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PubMed2002

[Localization of non-monoaminergic aromatic L-amino acid decarboxylase neurons (D-neurons) in the human striatum and their functional significance].

It has recently been reported that the human corpus striatum, especially its ventral part, named as the nucleus accumbens, contains numerous non-monoaminergic aromatic L-amino acid decarboxylase (AADC; the second-step monoamine synthesizing enzyme) neurons (D-neurons). D-neurons are the neurons immunoreactive for AADC but not immunoreactive for dopamine or serotonin. They lack the first-step monoamine synthesizing enzymes, tyrosine hydroxylase and tryptophan hydroxylase. AADC is also the rate-limiting enzyme of phenylethylamine (PEA) synthesis. D-neurons might participate in the manifestation of efficacy of pharmacotherapy for Parkinson's disease by uptaking monoamine precursors including L-dopa or droxidopa (L-threo-DOPS) and by converting them to dopamine or noradrenaline, respectively. As the nucleus accumbens is one of the brain regions that are involved in the pathogenesis of schizophrenia and drug dependence, D-neurons might be related to the etiology of these mental disorders. It has also been suggested that striatal D-neurons are the pluripotential cells that have compensating functions against aging or degeneration.

Aromatic-L-Amino-Acid Decarboxylases↗
PubMed2002

[Types of neuron death induced by recurrently epileptic discharge in cultured hippocampal neurons].

OBJECTIVE: To explore the mechanism of hippocampal neuron loss in temporal epileptic patients. METHODS: Hippocampal neurons from neonatal rats were taken and a Sombati's epileptic model was established. DNA ladder electrophoresis, TUNEL staining, fluorescence labeling and flow cytometry were used to detect and to quantitate dead neurons. RESULTS: After the treatment of culture solution without magnesium, epileptic discharge occurred. Three to twenty-four hours after treatment, the percentage of necrotic cells in the model group was higher than that in the control group. The difference of percentage of necrotic cells between the two groups was the greatest 6 hours after the treatment (14.65% vs 8.33%). There was no difference in the percentage of necrotic cells between the 2 groups since 24 hours after the treatment. The neuronal apoptosis began at the 6th hour after epileptic discharge. The percentage of apoptic cells in the model group was 14.65%, significantly higher than that in the control group (11.2%, P < 0.01). With the going on of the epileptic process, the difference in percentage of apoptotic neurons between the 2 groups kept on increasing. CONCLUSION: Recurrent epileptic discharge leads to necrosis of neurons in the early stage and induces apoptosis of neurons in the latter stage. The specific death pattern depends on multiple factors.

Animals↗
PubMed1990

Kainic acid on neostriatal neurons intracellularly recorded in vitro: electrophysiological evidence for differential neuronal sensitivity.

The electrophysiological effects produced by different concentrations of kainic acid (KA) were studied by utilizing intracellular recordings from neostriatal slices. In most of the recorded cells (81%), concentrations of KA ranging between 10 and 300 nM produced reversible and dose-dependent membrane depolarizations. Higher concentrations of this agonist caused larger depolarizations and changes of the membrane properties of the recorded neurons not reversible during the time of recording. In a smaller percentage (19%) of the recorded cells, 10-100 nM KA did not produce significant membrane depolarizations; in these neurons, the depolarizations produced by higher concentrations of KA were small and reversible. The 2 populations of neurons showed similar electrophysiological properties and did not reveal differential sensitivity to quisqualic acid (QUIS; 10-30 microM) or to NMDA (10-30 microM). Tetrodotoxin (TTX; 1 microM) did not reduce the depolarizations produced by KA and by NMDA. Low-calcium, cobalt-containing solutions abolished the effects produced by NMDA, but not the KA-induced depolarizations. Kynurenic acid (500 microM) significantly antagonized the depolarizations produced by KA and reduced the changes of the membrane properties caused by high doses of this agonist. In several neurons, KA induced bicuculline-sensitive synaptic depolarizing potentials. Our findings suggest the presence of 2 subpopulations of neostriatal neurons showing differential postsynaptic sensitivity to KA. The differential sensitivity of neostriatal neurons to KA might influence the responses of these cells to glutamatergic cortical inputs and the degenerative changes observed in neostriatal neurons in some pathological conditions.

