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PubMed1999

Gene expression of histamine H1 receptor in guinea pig primary sensory neurons: a relationship between H1 receptor mRNA-expressing neurons and peptidergic neurons.

Pharmacological studies have suggested that a subgroup of primary sensory neurons is responsive to histamine via the histamine H1 receptor. We addressed this issue using in situ hybridization histochemistry with a cRNA probe for the guinea pig H1 receptor gene. About 15% of the trigeminal and lumber dorsal root ganglion (DRG) neurons, but none of nodose ganglion neurons, were intensely labeled with this probe. The H1 receptor mRNA-positive neurons were exclusively small in size, and were demonstrated to give rise to unmyelinated fibers by ultrastructural analysis of isolectin B4-labeling. However, the H1 receptor mRNA-expressing DRG neurons were not immunoreactive to substance P (SP) and calcitonin gene-related peptide (CGRP). A marked increase in the number of mRNA-positive DRG neurons were observed 1-5 days after a crush injury of the sciatic nerve (3-4-fold of the control value). These neurons turned mRNA-positive after the nerve crush were also mainly small-sized. The mRNA signals were detected in many peptidergic (SP/CGRP) neurons, in contrast to the normal state. On the other hand, in the neurons which showed intense labeling in the normal condition, the mRNA signals were down-regulated. These results suggest that primary sensory neurons include two kinds of H1 receptor-expressing sensory neurons, one expressing H1 receptor mRNAs in the normal state and the other up-regulating the mRNAs following the peripheral nerve damage.

Animals↗
PubMed1997

Expression of neuronal traits in pancreatic beta cells. Implication of neuron-restrictive silencing factor/repressor element silencing transcription factor, a neuron-restrictive silencer.

Pancreatic beta cells (insulin-producing cells) and neuronal cells share a large number of similarities. Here, we investigate whether the same mechanisms could control the expression of neuronal genes in both neurons and insulin-producing cells. For that purpose, we tested the role of the transcriptional repressor neuron-restrictive silencing factor/repressor element silencing transciption factor (NRSF/REST) in the expression of a battery of neuronal genes in insulin-producing cells. NRSF/REST is a negative regulator of the neuronal fate. It is known to silence neuronal-specific genes in non-neuronal cells. We demonstrate that, as in the case of the neuronal pheochromocytoma cell line PC12, mRNA coding for NRSF/REST is absent from the insulinoma cell line INS-1 and from three other insulin- and glucagon-producing cell lines. NRSF/REST activity is also absent from insulin-producing cell lines. Transient expression of REST in insulin-producing cell lines is sufficient to silence a reporter gene containing a NRSF/REST binding site, demonstrating the role of NRSF/REST in the expression of neuronal markers in insulin-producing cells. Finally, by searching for the expression of NRSF/REST-regulated genes in insulin-producing cells, we increased the list of the genes expressed in both neurons and insulin-producing cells.

3T3 Cells↗
PubMed1993

Principal neurons as local circuit neurons in the rat superior cervical ganglion: the synaptology of the neuronal processes revealed by intracellular injection of biocytin.

To analyze the local circuitry of the sympathetic ganglion, the synaptic relations of the neuronal processes of the principal neurons in the rat superior cervical ganglion were investigated by correlated light and electron microscopy combined with intracellular injection of biocytin. Intracellular iontophoresis of biocytin followed by avidin-biotinylated horseradish peroxidase cytochemistry allowed complete visualization of the neuronal processes of the principal neurons. The stained principal neurons have a single process (axon), which leaves the ganglion, and several intraganglionic processes (dendrites), some of which show specific terminal arborizations. Some terminals of the dendritic collaterals formed pericellular plexuses or intercellular glomerular plexuses. Electron microscopically, the dendrites and their collaterals contain numerous small vesicles. Synaptic membrane specializations were observed between the stained dendritic collaterals and unlabeled neurites. These may be both preganglionic axon terminals and processes of principal neurons. The likely direction of neurotransmission often could not be determined because of the bidirectional synaptic structures. Our findings show that the dendritic collaterals of principal neurons appear to make both post- and presynaptic contacts with both the principal neurons and the preganglionic axons. It is suggested that the principal neurons might participate in local circuits involving not only preganglionic axons but also neighboring principal neurons.

