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PubMed2002

Evaluation of preconditioning treatments to protect near-pure cortical neuronal cultures from in vitro ischemia induced acute and delayed neuronal death.

We evaluated the efficacy of cycloheximide, heat stress, NMDA receptor blockade (MK801/AP-5), oxygen--glucose deprivation, hypoxia, hypothermia and TNFalpha preconditioning to protect cortical neurons from in vitro ischemic insults that result in acute necrotic and delayed apoptotic neuronal death. Preconditioning treatments were performed 22--24 h before in vitro ischemia. In vitro ischemia was carried out in 96-well microtitre strip-plates by washing neuronal cultures with a balanced salt solution containing 25 mM 2-deoxy-D-glucose and incubating in an anaerobic chamber. Glutamate receptor blockers were present during in vitro ischemia to induce delayed neuronal death. Cycloheximide, heat stress, MK801 and oxygen--glucose deprivation preconditioning were neuroprotective in both acute and delayed in vitro ischemic neuronal death models. AP-5 preconditioning and a 12 h post-MK801 preconditioning interval protected neurons from acute ischemic neuronal death only. Hypoxia, TNFalpha and hypothermic preconditioning provided no neuronal protection in the in vitro ischemia models. This study has confirmed for the first time that several preconditioning treatments can protect neurons from in vitro ischemia induced acute necrotic and delayed apoptotic neuronal death. In addition, a unique feature of this study is the finding that preconditioning could be induced in near-pure primary cortical neuronal cultures, thus confirming that ischemic tolerance is an intrinsic property of neurons and provides a simplified culture system for identifying neuroprotective proteins.

Animals↗
PubMed1997

Preferential localization of monoamine oxidase type A activity in neurons of the locus coeruleus and type B activity in neurons of the dorsal raphe nucleus of the rat: a detailed enzyme histochemical study.

Using enzyme histochemistry for monoamine oxidase (MAO) activity, we have examined whether MAO type A or type B or both are localized in neurons of the locus coeruleus (LC) and dorsal raphe nucleus (DR) of the rat. After pretreatment with various concentrations of the MAO type A inhibitor clorgyline or the type B inhibitor deprenyl, non-fixed frozen sections of the brain were histochemically stained for MAO activity with tyramine as a common substrate for the two types. MAO activity of the stained neuron was determined by measuring optical density of the staining. Percentage inhibition of the control MAO activity was plotted against increasing concentrations of the inhibitors. MAO activity of LC neurons was inhibited by low concentrations of clorgyline with a monophasic dose-response curve but not with a biphasic curve. Higher concentrations of deprenyl were needed to inhibit of LC neurons. MAO activity of DR neurons was inhibited by low concentrations of deprenyl with a monophasic dose-response curve. Clorgyline inhibited the MAO activity of DR neurons at only higher concentrations. When the sections without inhibitor pretreatment were incubated with the type A preferential substrate serotonin, the MAO activity was strongly stained in LC neurons but very weakly in DR neurons. With the type B preferential substrate beta-phenylethylamine, the staining was intense in DR neurons while very faint in LC neurons. These findings suggest that (i) almost all the MAO activity in LC neurons is of type A, and (ii) the MAO activity in DR neurons is predominantly of type B.

Animals↗
PubMed1996

The kindling-activated neuronal network: recruitment of somatostatin-synthesizing neurons.

The present study demonstrates the anatomical extent of the kindling-activated neuronal network in general, and specifically the recruitment of extrahippocampal somatostatin (SST)-synthesizing neurons into this network. It has been known that SST neurons of the hippocampal formation are activated during episodes of seizure, however, it was not known if this activation was a local event or extended to other areas in the brain. We were therefore interested in determining if and which SST neurons outside the hippocampal formation might be recruited into this seizure-activated neuronal network. Using the kindling model of seizure elicitation, expression of the Fos protein in activated, depolarized neurons was utilized to identify seizure-activated neurons. Subsequently, the mRNA for SST was identified through in situ hybridization in the same tissue section, allowing the identification of seizure-activated, SST-synthesizing neurons. The results show that: (a) the majority of SST-synthesizing neurons in the forebrain and diencephalon became activated during the kindling development; (b) their recruitment into the kindling-activated neuronal network occurred progressively; and, (c) these SST-synthesizing neurons represented a component of the kindling-activated neuronal network throughout the development of kindling-induced seizures.