Action Potentials↗
PubMed1996

Myelin basic protein gene expression in neurons: developmental and regional changes in protein targeting within neuronal nuclei, cell bodies, and processes.

The myelin basic protein (MBP) gene is part of the golli-mbp gene complex. In mouse, the golli-mbp gene produces two families of mRNAs from different transcription start sites that generate either MBPs or golli proteins (which contain MBP sequences in addition to unique peptide sequences). In situ hybridization and immunocytochemical analyses indicate that golli products are expressed in selected neuronal populations in postnatal mouse brain, in addition to oligodendrocytes, as shown earlier. The principal subcellular location of golli proteins in neurons was in axonal and dendritic processes. In a small subset of neurons, golli proteins were located in nuclei. With development and neuronal maturation, golli-mbp expression decreased and/or there was a striking shift in subcellular localization from nuclei and cell soma to the cell processes in specific neuronal populations. Golli protein was localize in neurites of migrating cerebellar granule cells, but it shifted to a nuclear localization when the cells took up residence in the internal granule cell layer. In some regions, (e.g., olfactory bulb and cerebellum) golli proteins were expressed over the entire postnatal period examined (birth to 75 d). The unique patterns of developmental expression within individual populations of neurons, and the unusual shift in subcellular localization of golli proteins with neuronal migration and maturation, suggest a complex regulation of this gene at both the transcriptional and posttranslational levels. The data also suggest that the cellular function(s) of the golli proteins is very different from the structurally related MBPs.

Animals↗
PubMed1998

Selective neuronal expression of green fluorescent protein with cytomegalovirus promoter reveals entire neuronal arbor in transgenic mice.

In simple nervous systems, identified groups of neurons can be studied in depth. To allow the same advantage in the mammalian brain, we have generated green fluorescent protein (GFP) transgenic mice in which only a few types of neurons are strongly labeled with a fluorescent molecule, which the neurons synthesize internally, allowing the cells, their dendrites, filopodia, and axons to be identified in both living and fixed CNS, in slices and culture. The same neurons, with GFP expression controlled by part of the major immediate early promoter of human cytomegalovirus (CMV), show GFP beginning early in development, from one generation to the next, allowing cellular and physiological studies of axonal and dendritic growth, fate mapping, anatomical connections, and synapse formation in identified neurons. The human CMV promoter sequence we used was different from that used in previous work with other reporter genes and gave a dramatically different pattern of expression. Two transgenic lines with the same CMV promoter show similar anatomical patterns of expression in the present study. Strong GFP labeling was found in a subpopulation of mossy fibers that innervated parasagittal bands in the cerebellar cortex and olfactory axons that projected into the olfactory bulb, subsets of motoneurons and dorsal root ganglion cells, granule but not mitral cells of the olfactory bulb, and a group of neurons in the hypothalamic suprachiasmatic nucleus. A novel type of neuron was strongly labeled in the olfactory bulb external plexiform layer. In normal brains, CMV does not constitute a threat, but in the developing brain, CMV can cause debilitating neurodegeneration and death; studies using the CMV promoter aid in understanding the affinity of CMV that has been suggested for specific brain regions.

Animals↗
PubMed1997

Local circuit neurons of macaque monkey striate cortex: IV. Neurons of laminae 1-3A.