Animals↗
PubMed1997

Barosensitive cardioinhibitory neurons in the medulla: comparison of FosB/ChAT-positive neurons with CT-HRP-labeled neurons.

The purpose of this study was to survey the distribution pattern of barosensitive cardioinhibitory preganglionic neurons in the medulla. This was done using Wistar rats anesthetized with fentanyl/midazolam. After stimulating arterial baroreceptors by blood pressure increase due to phenylephrine, c-Fos, FosB, c-Jun and JunD/choline acetyltransferase (ChAT)-positive neurons were surveyed in the medulla. After placing HRP conjugated by cholera toxin (CT-HRP) on the sino-atrial node, CT-HRP-labeled neurons were surveyed in the medulla. In the phenylephrine pressor test experiment, we ascertained that in the target neurons fosB was more sensitive to baroreceptor stimulation than any other immediate early genes such as c-fos, c-jun and junD. Using the FosB/ChAT method, we succeeded in determining sites of the barosensitive cardioinhibitory neurons that had never been found with the c-Fos/ChAT method. The distribution pattern of the FosB/ChAT-positive neurons was compared with that of the CT-HRP-labeled neurons. We found that the distribution pattern of the FosB/ChAT-positive neurons in the dorsal motor nucleus of the vagus nerve (DMX) and ambiguus nucleus (AMB) was similar to that of the CT-HRP-labeled neurons at the level between the caudal end of the area postrema (AP) and the caudal end of the nucleus of the trapezoid body. This suggests that the barosensitive FosB/ChAT-positive neurons in the DMX and AMB mediate the cardioinhibitory baroreceptor reflex.

Animals↗
PubMed1998

Neuronal injury increases retrograde axonal transport of the neurotrophins to spinal sensory neurons and motor neurons via multiple receptor mechanisms.

We investigated the retrograde axonal transport of 125I-labeled neurotrophins (NGF, BDNF, NT-3, and NT-4) from the sciatic nerve to dorsal root ganglion (DRG) sensory neurons and spinal motor neurons in normal rats or after neuronal injury. DRG neurons showed increased transport of all neurotrophins following crush injury to the sciatic nerve. This was maximal 1 day after sciatic nerve crush and returned to control levels after 7 days. 125I-BDNF transport from sciatic nerve was elevated with injection either proximal to the lesion or directly into the crush site and after transection of the dorsal roots. All neurotrophin transport was receptor-mediated and consistent with neurotrophin binding to the low-affinity neurotrophin receptor (LNR) or Trk receptors. However, transport of 125I-labeled wheat germ agglutinin also increased 1 day after sciatic nerve crush, showing that increased uptake and transport is a generalized response to injury in DRG sensory neurons. Spinal cord motor neurons also showed increased neurotrophin transport following sciatic nerve injury, although this was maximal after 3 days. The transport of 125I-NGF depended on the expression of LNR by injured motor neurons, as demonstrated by competition experiments with unlabeled neurotrophins. The absence of TrkA in normal motor neurons or after axotomy was confirmed by immunostaining and in situ hybridization. Thus, increased transport of neurotrophic factors after neuronal injury is due to multiple receptor-mediated mechanisms including general increases in axonal transport capacity.

Animals↗
PubMed1994

Identification and characterization of pleural neurons that inhibit tail sensory neurons and motor neurons in Aplysia: correlation with FMRFamide immunoreactivity.

