxide, and platelet activating factor participate in the mechanism of selective neural death in CA1 neurons.

We prepared neuron-rich cultures from cortical and hippocampal CA1 regions of postnatal day 1 (P1) rats. Using these cultures, we investigated the sensitivity of neurons to hypoxic insults. The effects of MK-801, cycloheximide, NG-nitro-L-arginine (L-NNA), and anti-platelet-activating factor (anti-PAF) IgG on neuronal injury under hypoxic conditions also were examined. The percentage of astroglial cells was higher in CA1 than cortical cultures despite use of the same culture procedure. Despite this finding, the percentage of lactate dehydrogenase (LDH) released into the medium was greater in CA1 than cortical cultures under the conditions of 24-h hypoxia and 24-h incubation (P < 0.05). We then added MK-801 (500 nM), cycloheximide (3 microM), L-NNA (100 microM) and anti-PAF IgG (50 micrograms/ml) prior to inducing the hypoxia and measured LDH in the medium after 24-h hypoxia and 48-h incubation. Under the hypoxic condition, MK-801, L-NNA, and anti-PAF IgG significantly protected the CA1 neurons from hypoxic injury compared with cortical neurons, while cycloheximide protected both cultures equally. These results suggest that CA1 neurons are more sensitive to hypoxia than cerebral cortical neurons, and glutamate, nitric oxide, and PAF may participate in the mechanism of selective neural death in neurons of the CA1 region due to hypoxia.

Animals↗
PubMed1998

Enhanced neuronal differentiation of NTera-2 cells expressing neuronally restricted beta2 adrenergic receptor.

NTera-2/D1 (NT2) is a human teratocarcinoma cell line which can be cultured as a dividing population of precursor cells that can be manipulated with retinoic acid (RA) to yield post-mitotic neurons. Precursor cells were transfected with the human beta2 adrenergic receptor, controlled by the neuronal cell specific rat synapsin-1 promoter. Transfected precursor cells did not display elevated expression of the beta2 adrenergic receptor. Upon differentiation to a neuronal phenotype with RA, betaSyn2 and betaSyn4 (beta2Syn-NT2; ATCC CRL-12356) displayed elevated beta2 adrenergic receptor levels, and an elevated coupling to cAMP production. It was also observed that the elevated expression of the beta2 adrenergic receptor in the neuronal NT2 cells resulted in an enhanced level of neuronal differentiation compared to the wild type cells. These results demonstrate that the neuronally restricted expression of the human beta2 adrenergic receptor in NT2 neurons results in increased receptor levels and receptor stimulated generation of cAMP, this may result in the observed improvement in neuronal differentiation.

Animals↗