Animals↗
PubMed2003

Aging of the myenteric plexus: neuronal loss is specific to cholinergic neurons.

Neuron loss occurs in the myenteric plexus of the aged rat. The myenteric plexus is composed of two mutually exclusive neuronal subpopulations expressing, respectively, nitrergic and cholinergic phenotypes. The goal of the present study, therefore, was to determine if neuron loss is specific to one phenotype, or occurs in both. Ad libitum fed virgin male Fischer 344 rats of 3 and 24 months of age were used in each of two neuronal staining protocols (n=10/age/neuron stain). The stomach, duodenum, jejunum, ileum, colon, and rectum were prepared as whole mounts and processed with either NADPHd or Cuprolinic Blue to stain, respectively, the nitrergic subpopulation or the entire population of myenteric neurons. Neuron numbers and sizes were determined for each preparation. Neuron counts from 24-month-old rats were corrected for changes in tissue area resulting from growth. There was no age-related loss of NADPHd-positive neurons for any of the regions sampled, whereas significant losses of Cuprolinic Blue-labeled neurons occurred in the small and large intestines of 24-month-old rats. At the two ages, the average neuron sizes were similar in the stomach and small intestine for both stains, but neurons in the large intestine were significantly larger at 24 months. In addition, numerous swollen NADPHd-positive axons were found in the large intestine at 24 months. These findings support the hypothesis that age-related cell loss in the small and large intestines occurs exclusively in the cholinergic subpopulation. It appears, however, from the somatic hypertrophy and the presence of swollen axons that the nitrergic neurons are not completely spared from the effects of age.

Aging↗
PubMed1974

The influence of non-neuronal cells on catecholamine and acetylcholine synthesis and accumulation in cultures of dissociated sympathetic neurons.

The effects of several non-neuronal cell types on neurotransmitter synthesis in cultures of dissociated sympathetic neurons from the new-born rat were studied. Acetylcholine synthesis from radioactive choline was increased 100- to 1000-fold in the presence of non-neuronal cells from sympathetic ganglia. This increase was roughly dependent on the number of ganglionic non-neuronal cells present. The effect did not appear to be due to an increased plating efficiency of neurons, since the non-neuronal cells were capable of increasing acetylcholine synthesis after only 48-hr contact with neurons that had been previously grown without non-neuronal cells for 2 weeks. C6 rat glioma cells were also able to stimulate acetylcholine synthesis, but 3T3 mouse fibroblast cells had little or no effect. None of the non-neuronal cell types synthesized detectable acetylcholine in the absence of the neurons. The ganglionic non-neuronal cells had no significant effect on catecholamine synthesis (which occurs in the absence of non-neuronal cells).

Acetylcholine↗
PubMed1998

The p75 neurotrophin receptor mediates neuronal apoptosis and is essential for naturally occurring sympathetic neuron death.

To determine whether the p75 neurotrophin receptor (p75NTR) plays a role in naturally occurring neuronal death, we examined neonatal sympathetic neurons that express both the TrkA tyrosine kinase receptor and p75NTR. When sympathetic neuron survival is maintained with low quantities of NGF or KCl, the neurotrophin brain-derived neurotrophic factor (BDNF), which does not activate Trk receptors on sympathetic neurons, causes neuronal apoptosis and increased phosphorylation of c-jun. Function-blocking antibody studies indicate that this apoptosis is due to BDNF-mediated activation of p75NTR. To determine the physiological relevance of these culture findings, we examined sympathetic neurons in BDNF-/- and p75NTR-/- mice. In BDNF-/- mice, sympathetic neuron number is increased relative to BDNF+/+ littermates, and in p75NTR-/- mice, the normal period of sympathetic neuron death does not occur, with neuronal attrition occurring later in life. This deficit in apoptosis is intrinsic to sympathetic neurons, since cultured p75NTR-/- neurons die more slowly than do their wild-type counterparts. Together, these data indicate that p75NTR can signal to mediate apoptosis, and that this mechanism is essential for naturally occurring sympathetic neuron death.