We continue our Golgi studies (Lund [1987] J. Comp. Neurol. 257:60-92; Lund et al. [1988] J. Comp. Neurol. 276:1-29; Lund and Yoshioka [1991] J. Comp. Neurol. 331:234-258) of the organization of local circuit, largely gamma-aminobutyric acid (GABA)-containing neurons in macaque monkey visual cortex, area V1, with this account of the local circuit neurons lying in layers 1 and 2/3A. These layers receive intrinsic interlaminar excitatory and inhibitory relays from layers 3B, 4A, 4B, and 5. We describe seven varieties of local circuit neurons with somata within layers 1-2/3A, and we compare the lateral scale of spread of the axons and dendrites of these neurons with the size of the columnar connectional patch domains made by the laterally spreading axon collaterals of pyramidal neurons within the superficial layers (Lund et al. [1993] Cerebral Cortex 3:148-162). We conclude from this comparison that all of the neurons have dendritic fields that are limited to single patch domains. Furthermore, only two of the seven local circuit neuron varieties have sufficient axon spread to influence territory beyond single domains, reaching into neighboring territory likely to differ in function from that occupied by their dendrites. We have identified descending projections from particular varieties to layers 3B, 4A, 4B, and 5 and to the white matter. We discuss the contributions that these interneurons may make to function within the superficial cortical layers, and we summarize our overall conclusions, so far, from our set of studies on interneurons within area V1 of the macaque.

Animals↗
PubMed1999

Protein kinase C and cAMP-dependent protein kinase regulate the neuronal differentiation of immortalized raphe neurons.

These studies examined the extent to which protein kinase C (PKC) and cAMP-dependent protein kinase (PKA) regulate the neuronal differentiation of the raphe-derived neuronal cell line, RN33B. A differentiation-specific 2.25-fold increase in soluble PKA activity was observed. Neither membrane-associated-PKA, -PKC, or soluble PKC activities changed concomitant with differentiation. The PKC activity was derived from PKC alpha, gamma, epsilon, and theta isoenzymes. Activation of PKC inhibited the immunocytochemical expression of low and medium molecular weight neurofilament proteins, an effect due at least in part to decreased steady-state levels of protein. PKC activation also decreased glutamate immunoreactivity and increased cell number, protein synthesis, and bromodeoxyuridine uptake by 2.4-fold, 25%, and 32%, respectively. Coupled with the decrease in mature neuronal antigen expression, these data suggest that PKC activation inhibits neuronal differentiation by inducing proliferation. Inhibition of PKC markedly upregulated glutamate immunoreactivity. PKA activation potentiated the glutamatergic phenotype of RN33B cells, but inhibition of PKA was without effect on the expression of all neuronal antigens examined. Thus, both PKC and PKA regulate the differentiation of RN33B cells, although neither is absolutely necessary for expression of the differentiated neuronal phenotype. These results suggest the existence of parallel pathways regulating raphe neuronal differentiation.

Animals↗
PubMed1989

Expression of synaptophysin and neuron-specific enolase during neuronal differentiation in vitro: effects of dimethyl sulfoxide.

Neural development in dissociated cell cultures of fetal rat brain can be expected to depend on synaptic interactions between cultured neurons. Therefore, an attempt was made to obtain a quantitative measure of the time course of synaptogenesis in such a culture system by assessing the level of the secretory vesicle-associated protein synaptophysin (p38). The developmental schedule of p38 was compared to that of neuron-specific enolase (NSE), an established marker of neuronal differentiation. Cultures were raised from dissociated 14 day-old fetal rat diencephalon. In cultures grown for 1-2 days in vitro (DIV), p38-immunoreactivity was preferentially located in neuronal perikarya. After 10-16 DIV, neurons in culture had formed a dense neuritic network, and almost all of the p38-immunoreactivity occurred in the form of fine punctate deposits associated with neuronal processes that often outlined neuronal cell bodies in a basket-like fashion. Electron-microscopic immunocytochemistry proved the punctate deposits to be presynaptic elements, mostly in the form of axonal varicosities. Quantitative immunoblotting showed that levels of p38 increased from the start of cultivation to DIV 4, stayed fairly constant from DIV 4 to DIV 8, and rose again steeply to peak at DIV 12. In contrast, levels of NSE rose continuously up to DIV 12. After DIV 12, levels of both p38 and NSE fell again. Treatment of cultures with dimethyl sulfoxide (DMSO), an agent known to induce differentiation in various normal and malignant cell types, resulted in a significant increase of p38 levels and in a decrease of NSE levels. The amount of p38 continued to increase beyond DIV 12, whereas NSE diminished after having reached a maximum at DIV 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Increased neuronal responsiveness to cholecystokinin and dopamine induced by lesioning mesolimbic dopaminergic neurons: an electrophysiological study in the rat.