Neurons on the rostral edge of the ventral surface of the right pleural ganglion were identified as elements of the circuit mediating the defensive tail withdrawal reflex of Aplysia. These neurons produced IPSPs in tail sensory neurons and were classified into two groups, RPI4 and RPI5, according to their affinity for an antibody directed against FMRFamide. RPI4 was not FMRFamide immunoreactive, and RPI5 was. RPI4 and RPI5 were found to have different electrophysiological profiles. The summated IPSPs in sensory neurons produced by RPI4 developed more rapidly and had a shorter duration than those produced by RPI5. In addition, RPI4 produced IPSPs in the tail motor neurons, whereas RPI5 did not. Both RPI4 and RPI5 received excitatory synaptic inputs from stimulation of the pleural-abdominal connective as well as peripheral nerves P8 and P9, which innervate the tail and posterior part of the animal's body. These inputs were sufficient to elicit spikes. In RPI4, the excitatory synaptic inputs were followed by short and transient hyperpolarization, whereas in RPI5, the excitatory synaptic inputs were followed by slow and long-lasting hyperpolarization. Excitatory inputs elicited in RPI4 by stimulation of peripheral nerves appeared to be mediated, at least in part, by activation of tail sensory neurons. Intracellular stimulation of sensory neurons produced EPSPs in RPI4 that appeared to be monosynaptic. These results suggest that inhibitory interneurons underlying the circuit of the tail withdrawal reflex may play roles in mediating or modulating neuronal responses to tail stimulation. By inhibiting tail sensory and motor neurons, these interneurons may reduce the effectiveness of an animal's response to stimulation of the tail.

Animals↗
PubMed1992

Structure, expression, and function of Ng-CAM, a member of the immunoglobulin superfamily involved in neuron-neuron and neuron-glia adhesion.

The neuron-glia cell adhesion molecule (Ng-CAM) mediates neuron-neuron adhesion by a homophilic mechanism and neuron-astrocyte adhesion by a heterophilic mechanism. The protein is expressed on neurons and Schwann cells but not on astrocytes. It is most prevalent during development on cell bodies of migrating neurons and on axons during formation of nerves. Ng-CAM expression is greatly increased following nerve injury. Anti-Ng-CAM antibodies inhibited migration of granule cells along Bergmann glia in cerebellar explants and fasciculation of neurites in outgrowths from explants of dorsal root ganglia. The combined results indicate that Ng-CAM on neurons binds to Ng-CAM on adjacent neurons and to as yet unidentified ligands on astrocytes. Ng-CAM is synthesized in chicken neurons from a 6 kb mRNA as Mr approximately 200,000 forms which are cleaved to yield two components of Mr 135,000 and 80,000. It is glycosylated and can be phosphorylated. Amino acid sequence analysis indicates that it contains six immunoglobulin domains, five fibronectin type III repeats, a transmembrane domain and a cytoplasmic region. Structural analyses indicate that Ng-CAM is most closely related to the mammalian glycoprotein L1 but significant differences between them strongly suggest that they are not equivalent molecules. The recent identification of another structurally related molecule in the chicken called Nr-CAM underscores the notion that these molecules are members of a subfamily of neural cell adhesion molecules within the immunoglobulin superfamily that have related or complementary functions in the nervous system.

Animals↗
PubMed2006

Neuronal differentiation is accompanied by increased levels of SNAP-25 protein in fetal rat primary cortical neurons: implications in neuronal plasticity and Alzheimer's disease.

