Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “neurons”

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

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

At least 19 recordsLinked to original sources
PubMed1979

Projections of intestinal neurons showing immunoreactivity for vasoactive intestinal polypeptide are consistent with these neurons being the enteric inhibitory neurons.

Experiments were performed to determine if the distribution of vasoactive intestinal peptide(VIP)-like immunoreactivity in nerve cell bodies and axons of the myenteric plexus and circular muscle of the small intestine is consistent with VIP being the transmitter of enteric inhibitory neurons. Immunoreactivity for VIP was found in nerve cell bodies of the myenteric plexus and in axons within the myenteric plexus and circular muscle. When the axons in the myenteric plexus were interrupted, there was accumulation of material showing reactivity for VIP on the oral side, indicating that the neurons project in an anal direction. The VIP-like immunoreactivity in axons which supply the circular muscle disappeared after a myectomy in which the overlying myenteric plexus was removed, but remained intact when extrinsic nerves were served. The projections of VIP neurons from the myenteric plexus to the circular muscle correspond to the expected projections of enteric inhibitory neurons determined by functional studies.

Animals↗
PubMed1979

The location of spinal neurons with long descending axons (long descending propriospinal tract neurons) in the cat: a study with the horseradish peroxidase technique.

The distribution spinal neurons with long descending axons was studied in the cat by means of retrograde transport of horseradish peroxidase. Labeled neurons appeared bilaterally in the cervical and the thoracic cord following injections in the lumbosacral cord. In some cases hemisections were made rostrally and contralaterally to the injections in an attempt to determine whether or not the axons crossed. Neurons with uncrossed descending axons were located in laminae I, V, VII and VIII. Lamina I neurons were present in all the spinal segments. In lamina V labeled neurons were distributed mainly laterally in the cervical cord but medially and laterally in the thoracic cord. In the upper cervical and the thoracic cord laminae VII and VIII neurons were distributed very densely along the lateral cord, accounting for 30 and 40 of the total labeled neurons, respectively. In the cervical enlargement they were located in the middle part of lamina VII and in lamina VIII, accounting for about 25% of the total labeled neurons. Neurons with crossed descending axons were found in laminae V, VII and VIII, in the medial part of lamina VII including the intermediomedial nucleus of the thoracic levels and close to the central canal. Lamina V neurons were very small in number. The largest collections of labeled neurons were present in the medial part of laminae VII and VIII. They accounted for about 45% to 55% and 37% of the total in the cervical and the thoracic cord. These neurons may function as the long spinal reflex paths for forelimb-hindlimb synergies and the intercalated paths between the supraspinal descending tracts and the spinal motor centers.

Animals↗
PubMed1975

Ultrastructural studies on the hypothalamic neurosecretory neurons of the rat. III. Paraventricular and supraoptic neurons during lactation and dehydration.

The ultrastructural features of paraventricular (PVN) and supraoptic (SON) neurons and of their axons were studied in lactating and dehydrated rats. Under both conditions of stimulation, the PVN and SON neurons and their axons enlarge. The protein synthesizing apparatus of the neurons becomes activated, but the number of neurosecretory granules (NSG) is decreased. No differences are seen between the PVN and SON neurons during lactation or dehydration. The similarity and simultaneity of the response of the PVN and SON neurons to these two different stimuli is discussed in the light of the theory of nuclear and neuronal specialization for the production of only one hormone. After prolonged lactation of over 2 1/2 weeks' duration, neurons with extreme vacuolation of the rough endoplasmic reticulum (RER) appear in the PVN and SON; the vacuolated neurons appear earlier and predominantly in the PVN involving a maximum of 10-15% of all PVN neurons. Vacuolated neurons were never seen in either nucleus during dehydration of up to 6 days' duration. The vacuolation is suggested to represent an exhaustion phenomenon due to an intense, long-lasting stimulus for oxytocin synthesis. The predominant location of the vacuolated neurons in the PVN supports the theory that oxytocin is produced predominantly in the PVN. The decrease in the number of NSGs during these states of enhanced hormone secretion is considered to corroborate the proposed existence of an extragranular fast axoplasmic transport mechanism in PVN and SON neurons. The possible existence of a reuptake mechanism into NSGs, similar to that in the vesicles of monoaminergic nerve endings is discussed.