In the rat, cholecystokinin (CCK) and dopamine (DA) coexist in a subpopulation of neurons of the ventral tegmental area (VTA) projecting to the nucleus accumbens. However, in the dorsal hippocampus, dopaminergic projections from the VTA do not contain CCK, the latter neurotransmitter being mainly localized in intrinsic hippocampal neurons. The present experiments were undertaken in order to compare the interactions of CCK and DA and the effects of lesioning VTA dopaminergic neurons in a region where these neurotransmitters coexist and in one where they do not. The effects of microiontophoretic applications of CCK, kainate (KA), glutamate (GLU) and DA were determined in control rats and in rats pretreated with a local injection of 6-hydroxydopamine (6-OHDA) in the VTA. In the nucleus accumbens and in the hippocampus of intact rats, DA exerted a similar depressant effect whether applied during CCK-, KA- or GLU-induced activations. The 6-OHDA lesion enhanced responsiveness of accumbens neurons to KA, GLU and CCK (the responsiveness to this latter peptide being increased by more than 15-fold) and the depressant effect of DA when applied during neuronal activation by KA or GLU but not when the same neurons were activated with CCK. In the dorsal hippocampus, the 6-OHDA lesion enhanced neuronal responsiveness to KA and DA in the CA1, but not in the CA3 region, whereas the responsiveness to CCK remained unchanged in both regions. These results suggest a physiological role for the coexistence of CCK and DA in the nucleus accumbens. The induction of a supersensitivity to DA in the CA1, but not in the CA3, region of the dorsal hippocampus following a VTA lesion is consistent with the regional distribution of the dopaminergic innervation in this structure.

Action Potentials↗
PubMed1989

Effect of fluorodeoxyuridine on neurons and non-neuronal cells in cerebral explants.

Fetal rat brain neurons are reported to show enhanced neurite development when treated with the mitotic inhibitors fluorodeoxyuridine (FUdR) or cytosine arabinoside (AraC). For AraC-treated rat cerebral explants, increased neurite growth occurs along with a change in the composition of the non-neuronal cell population and diminished non-neuronal cell proliferation. FUdR-treated rat cerebral explants were therefore cultured in an attempt to determine whether FUdR encourages neurite outgrowth by changing the composition and number of non-neuronal cells. Quantitative morphological analyses revealed a significant decrease in the incidence of non-neuronal cells, and an increase in neurite outgrowth for the FUdR-treated explants. These explants also exhibited an increased proportion of protoplasmic astrocytic-epithelial cells and a decreased proportion of fibroblastic-reactive microglial cells. Thus, FUdR may encourage neurite outgrowth through a curtailment of non-neuronal cell proliferation (primarily by fibroblastic-reactive microglial cells) and through the creation of a non-neuronal cell environment consisting almost entirely of protoplasmic astrocytes.

Animals↗
PubMed1995

Action of intravenously administered talipexole on the rat striatal neurons receiving excitatory input from nigral dopamine neurons.