Alzheimer's disease (AD) is accompanied by progressive memory loss and decline in general cognitive abilities. Neuropathological hallmarks include amyloid plaque formation, neurofibrillary tangles, and neuronal and synaptic loss. To improve research models in AD, we have characterized several aspects of the primary rat neuronal cell culture model, which relate directly to the study of neuroexocytosis, neuronal plasticity, and amyloidosis. We have attempted to isolate and assess the neuronal enrichment of a primary cortical cell culture by morphological and molecular techniques, following progress of these cultured cells for up to 18 days in culture to identify the optimum timeframe for the manipulation and data collection in these cells. We observed maximum neuronal differentiation around day 15, which was in decline by day 18, thus, the critical window for manipulations in these cultures seems to be between days 12-15. The substantial increase in neuritic length and density was apparent at very early time points and peaked at day 15. In parallel to morphological assessments, we measured levels of a group of selected neuronally important proteins, including cytoskeletal and synaptic proteins. Change in the levels of cell-associated APP and synaptophysin were not as dramatic as that of SNAP-25 or secreted APP. Notably, this increased differentiation is accompanied by a dramatic increase in levels of SNAP-25 protein, which peaked at day 15 and declined thereafter. These results suggest that this neuronal population contains quantifiable presynaptic terminals. Thus, the establishment and molecular characterization of this neuronal model would have many implications in neuroscience research including synaptic differentiation and neuronal plasticity and for the evaluation of pharmacological interventions in the disease process.

Alzheimer Disease↗
PubMed2006

Multiprotein complexes of the survival of motor neuron protein SMN with Gemins traffic to neuronal processes and growth cones of motor neurons.

Spinal muscular atrophy (SMA), a progressive neurodegenerative disease affecting motor neurons, is caused by mutations or deletions of the SMN1 gene encoding the survival of motor neuron (SMN) protein. In immortalized non-neuronal cell lines, SMN has been shown to form a ribonucleoprotein (RNP) complex with Gemin proteins, which is essential for the assembly of small nuclear RNPs (snRNPs). An additional function of SMN in neurons has been hypothesized to facilitate assembly of localized messenger RNP complexes. We have shown that SMN is localized in granules that are actively transported into neuronal processes and growth cones. In cultured motor neurons, SMN granules colocalized with ribonucleoprotein Gemin proteins but not spliceosomal Sm proteins needed for snRNP assembly. Quantitative analysis of endogenous protein colocalization in growth cones after three-dimensional reconstructions revealed a statistically nonrandom association of SMN with Gemin2 (40%) and Gemin3 (48%). SMN and Gemin containing granules distributed to both axons and dendrites of differentiated motor neurons. A direct interaction between SMN and Gemin2 within single granules was indicated by fluorescence resonance energy transfer analysis of fluorescently tagged and overexpressed proteins. High-speed dual-channel imaging of live neurons depicted the rapid and bidirectional transport of the SMN-Gemin complex. The N terminus of SMN was required for the recruitment of Gemin2 into cytoplasmic granules and enhanced Gemin2 stability. These findings provide new insight into the molecular composition of distinct SMN multiprotein complexes in neurons and motivation to investigate deficiencies of localized RNPs in SMA.

Animals↗
PubMed1984

Delayed neuronal recovery and neuronal death in rat hippocampus following severe cerebral ischemia: possible relationship to abnormalities in neuronal processes.

Mechanisms involved in the postischemic delay in neuronal recovery or death in rat hippocampus were evaluated by light and electron microscopy at 3, 15, 30, and 120 min and 24, 36, 48, and 72 h following severe cerebral ischemia that was produced by permanent occlusion of the vertebral arteries and 30-min occlusion of the common carotid arteries. During the early postischemic period, neurons in the Ca1 and Ca3 regions both showed transient mitochondrial swelling followed by the disaggregation of polyribosomes, decrease in rough endoplasmic reticulum (RER), loss of Golgi apparatus (GA) cisterns, and decrease in GA vesicles . Recovery of these organelles in Ca3 neurons was first noted between 24 and 36 h and was accompanied by a marked proliferation of smooth endoplasmic reticulum (SER). Many Ca1 neurons initially recovered between 24 and 36 h, but subsequent cell death at 48-72 h was often preceded by peripheral chromatolysis, constriction and shrinkage of the proximal dendrites, and cytoplasmic dilatation that was continuous with focal expansion of RER cisterns. Because SER accumulates in resistant Ca3 neurons and proximal neuronal processes are damaged in vulnerable Ca1 neurons, we hypothesize that delayed cell recovery or death in vulnerable and resistant postischemic hippocampal neurons is related to abnormalities in neuronal processes.