Animals↗
PubMed1976

Metabolic control of respiratory neuronal activity and the accompanying changes in breathing movements of the rabbit. 1. Mainpulation of inspiratory and expiratory-inspiratory neurons.

The property of the neuronal membrane to be permeable to metabolic modifiers of two regulatory enzymes has been utilized to manipulate the spike activity of inspiratory (I) and expiratory-inspiratory (EI) neurons of the bulbar respiratory centre. The neurons have been classified according to their response to lung distention or collapse (alpha- or beta-type) and to hyperventilation (tonic firing denoted by "+", cessation of activity by "-"). Using extracellular microelectrodes for single unit recording, the medulla oblongata was superfused with a metabolite-containing CSF. The various neuronal sub-types exhibited a differential activating or inhibitory response to one or several metabolic effectors. For example Ialpha+ units were activated by 5 mM glucose-6-phosphatase (G-6-P) and 3.5 mM 3-phosphoglycerate (3-PGA), which both inhibited Ibeta+ neurons, while 5 mM AMP inhibited Ialpha+ much more strongly than Ibeta+ cells. The spike density of Ialpha- and Ibeta- neurons was increased in the presence of 2.5 mM fructose-6-phosphate and 3.5--5 mM AMP, but became reduced by G-6-P. In contrast, 3 mM fructose-1,6-diphosphate and 5 mM 3-PGA activated the Ialpha- but inhibited the Ibeta- neurons. The EIbeta units were characteristically activated by 10 mM citrate, which inhibited all I-type neurons. Activations of the Ialpha and Ibeta neurons led to an accelerated respiratory rate and a higher tidal volume, while the opposite was true for EIbeta neurons. Intravenous injection of metabolites could not duplicate the striking effects under local applications.

Animals↗
PubMed1978

Stimulation of non-neuronal cell proliferation in vitro by mitogenic factors present in highly purified sympathetic neurons.

Sympathetic neurons have been demonstrated to contain one or more mitogens which are active on highly purified non-neuronal cells cultured in medium containing an optimal concentration of fetal calf serum. Neurons and homologous non-neuronal cells were separated by a method recently developed in this laboratory. The highly purified neurons were either sonicated or homogenized prior to addition to nonneuronal cultures. The presence of neuronal sonicate (1) greatly stimulated [3H]thymidine incorporation into acid-precipitable macromolecules without altering the soluble [3H]thymidine pool, (2) increased both the fraction of non-neuronal cells which took up [3H]thymidine and the density of labeling as observed by autoradiography, and (3) increased the number of cells present in treated cultures after 40 h. The enhancement of [3H]thymidine incorporation was dose-dependent and did not involve cyclic AMP. Addition of neuronal sonicate also caused marked non-neuronal cell elongation which resulted in the elaboration of very long cell processes. The active factor(s) in the neuronal sonicate were partially heat-labile. Norepinephrine was ruled out as a possible mitogenic factor.

Animals↗
PubMed2026

Optimizing NGN2 Dosage Enhances the Neuronal Enrichment of iPSC-Derived Neuronal Cultures.