Animals↗
PubMed1997

Synchronization of neuronal activity promotes survival of individual rat neocortical neurons in early development.

Neural activity is thought to play a significant role during the development of the cerebral cortex. In this study, we examined the effects of global activity block or enhancement and the effects of patterned firing on the ability of cultured rat neocortical neurons to survive during the second week in vitro, beyond the beginning of synaptogenesis. Blockade of neuronal activity by adding tetrodotoxin (TTX) and increasing magnesium concentration in the medium strongly reduced the survival of cortical cells. Increasing neuronal activity by raising the external potassium concentration significantly improved the survival of cortical neurons. We postulated that in a developing neuronal network the survival of nerve cells is regulated by synaptically mediated events that involve changes in the intracellular calcium concentration. To examine this question further, we monitored the activity of the developing network by optically recording the intracellular calcium signals of many neurons simultaneously. These recordings show that in low magnesium neocortical neurons express synchronized oscillation of their intracellular calcium concentration. The ability of a network to synchronize the changes in intracellular calcium of multiple cells appeared gradually during the second week in culture, paralleled by both an increase in the synaptic density and a decline in the number of surviving neurons. By examining the fate of identified cells several days after a recording session, we found that those nerve cells that were co-activated with other neurons had a significantly higher chance to survive than cells that did not participate in synchronized events. These experiments demonstrate that during early cortical network development cortical neurons show synchronized firing activity and that the survival of neurons is at least partially dependent on this pattern of neuronal activity.

Animals↗
PubMed1995

Identification and characterization of cerebral ganglion neurons that induce swimming and modulate swim-related pedal ganglion neurons in Aplysia brasiliana.

1. We have identified and characterized a family of several pairs of neurons in the cerebral ganglion of Aplysia brasiliana that are capable of inducing, maintaining, or modulating a motor program that underlies swim locomotion in this marine mollusk. We have operationally defined these cells as command neurons (CNs) for swimming. 2. The command cells occur in bilateral pairs in the cerebral ganglion and make direct and indirect outputs to neurons in the pedal ganglia, including motor neurons, a central pattern generator circuit, and modulatory neurons that enhance muscle contractions during swimming. Several of the CNs are sufficient individually to induce the swim motor program (SMP), all receive sensory feedback from the periphery, and several interconnect with other swim-related CNs. 3. Tonic discharges of approximately 10 Hz in CN types 1-3 (CN1-CN3) are capable of eliciting the oscillatory, phasic SMP as recorded in peripheral nerves that innervate the swim appendages, the parapodia. CN1, CN2, and CN3 make monosynaptic excitatory connections onto ipsilateral, contralateral, and bilateral pedal swim-modulatory neurons [parapodial opener-phase (POP) cells], respectively; and each command cell type activates the pedal central pattern generator (CPG), leading to sustained phasic output of motor neurons and POP cells. 4. Tonic firing of CN4 causes weak activation of the SMP contralaterally. These neurons occur as two pairs of neurons in each cerebral hemiganglion, with mutual electrical and chemical synaptic interconnections. CN4 cells also excite CN1 and CN2 cells. Thus CN4 is classified as a higher-order swim command cell type. 5. Command cells classified as types 5-8 (CN5-CN8), although not capable of inducing the SMP individually, nonetheless have strong synaptic connections with pedal POP cells and/or with other command neurons. These command cells may excite or inhibit follower cells on the same or opposite sides of the preparation and modulate the swim output. 6. All the command cells tested received strong input from mechanical stimulation, either stretch or pinching, of either parapodium. Mechanosensory input from the parapodia was shown to depend on the presence of the pedal ganglion, but not the pleural. Sensory stimulation activated command cells and motor neurons, but POP cells received input from sensory stimuli only through the cerebral ganglion, probably via command cells. The effects of applied mechanosensory stimuli could be entirely mimicked by motor neuron-induced contractions of the parapodia.