Electrophysiological studies using rats anesthetized with chloral hydrate were performed to elucidate whether or not intravenously injected talipexole acted as a D2 receptor agonist on the striatal neurons in comparison with the action of bromocriptine. The activities of the striatal neurons were extracellularly recorded using a glass microelectrode attached along a seven-barreled micropipette, each barrel of which was filled with talipexole, bromocriptine, SCH23390 (D1 antagonist), domperidone (D2 antagonist), glutamate or 2 M NaCl. These drugs were iontophoretically applied to the immediate vicinity of the target neuron being recorded. The effects of talipexole and bromocriptine were examined on the neurons, whose spikes (induced by the stimulation of the substantia nigra pars compacta) were inhibited by the iontophoretic application of domperidone. Iontophoretic application of talipexole or bromocriptine increased spontaneous firing of these neurons and this increase in firing was also inhibited by iontophoretically applied domperidone. In the same neurons, intravenously administered talipexole (0.01, 0.02 and 0.04 mg/kg) dose-dependently increased firing, and this increase was inhibited by microiontophoretically applied domperidone, but not by SCH23390. On the other hand, the intravenous injection of bromocriptine (0.1, 0.2 and 0.4 mg/kg) also increased the firing rate. However, the increase was not dose-dependent and fluctuated; the firing transiently decreased during the increase in firing with intravenously administered bromocriptine. However, the bromocriptine-induced increase in firing was also suppressed by domperidone, and decrease in firing was inhibited by SCH23390. These findings suggest that talipexole acts as a D2 agonist on the striatal neurons receiving input from substantia nigra pars compacta and increases firing when intravenously applied.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Single unit activity of noradrenergic neurons in locus coeruleus and serotonergic neurons in the nucleus raphe dorsalis of freely moving cats in relation to the cardiac cycle.

Single unit activity of serotonergic (5-HT) neurons in the nucleus raphe dorsalis (NRD) and of noradrenergic (NE) neurons in the locus coeruleus (LC) was recorded in relation to the cardiac cycle in awake, freely moving cats. The discharge of NRD-5-HT neurons showed no relationship to the cardiac cycle, while LC-NE neurons displayed a cardiac periodicity such that the units were most likely to fire from 80 to 180 ms after the peak of the cardiac r-wave (diastole), and least likely to fire during the period from 40 ms before to 60 ms after the r-wave (systole). The strength of this periodicity was inversely related to the discharge rate of individual cells. Exposure to a noxious environmental stimulus (15 min of 100 dB white noise) greatly attenuated the cardiac relationship of LC-NE neurons. A blood volume expansion of approximately 15% (9.0 ml/kg b. wt.) decreased unit rate by about 25%, but did not alter either the timing or the magnitude of the LC-NE cardiac relationship. These data are discussed in terms of the participation of NRD-5-HT and LC-NE neurons in cardiovascular function, and the possible role of LC-NE neurons in short- and long-term volume homeostasis.

Action Potentials↗
PubMed1995

Cultured rat striatal and cortical astrocytes protect mesencephalic dopaminergic neurons against hydrogen peroxide toxicity independent of their effect on neuronal development.

Reactive oxygen species (ROS), including hydrogen peroxide, are supposed to be involved in the degeneration of dopaminergic neurons in Parkinson's disease. The potential role of astrocytes against neurotoxic effects of ROS was studied in cocultures of rat mesencephalic neurons and rat striatal or cortical astrocytes. Neuronal [3H]dopamine uptake, a marker of dopaminergic neuron integrity, was enhanced by striatal astrocytes, but not by cortical astrocytes, compared to uptake in mesencephalic neurons cultured alone. Whereas hydrogen peroxide at concentrations up to 100 microM reduced the [3H]dopamine uptake in neuronal cultures, no reduction of the uptake was observed in cocultures, regardless of the origin of the supporting astrocytes. These results suggest that astrocyte mediated protection of neurons against hydrogen peroxide induced toxicity is not directly related to a region-specific neurotrophic effect.

Animals↗
PubMed1985

Cerebral neocortical neurons in the aged rat: spontaneous activity, properties of pyramidal tract neurons and effect of acetylcholine and cholinergic drugs.