Animals↗
PubMed2004

Localization of wild-type and mutant neuronal ceroid lipofuscinosis CLN8 proteins in non-neuronal and neuronal cells.

Neuronal ceroid lipofuscinoses (NCLs) are a group of childhood-onset neurodegenerative disorders characterized by accumulation of autofluorescent lipopigment in many tissues, especially in neurons. Mutations in the CLN8 gene underlie Northern epilepsy (progressive epilepsy with mental retardation [EPMR], OMIM 600143) and a subset of Turkish variant late infantile NCL, but the pathogenetic mechanisms have remained elusive. The CLN8 transmembrane protein is an endoplasmic reticulum (ER) resident protein that recycles between ER and ER-Golgi intermediate compartment (ERGIC) in non-neuronal cells. To explore the disease mechanisms, we have characterized the neuronal localization of wild-type CLN8 protein as well as CLN8 proteins representing patient mutations. Semliki Forest virus-mediated CLN8 protein localized in the ER of mouse hippocampal primary neurons when compared to subcellular markers by immunofluorescence analysis. We also analyzed the possible polarized targeting of CLN8 and observed basolateral targeting in polarized epithelial CaCo-2 cells, suggesting that CLN8 may locate outside the ER or in a specialized subcompartment of the ER. We were not able, however, to demonstrate differential distribution of CLN8 between axons and dendrites of neurons. Fractionation of mouse brain tissue indicated that endogenous mouse Cln8 is observed in light membrane fractions, different from ER, which further suggested differential localization for CLN8 in polarized cells. The disease mutations did not affect intracellular localization of CLN8 in non-neuronal or neuronal cells. Consequently, there is no obvious genotype-phenotype correlation at the level of protein localization and thus mutations most likely directly affect functionally important domains of CLN8.

Animals↗
PubMed2000

Outputs of radula mechanoafferent neurons in Aplysia are modulated by motor neurons, interneurons, and sensory neurons.

The gain of sensory inputs into the nervous system can be modulated so that the nature and intensity of afferent input is variable. Sometimes the variability is a function of other sensory inputs or of the state of motor systems that generate behavior. A form of sensory modulation was investigated in the Aplysia feeding system at the level of a radula mechanoafferent neuron (B21) that provides chemical synaptic input to a group of motor neurons (B8a/b, B15) that control closure and retraction movements of the radula, a food grasping structure. B21 has been shown to receive both excitatory and inhibitory synaptic inputs from a variety of neuron types. The current study investigated the morphological basis of these heterosynaptic inputs, whether the inputs could serve to modulate the chemical synaptic outputs of B21, and whether the neurons producing the heterosynaptic inputs were periodically active during feeding motor programs that might modulate B21 outputs in a phase-specific manner. Four cell types making monosynaptic connections to B21 were found capable of heterosynaptically modulating the chemical synaptic output of B21 to motor neurons B8a and B15. These included the following: 1) other sensory neurons, e.g. , B22; 2) interneurons, e.g., B19; 3) motor neurons, e.g., B82; and 4) multifunction neurons that have sensory, motor, and interneuronal functions, e.g., B4/5. Each cell type was phasically active in one or more feeding motor programs driven by command-like interneurons, including an egestive motor program driven by CBI-1 and an ingestive motor program driven by CBI-2. Moreover, the phase of activity differed for each of the modulator cells. During the motor programs, shifts in B21 membrane potential were related to the activity patterns of some of the modulator cells. Inhibitory chemical synapses mediated the modulation produced by B4/5, whereas excitatory and/or electrical synapses were involved in the other instances. The data indicate that modulation is due to block of action potential invasion into synaptic release regions or to alterations of transmitter release as a function of the presynaptic membrane potential. The results indicate that just as the motor system of Aplysia can be modulated by intrinsic mechanisms that can enhance its efficiency, the properties of primary sensory cells can be modified by diverse inputs from mediating circuitry. Such modulation could serve to optimize sensory cells for the different roles they might play.