Animals↗
PubMed1999

Electrophysiological and morphological properties of neurons in the rat superior colliculus. I. Neurons in the intermediate layer.

To begin characterizing the neural elements underlying the dynamic properties of local circuits in the mammalian superior colliculus (SC), electrophysiological and morphological properties of individual neurons in the intermediate layer [stratum griseum intermediale (SGI)] were investigated using whole cell patch-clamp recording and intracellular staining with biocytin in slice preparations from young (17-22 days old) and adult rats (7-8 wk old). Voltage responses to depolarizing current pulses of 223 neurons recorded in young rats were classified into six subclasses: regular-spiking neurons (n = 113), interspike intervals during depolarizing current pulses were constant; late-spiking neurons (n = 48), initiation of repetitive firing was delayed markedly from the onset of depolarizing pulses because of a transient hyperpolarization caused by A-like currents; burst-spiking neurons (n = 29), transient burst firing due to low-threshold Ca(2+) channels were observed at the firing threshold level; fast-spiking neurons (n = 19), constant repetitive firings at frequencies >100 Hz were observed for the duration of the depolarizing pulse; neurons with marked spike frequency adaptation (n = 11), interspike intervals more than doubled due to spike frequency adaptation during depolarizing pulses; and neurons with rapid spike inactivation (n = 3), spike amplitude rapidly reduced, width increased during depolarizing pulses, and spiking was terminated after generating a few spikes. In response to hyperpolarizing current pulses, two different types of inward rectification were observed; time-dependent inward rectification by hyperpolarization-activated current (I(h); n = 29) and time-independent inward rectification (n = 111). Morphological analysis showed that neurons expressing time-dependent inward rectification by I(h) had large somata, extended divergent dendrites dorsally into the superficial layers, and projected axons ventrally and sometimes dorsally, all characteristic features of wide-field vertical cells. Other neurons exhibited heterogeneous morphological properties, such as multipolar, fusiform, horizontal, or pyramidal-shaped cells. In adult rats, a total of 44 neurons showed similar electrophysiological properties except for the last type. These results indicate that the local circuits of the SC include neurons with at least five different firing properties and two different rectification properties; each with distinct electrophysiological and morphological characteristics that may be correlated with the functional output of the SC.

Action Potentials↗
PubMed1995

Histochemical localization of nitric oxide neurons in the hypothalamus: association with gonadotropin-releasing hormone neurons and co-localization with N-methyl-D-aspartate receptors.