The properties of cortical cerebral neurons have been studied and compared in 2, 22 and 26 month-old Sprague-Dawley rats, using electrophysiological techniques. The mean spontaneous activity of the neurons in old animals (unidentified as well as pyramidal tract neurons) was not different from that of young adult rats. In contrast the mean latency of the antidromic response of pyramidal tract neurons to pyramidal tract stimulation was significantly longer in 26 month-old animals. No difference was observed in the effects of the excitatory amino acid glutamate applied by iontophoresis. The percentage of cortical neurons excited by the iontophoretic application of acetylcholine was similar in young and old animals. Neither the laminar distribution, nor the individual sensitivity of these neurons to acetylcholine were found to be modified. The pharmacological properties of the acetylcholine-induced excitations were unchanged, exhibiting muscarinic as well as nicotinic properties. These results are consistent with the suggestion that the impairment of the cholinergic system with aging is for a large part presynaptic. They also emphasize the fact that several physiological and pharmacological properties of the cerebral cortical neurons show little change with age in Sprague-Dawley rats.

Acetylcholine↗
PubMed1986

Behavior of neurons in the abducens nucleus of the alert cat--II. Internuclear neurons.

The activity of 43 antidromically identified abducens internuclear neurons with conduction velocities ranging from 14 to 54 m/s was analyzed in alert cats during spontaneous and vestibular induced eye movements. The discharge rate of internuclear neurons significantly increased with successive adducting positions of the contralateral eye. Slopes of rate-position (k) relationships ranged from 3.1 to 17.9 spikes/deg (mean 12.01 +/- 3.1). Threshold ranged from -19 degrees to +3 degrees. Frequency saturation was never observed for any internuclear neuron within the oculomotor range. Although straight lines were selected to illustrate the rate-position relationships, exponential curves always provided the best statistical fit demonstrating that an enhancement in frequency potentiation (k) must accompany more eccentric fixations in the on direction. Internuclear neurons showed a low variability in firing rate (less than 3.0%) for fixations less than 1 s. Variability increased with both longer and repeated fixations of the same eye position. Discharge rates were found to depend upon both the direction of the preceding eye movement and the animal's level of alertness. Separate regression lines of rate-position relations following saccades in the on and off directions differed significantly in slope (100%), but not threshold. The observed static hysteresis in an identified non-motoneuron shows this property to be in a central neural circuit prior to the extraocular motoneuron. The slopes (k) of rate-position plots for all internuclear neurons decreased significantly (100%) when level of alertness changed from "alert" (1 +/- 0.2 saccades/s) to "drowsy" (0.5 +/- 0.2 saccades/s). Thresholds, however, were not significantly altered. Discharge rate of abducens internuclear neurons increased abruptly 10.4 +/- 2.5 ms preceding saccades in the on direction, and decreased 20.5 +/- 7.8 ms before saccades in the off direction. Internuclear neuronal activity was not affected by pure vertical saccades. During on direction saccades, firing frequency did not saturate, but increased with velocity in a linear fashion. Exponential functions often fit the data better due to the difference in slopes of rate-velocity plots for on vs off direction saccades. Slopes (rs) of rate-velocity regression lines during spontaneous saccades ranged from 0.99 to 4.10 spikes/s/deg/s (mean 2.16 +/- 0.93). During saccades in the off direction activity always decreased, but it seldom ceased. Rate-velocity regression lines measured during the fast phase of vestibular nystagmus (rsv = 2.09 +/- 0.88) showed no significant differences from rs slopes in 82% of the cases.(ABSTRACT TRUNCATED AT 400 WORDS)

Abducens Nerve↗
PubMed1990

Inhibition of an identified snail postsynaptic neuron evoked by stimulation of a peptidergic interneuron initiating bursting pacemaker activity in another neuron.