Animals↗
PubMed2007

Telomerase and neuronal marker status of differentiated NT2 and SK-N-SH human neuronal cells and primary human neurons.

Upon treatment with retinoic acid, NTera-2 (NT2) human teratocarcinoma and SK-N-SH neuroblastoma cells can be induced to terminally differentiate into postmitotic neuronal cells. The neuronal cell yield obtained from the NT-2 cells is partially dependent on the time of differentiation (24-55 days). SK-N-SH cells differentiate into a mixed population of neuronal and epithelium-like cells. Here we report modified protocols that increase the number of differentiated NT-2 and SK-N-SH cells and that establish an enriched neuronal SK-N-SH-derived cell population essentially devoid of nonneuronal cells. Differentiated cells express the cytoskeleton-associated protein tau and other typical neuronal markers, such as Map2, Ngn1, NeuroD, Mash1, and GluR which are also expressed in primary human fetal neurons. Telomerase activity is down-regulated in differentiated cells, which is consistent with the telomerase status of primary fetal human neurons. Thus, differentiated NT2 and SK-N-SH cells may represent an excellent source for studies investigating the role of telomerase or other survival-promoting activities in protecting human neuronal cells from cell death-mediating stresses associated with neurodegenerative diseases.

Cell Adhesion↗
PubMed1980

Neurons switch from non-neuronal enolase to neuron-specific enolase during differentiation.

The enolase (EC 4.2.1.11) isoenzymes, neuron-specific enolase (NSE, gamma gamma) and non-neuronal enolase (NNE, alpha alpha), are markers for neurons and glia, respectively, in adult mammalian brain. In developing fetal and early postnatal brain, levels of non-neuronal enolase (NNE) are high. Neuron-specific enolase (NSE) appears only after neurogenesis begins in a given region and only slowly attains adult levels. Immunocytochemistry in developing rat and rhesus monkey brain reveals that proliferative zones that give rise to neurons are NNE(+). Thus, nerve cells must undergo a switch from NNE to NSE. In addition, study of neurons in cerebellum and neocortex reveals that they are NNE(+) during migration and only become NSE(+) in their final location, presumably after making full synaptic connections. Such migrating cells may contain hybrid enolase (alpha gamma) and some (e.g. cerebellar stellate/basket cells) may not completely switch over to NSE even in the adult. Neuron-specific enolase is not only a specific molecular marker for mature nerve cells, but is closely correlated to the differentiated state.

Animals↗
PubMed1982

Neuron-specific and non-neuronal enolase in developing chick brain and primary cultures of chick neurons.

Developmental changes of the neuron-specific enolase (NSE) and the non-neuronal enolase (NNE) were determined in pure neuronal, or mixed cultures of neuronal and glial cells, prepared from brains of 8-day-old chick embryos, as a function of cellular development with time in culture. The modifications observed in culture were compared to those measured in brain during the development of the nervous tissue in the embryo and during the post-hatching period. In the whole brain, the total enolase activity increases progressively until the adult level, the NSE appears only 4 days before hatching. The total enolase activity of pure neurons increases until 8 days of culture but the NSE never appears during this period. Mixed cultures of neurons and glial cells present an increase of total activity until 14 days of culture and neuron-specific form of the enzyme can be observed after 6 days of culture. Our results suggest that NSE appears only in the functional brain and is expressed in cultivated neurons only when glial cells are present simultaneously.

Animals↗
PubMed1986

Influence of the extracellular potassium environment on neurite growth in sensory neurons, spinal cord neurons and sympathetic neurons.