The neurotransmitter glutamate plays an important role in the control of gonadotropin-releasing hormone (GnRH) secretion. Recent evidence suggests that the novel transmitter nitric oxide may also play a role in controlling GnRH release and may be an important mediator of glutamate effects. To explore the role of nitric oxide in these events, the present study determined the distribution of the enzyme which catalyzes nitric oxide production, nitric oxide synthase (NOS) in the hypothalamus, its association with GnRH neurons, and whether NOS neurons contain NMDA receptors. NOS was localized by staining hypothalamic sections from female rats for NADPH-diaphorase activity. Specific antibodies for GnRH and the NMDAR1 receptor subunit were used for double-staining to determine NOS association with GnRH neurons and the presence of NMDA R1 receptor subunits in hypothalamic NOS neurons. The studies showed intense NOS cell body and fiber staining in the organum vasculosum of the lamina terminalis (OVLT) where numerous GnRH cell bodies are located. Other major GnRH cell body sites such as the median preoptic nucleus (MPN) and medial preoptic area (MPOA) displayed moderate staining of NOS cell bodies and fibers. Intense NOS staining was also observed in the median eminence, ventromedial nucleus, paraventricular nucleus and supraoptic nucleus of the hypothalamus. While no GnRH neurons were found to double stain for NOS in the hypothalamus, GnRH neurons were frequently surrounded by NOS neurons in the OVLT, MPN and MPOA with potential contacts between NOS and GnRH neurons in these areas. In addition, there was significant overlap of GnRH and NOS fibers in the lateral portion of the internal zone of the median eminence where GnRH fibers and terminals converge. Double-staining studies for NADPH-diaphorase and NMDA R1 receptor subunit showed that many NOS neurons in the OVLT, MPOA, ventromedial nucleus, paraventricular nucleus and supraoptic nucleus co-localize the NMDA R1 receptor subunit. Localization of NMDA R1 receptor subunit immunoreactivity in B-NOS neurons in the hypothalamus was further confirmed by using combined immunohistochemistry-in situ hybridization. Finally, the functional importance of this co-localization was shown by the finding that central administration of a nitric oxide synthase inhibitor blocked the ability of NMDA to induce LH secretion. Taken as a whole, these studies provide evidence which support a role for nitric oxide as an important regulator of GnRH neurons in the female. They also suggest that hypothalamic NOS neurons are targets for glutamate regulation as evidenced by co-localization of the NMDA R1 receptor subunit.

Animals↗
PubMed1999

Differential effects on the survival of neuronal and non-neuronal cells after infection by herpes simplex virus type 1 mutants.

Replication-defective mutants of herpes simplex virus type 1 (HSV-1) are powerful tools to transfer genes into postmitotic neurons and show promise for gene therapy protocols in vivo. To evaluate the efficacy and safety of these vectors for the treatment of deafness we infected dissociated cochlear ganglia with HSV mutants defective in the immediate early genes IE 2 (5dl1.2) or IE 3 (d120). Our results reveal striking differences in the survival of neuronal and non-neuronal cells caused by these mutants. Surprisingly, cochlear neurons infected with 5dl1.2 at various concentrations show a significant increase in survival after 2 days in culture. In contrast, many non-neuronal cells undergo apoptosis reducing cell number to less than 50%. In both neuronal and non-neuronal cell types we also observe a population of cells with important changes in morphology. Analysis of dissociated cochlear ganglia infected with d120 reveals a decrease of neuronal survival, whereas non-neuronal cells were almost unaffected. To further characterize and compare the effects of 5dl1.2 and d120 we transduced central nervous system-derived cell types including cortical neurons and astrocytes. Similarly, as observed for cochlear neurons, infection with 5dl1.2 results in increased survival of cortical neurons, whereas d120 shows cytotoxic effects. Survival of astrocytes is equally reduced by both HSV deletion mutants. We conclude that HSV-1 mutants defective in immediate early genes cause very distinct cytopathic phenotypes depending on the cellular context. Possible reasons for these differences, like various patterns of cellular and viral gene expression, and the implications for the use of HSV-1 vectors for gene transfer are discussed.

Animals↗
PubMed2000

GABA neurons provide a rich input to microvessels but not nitric oxide neurons in the rat cerebral cortex: a means for direct regulation of local cerebral blood flow.