Beating neuron V8, whose activity is abolished upon interneuronal stimulation, has been found and identified in the CNS of the snail, Helix pomatia. It was found earlier that stimulation of the same interneuron initiates bursting pacemaker activity in another neuron. Under voltage clamp conditions interneuronal stimulation evoked a slow outward current in the V8 neuron with a latency of about 2 s. Intracellular injection of tetraethylammonium or Cs+ ions into the interneuron greatly increased the slow outward current amplitude. External application of CdCl2 (1 mM), LaCl3 (5 mM) or replacement of Ca2+ by Mg2+ ions reversibly abolished transmission between the interneuron and the V8 neuron. The neuronal membrane conductance increased by about three times on the maximum of the slow outward current development. Computer fitting showed that a decay of the slow outward current can be approximated by the sum of two exponentially decaying components with time constants of about 1 s and 16 s. Extrapolated reversal potential for a fast (1 s) component of the current was about -70 mV. A slow (16 s) component asymptotically decreased upon hyperpolarization and it was observed at even more negative potential than Ek. Theophylline (1 mM) and 3-isobutyl-1-methylxanthine (0.1 mM) reversibly increased the slow outward current amplitude, whereas imidazole (5 mM) and tolbutamide (5 mM) caused its reversible decrease. It is concluded that inhibitory monosynaptic transmission exists between the interneuron and the beating V8 neuron. Interneuronal simulation evokes an increase in the membrane potassium conductance and probably a decrease in stationary potential-dependent sodium conductance of the postsynaptic V8 neuron. The cellular cyclase system seems to be involved in the postsynaptic response.

Action Potentials↗
PubMed2005

The UNC-3 Olf/EBF protein represses alternate neuronal programs to specify chemosensory neuron identity.

Neuronal identities are specified by the combinatorial functions of activators and repressors of gene expression. Members of the well-conserved Olf/EBF (O/E) transcription factor family have been shown to play important roles in neuronal and non-neuronal development and differentiation. O/E proteins are highly expressed in the olfactory epithelium, and O/E binding sites have been identified upstream of olfactory genes. However, the roles of O/E proteins in sensory neuron development are unclear. Here we show that the O/E protein UNC-3 is required for subtype specification of the ASI chemosensory neurons in Caenorhabditis elegans. UNC-3 promotes an ASI identity by directly repressing the expression of alternate neuronal programs and by activating expression of ASI-specific genes including the daf-7 TGF-beta gene. Our results indicate that UNC-3 is a critical component of the transcription factor code that integrates cell-intrinsic developmental programs with external signals to specify sensory neuronal identity and suggest models for O/E protein functions in other systems.

Animals↗
PubMedDate not supplied

The origin of fluorescence in the neuronal ceroid lipofuscinoses (Batten disease) and neuron cultures from affected sheep for studies of neurodegeneration.

Lipofuscin and ceroid are usually held responsible for impaired cellular performance, via oxidative damage and the irreversible accumulation of fluorescent products of lipid peroxidation. The neuronal ceroid lipofuscinoses (NCLs, Batten disease) are inherited neurodegenerative diseases characterized by intracellular accumulation of fluorescent lipofuscin-like bodies. However these bodies are lysosomes packed with a particular protein, subunit c of mitochondrial ATP synthase; not the result of oxidative damage. No individual storage body component was fluorescent nor were solutions of total storage bodies. UV-vis spectra confirmed the lack of a fluorophor. Crystals of non-fluorescent albumin and reconstituted storage bodies were fluorescent in glycerol suspensions. This fluorescence is probably caused by interference of light reflected from the protein array, as is often observed in protein crystals. Other lipofuscins may be secondary lysosomes with a high protein content and the source of fluorescence the same. The neurodegeneration associated with lipofuscin accumulation may be caused by that accumulation, or may be a separate manifestation of aging. Neuronal cell cultures offer a way to study these processes. Subunit c accumulation has been observed in cerebral bipolar neurons cultured from 90 day NCL affected sheep foetuses. Neurons from different parts of the brain behave differently. Normal 108 day cerebellar granule neurons migrated into clumps when cultured with tri-iodothyronine, but affected cerebellar neurons did not, nor did normal or affected cerebral neurons.

Journal Article↗