The influence of the extracellular potassium concentration ([K+]o) on neurite growth in rat sensory neurons, spinal cord neurons and sympathetic neurons was investigated. Experiments carried out in 3-compartment culture dishes showed that although neurites from sensory and spinal cord neurons were capable of growing in both 5 mM [K+]o and 20 mM [K+]o, they were virtually unable to grow from a region of 5 mM [K+]o into a region of 20 mM [K+]o. Neurites from sympathetic neurons behaved similarly although [K+]o exceeding 20 mM was required to exclude sympathetic neurites. We suggest the possibility of a negative chemotaxis to [K+]o by growth cones in these neurons. Neurite regeneration following axotomy in sensory neurons was partially inhibited distal to a proximo-distal increase in [K+]o. The nature of this inhibition was somewhat different from that described previously in sympathetic neurons. The possibility is raised that [K+]o plays a role in the development of the nervous system.

Animals↗
PubMed1998

Dendritic integration in olfactory sensory neurons: a steady-state analysis of how the neuron structure and neuron environment influence the coding of odor intensity.

Response properties of the receptor potential at steady state were analyzed in a biophysical model of an olfactory sensory neuron embedded in a multicell environment. The neuron structure was described as a set of several identical dendrites (or cilia) bearing the transduction mechanisms, joined to a nonsensory part--dendritic knob, soma, and axon. The different ionic compositions of the media surrounding the neuron sensory and nonsensory parts and the extraneuronal voltage sources, which both result from the presence of auxiliary cells, were also taken into account. Analytical solutions were found to describe how the receptor potential at the nonsensory part responds to a uniform change in the odorant-dependent conductance resulting from odorant stimulation of the sensory dendrites. We investigated the influence of various geometrical and electrical parameters on the receptor-potential response in the classical model neuron within a homogeneous environment and in the model neuron surrounded with auxiliary cells. First, it was found that the maximum amplitude of the receptor potential is independent of the neuron structure in the absence of auxiliary cells but not in their presence. In the latter case, the amplitude decreases with the length and number of sensory dendrites and with the input resistance of the nonsensory part. Second, the sensitivity (as measured by the increase in membrane conductance at half-maximum response) of the neuron model in the absence of auxiliary cells is higher, but its dynamic range is narrower than in their presence. The dynamic range is wide and the sensitivity low when the input resistance of the nonsensory part is small and the sensory dendrite is unbranched. Both sensitivity and dynamic range are higher for a longer dendrite. These results help understand the morphology of insect olfactory sensilla and can be generalized to other neuron types.

Animals↗
PubMed2001

Neuron-specific Bcl-2 homology 3 domain-only splice variant of Bak is anti-apoptotic in neurons, but pro-apoptotic in non-neuronal cells.

We have identified and characterized N-Bak, a neuron-specific isoform of the pro-apoptotic Bcl-2 family member Bak. N-Bak is generated by neuron-specific splicing of a novel 20-base pair exon, which changes the previously described Bak, containing Bcl-2 homology (BH) domains BH1, BH2, and BH3, into a shorter BH3-only protein. As demonstrated by reverse transcription-polymerase chain reaction and RNase protection assay, N-Bak transcripts are expressed only in central and peripheral neurons, but not in other cells, whereas the previously described Bak is expressed ubiquitously, but not in neurons. Neonatal sympathetic neurons microinjected with N-Bak resisted apoptotic death caused by nerve growth factor (NGF) removal, whereas microinjected Bak accelerated NGF deprivation-induced death. Overexpressed Bak killed sympathetic neurons in the presence of NGF, whereas N-Bak did not. N-Bak was, however, still death-promoting when overexpressed in non-neuronal cells. Thus, N-Bak is an anti-apoptotic BH3-only protein, but only in the appropriate cellular environment. This is the first example of a neuron-specific Bcl-2 family member.

Alternative Splicing↗