Basal forebrain neurons project to microvessels and the somata of nitric oxide (NO) synthase-containing neurons in the cerebral cortex, and their stimulation results in increases in cortical perfusion. gamma-Aminobutyric acid (GABA) is the second major neurotransmitter synthesized by these neurons and it has also been reported to modify cerebromicrovascular tone. We thus investigated by light and electron microscopy the association of GABA neurons (labeled for glutamic acid decarboxylase [GAD]) with cortical microvessels and/or NO neurons (identified by nicotinamide adenine dinucleotide [NADPH-D] histochemistry) within the frontoparietal and perirhinal cerebral cortex in the rat. On thick and semithin sections, a high density of GAD puncta was observed, several surrounded intracortical blood vessels and neuronal perikarya. In contrast, NADPH-D cell somata and proximal dendrites were only occasionally contacted by GAD nerve terminals. Perivascular and perisomatic GAD appositions were identified at the ultrastructural level as large (0.44-0.50 microm(2)) neuronal varicosities located in the immediate vicinity of, or being directly apposed to, vessels or unstained neuronal cell bodies. In both cortical areas, perivascular GAD terminals were located at about 1 microm from the vessels and were seen to frequently establish junctional contacts (synaptic frequency of 25-40% in single thin sections) with adjacent neuronal but not vascular elements. Ibotenic or quisqualic acid lesion of the substantia innominata did not significantly affect the density of cortical and perivascular GAD terminals, suggesting that they mostly originated locally in the cortex. These results suggest that GABA terminals can interact directly with the microvascular bed and that the somata and proximal dendrites of NO neurons are not a major target for cortical GABA neurotransmission. However, based on the colocalization of GABA and NADPH-D in a subset of cortical neurons, we suggest that these interneurons could be implicated in the cortical vascular response elicited by stimulation of basal forebrain neurons.

Animals↗
PubMedDate not supplied

Distribution of dopamine-immunoreactive neuronal perikarya and fibres in the brain of a teleost, Gasterosteus aculeatus L. comparison with tyrosine hydroxylase- and dopamine-beta-hydroxylase-immunoreactive neurons.

The distribution of dopamine in the brain of the teleost Gasterosteus aculeatus L. was demonstrated with the indirect peroxidase-antiperoxidase immunohistochemical method using highly specific antibodies against a dopamine-glutaraldehyde-thyroglobulin conjugate. Dopamine-immunoreactive (DAir) neuronal somata were observed in all main brain regions. In the forebrain, DAir neurons were located in a continuous cell column extending from the caudal part of the olfactory bulbs to the preoptic area. The neurons lie lateral to the dorsal (and caudally to the subcommissural) portion of the ventral telencephalic area, and ventromedial to the central nuclei of the dorsal area. In the diencephalon, cerebrospinal fluid-contacting neurons were located in the paraventricular organ and in the subependymal layers of the dorsal and caudal zones of the periventricular hypothalamus. Small DAir neurons were observed in the suprachiasmatic nucleus, in the parvocellular preoptic nucleus and in the ventromedial thalamic nucleus, while large perikarya were observed dorsolateral to the dorsal zone of the periventricular hypothalamus ('PVO-accompanying cells'), in the posterior tuberal nucleus and in the most rostral portion of the mammillary bodies. Numerous small DAir neurons were located in the periventricular pretectal nucleus. In the brainstem, DAir neurons were observed in the isthmus region, in the dorsal raphe nucleus and in the lateral parts of the nucleus of the solitary tract. DAir perikarya were also observed in the area postrema. Direct comparison with the distribution of tyrosine hydroxylase- and dopamine-beta-hydroxylase-immunoreactivity (THir and DBHir) gave the following results: THir neurons were found in all areas where DAir neurons were located, except for the paraventricular organ and the dorsal and caudal zones of the periventricular hypothalamus, which were devoid of THir. DBHir (putatively noradrenergic or adrenergic) neurons were observed in the lateral parts of the nucleus of the solitary tract, and in the isthmus region. The DBHir neurons in the isthmus region, which have previously been shown to be noradrenergic, appeared to be identical with the THir and DAir neurons of the same area. DAir axons were found in high numbers in most parts of the brain. Especially dense innervation was found in the ventrolateral and posterior parts of the dorsal telencephalic area, the region surrounding the lateral recesses of the third ventricle, the interpeduncular nucleus, the dorsal and median raphe nuclei (the rostral raphe nuclei), and in the nucleus of the solitary tract.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Relationship between differentiation and terminal mitosis: chick sensory and ciliary neurons differentiate after terminal mitosis of precursor cells, whereas sympathetic neurons continue to divide after differentiation.

A population of undifferentiated cells has been characterized during the early development of nodose and ciliary ganglia. This population is defined by the absence of surface markers specific for neurons (tetanus toxin receptor, Q211 antigen) and for glial cells (O4 antigen). These undifferentiated cell populations were isolated from the ganglia and were shown to contain neuronal precursor cells that were able to differentiate in vitro into neurons, as characterized by morphology and surface antigens. Undifferentiated cells were detected during the period of neuronal birth, indicating that dividing neuronal precursor cells do not express neuron-specific surface markers. This was directly shown by 3H-thymidine-labeling studies using nodose ganglia, ciliary ganglia, and dorsal root ganglia. In sympathetic ganglia, however, no undifferentiated neuronal precursor cells were detectable at developmental stages when sympathetic neurons are born. 3H-Thymidine injected during that stage at E7 was incorporated into cells expressing the neuronal markers tetanus toxin receptor and Q211 antigen. Quantitative fluorimetric determination of the DNA content of dissociated sympathetic ganglion cells demonstrated the presence of a population of Q211-positive sympathetic ganglion cells in the G2 phase of the cell cycle. E7 sympathetic ganglion cells expressing neuronal surface markers were also shown to be able to divide in vitro. We have concluded that the relationship between terminal mitosis and the onset of differentiation differs between ganglia of the chick peripheral nervous system: Sympathetic ganglion cells continue to divide after the acquisition of neuronal properties, whereas neuronal precursor cells from other autonomic and sensory ganglia start to differentiate after a terminal mitosis.

Animals↗
PubMed1985

Neural mechanisms of motor program switching in the mollusc Pleurobranchaea. III. Role fo the paracerebral neurons and other identified brain neurons.

Identified neurons in the cerebropleural ganglion (brain) of the mollusc Pleurobranchaea were stimulated and recorded from intracellularly while recording the identified motor program from buccal muscles (reduced preparation) or nerves (isolated central nervous system). Neurons studied included the metacerebral giant neurons (MCGs), phasic paracerebral neurons (PCp's), polysynaptic excitors of the PCp's (PSEs), type II electrotonic neurons (ETII's), type I electrotonic neurons (ETI's) and several other identified neurons or neuronal classes. Intracellular stimulation of the above identified neurons generally elicited the ingestion motor program or its characteristic components, but never the egestion motor program and seldom its characteristic components. Intracellular recordings from these neurons in the isolated central nervous system preparation while eliciting the ingestion and egestion motor program generally showed cyclic membrane potential oscillations in phase with both motor programs, indicating that these neurons receive synaptic feedback from the ingestion and egestion central pattern generator(s). This study is therefore consistent with the view that an interrelated cluster of brain neurons is specialized to command the ingestion motor program. A neural model of motor program switching in the buccal motor system is formulated, comprising separate command pathways for ingestion and egestion that converge on a common central pattern generator(s).

Animals↗
PubMed1995

Ontogenically related properties of N-methyl-D-aspartate receptors in rat hippocampal neurons and the age-specific sensitivity of developing neurons to lead.

The sensitivity of N-methyl-D-aspartate- (NMDA) induced whole-cell and single-channel currents to Pb2+ was studied in neurons acutely dissociated from the hippocampus of 3- to 30-day-old rats. The amplitude of NMDA-induced whole-cell currents in the neurons increased with age of the animals until they were 10 to 12 days old, thereafter remaining nearly unchanged. As in cultured hippocampal neurons, Pb2+ at both 10 and 30 microM inhibited NMDA-induced currents, and the sensitivity of the currents to Pb2+ decreased with age of the rats. The sensitivity correlated with the age-related expression of two components of the NMDA-induced currents, one that was fast decaying and more prominent in younger neurons, and the other slowly decaying. Inhibition of the fast component by Pb2+ was always greater than that of the slow component, which may explain the greater sensitivity of younger neurones to Pb2+. may explain the greater sensitivity of younger neurons to Pb2+. The use of trypsin during acute dissociation of the neurons did not qualitatively alter the findings, although in the trypsin-treated neurons the currents were 65% smaller, and the EC50 for NMDA and glycine for the slow component were both about two times greater than in the untreated neurons; in the case of the fast component, the EC50s for NMDA and for glycine were not significantly altered. In outside-out patches excised from acutely dissociated hippocampal neurons, Pb2+ decreased the frequency of NMDA-activated channel openings without altering the mean channel open time. Our results are in agreement with those reported for embryonic neurons that developed in culture, and indicate that NMDA receptors expressed in hippocampal neurons of young animals are key target sites for the neurotoxic actions of Pb2+.

Aging↗
PubMed1999

Synthesis of the antioxidant glutathione in neurons: supply by astrocytes of CysGly as precursor for neuronal glutathione.

Deficiency of the antioxidant glutathione in brain appears to be connected with several diseases characterized by neuronal loss. To study neuronal glutathione metabolism and metabolic interactions between neurons and astrocytes in this respect, neuron-rich primary cultures and transient cocultures of neurons and astroglial cells were used. Coincubation of neurons with astroglial cells resulted within 24 hr of incubation in a neuronal glutathione content twice that of neurons incubated in the absence of astroglial cells. In cultured neurons, the availability of cysteine limited the cellular level of glutathione. During a 4 hr incubation in a minimal medium lacking all amino acids except cysteine, the amount of neuronal glutathione was doubled. Besides cysteine, also the dipeptides CysGly and gammaGluCys were able to serve as glutathione precursors and caused a concentration-dependent increase in glutathione content. Concentrations giving half-maximal effects were 5, 5, and 200 microM for cysteine, CysGly, and gammaGluCys, respectively. In the transient cocultures, the astroglia-mediated increase in neuronal glutathione was suppressed by acivicin, an inhibitor of the astroglial ectoenzyme gamma-glutamyl transpeptidase, which generates CysGly from glutathione. These data suggest the following metabolic interaction in glutathione metabolism of brain cells: the ectoenzyme gamma-glutamyl transpeptidase uses as substrate the glutathione released by astrocytes to generate the dipeptide CysGly that is subsequently used by neurons as precursor for glutathione synthesis.

Animals↗
PubMed1986

Anatomy and physiology of saccadic burst neurons in the alert squirrel monkey. II. Inhibitory burst neurons.

Electrophysiological and intracellular labelling studies in the cat have identified a population of saccadic burst neurons in the medullary reticular formation that have an inhibitory, monosynaptic projection to the contralateral abducens nucleus. In the present study, intraaxonal recording and injection of horseradish peroxidase were used to identify and characterize the corresponding population of inhibitory burst neurons (IBNs) in the alert squirrel monkey. Squirrel monkey IBNs are located in the reticular formation ventral and caudal to the abducens nucleus and project contralaterally to the abducens. Additional contralateral projections are present to the vestibular nuclei, the nucleus prepositus, and the pontine and medullary reticular formation rostral and caudal to the abducens. All neurons fire a burst of spikes during saccades and are silent during fixation. In most neurons the burst begins 5-15 msec before saccade onset. The number of spikes in the saccadic burst is linearly related to the amplitude of the component of the saccade in the neuron's on-direction. Linear relationships also exist between burst duration and saccade duration and between firing frequency and instantaneous eye velocity. For all neurons, the on-direction is in the ipsilateral hemifield, with a vertical component that may be either upward or downward. Neurons with projections to the vertically related descending and superior vestibular nuclei tend to have on-directions with larger vertical components than neurons that lack these projections. These results, together with those on excitatory burst neurons reported in the preceding paper, demonstrate a reciprocal organization of burst neuron input to the abducens in the monkey similar to that found in the cat and indicate a major role for these neurons in generating the oculomotor activity in motoneurons as well as in other classes of premotor neurons.

Animals↗