Proteomic analysis of highly neuron-enriched iPSC-derived cultures can provide valuable insights into the pathogenesis of neurological disease by minimizing confounding signals from non-neuronal populations. However, single-cell iPSC clones with stable NGN2 integration at the AAVS1 locus exhibit spontaneous loss of the mCherry reporter. In addition, following NGN2 induction, cultures frequently contain proliferative progenitor cells that compromise neuronal physical integrity. Here, we show that increased DNA methylation of the EF1-α promoter is associated with mCherry silencing. Importantly, reporter silencing does not affect iNeuron derivation, as evidenced by two lines of evidence. First, single-cell proteomic analysis indicated that mCherry silencing does not drive detectable proteomic divergence in undifferentiated iPSCs. Second, bulk proteomics and immunofluorescence analyses indicated that iPSC-derived neuronal cultures, whether expressing or lacking mCherry, resemble cortical glutamatergic neurons. Instead, the primary confounding factor in iNeuron generation was suboptimal neuronal conversion, which led to cell aggregates comprised of actively proliferating progenitor cells and astrocytes as the culture developed. We found that a 4-day period of NGN2 induction substantially increases neuronal maturation and the expression of neuronal-specific markers. Moreover, transient inhibition of Notch signaling is consistent with a reduction in progenitor cells. Finally, we observed that monoallelic NGN2 integration, rather than biallelic integration, preferentially increases expression of the CNS neuronal marker GPM6A over PNS markers (PRPH, POU4F1, ILS1).

Basic Helix-Loop-Helix Proteins↗
PubMed1979

Neurogenesis and neuron regeneration in the olfactory system of mammals. II. Degeneration and reconstitution of the olfactory sensory neurons after axotomy.

This report describes the retrograde degeneration affecting olfactory sensory neurons of rats after severance of their axons and illustrates the reconstitution of new neurons originating from stem cells located at the base of the olfactory neuroepithelium. Degeneration of the mature, axotomized neurons, signalled by an increased electron density of their cytoplasmic matrix and by the appearance of lipofuscin-like granules, can be detected in the neuroepithelium as early as 24 h after surgery and becomes conspicuous between the second and the third day. Degenerating neurons can be observed in decreasing number up to the tenth post-operative day. They are removed by macrophages which invade the epithelium. The reconstitution of new neurons begins to occur after eight days, when the stem cells undergo vigorous mitotic activity and differentiate into neurons. The morphology of the reconstituted neurons has been described in detail at different stages of their maturation. After 30 days, the olfactory epithelium appears similar to controls. On the basis of both morphological (in rats) and autoradiographic ( in mice) observations, the basal cells have been recognized as stem cells of the olfactory neurons.

Animals↗
PubMed2025

Nfe2l1 dysfunction alters Parkinson's disease-related gene expression and impairs neuronal differentiation under ubiquitin stress in neuronal differentiated P19 Cells.

Proteostasis is essential for neuronal health, and its disruption is implicated in neurodegenerative diseases such as Parkinson's disease (PD). Nfe2l1, a key regulator of proteostasis and ubiquitination, plays a significant role in neuronal health, yet its molecular functions in neuronal cells remain unclear. Our study investigates the role of Nfe2l1 in RA-induced neuronal differentiation of P19 cells under proteasome inhibition. This condition significantly increased Nfe2l1 expression at both protein and RNA levels in wild-type and differentiated cells. In differentiated cells under proteasome inhibition, RNA sequencing revealed an enrichment of neurodegenerative pathways, particularly those associated with PD. Proteasome inhibition led to the upregulation of several PD-related genes, including Atf6, Camk2d, and Sod1. However, Nfe2l1 knockdown in differentiated cells significantly reduced the expression of these genes, highlighting the role of Nfe2l1 in the regulation of PD-related pathways. Knockdown of Nfe2l1 also decreased Neat1, a long non-coding RNA associated with PD pathology, and downregulated the neuronal marker Map2, indicating impaired neuronal differentiation. Furthermore, Nfe2l1 knockdown increased ubiquitination under proteasome inhibition, emphasizing its role in protein degradation and neuronal homeostasis under stress. These findings highlight Nfe2l1 as a critical regulator in neuronal cells and reveal its potential role in maintaining proteostasis and involvement in neurodegenerative disease mechanisms, such as PD.

Parkinson Disease↗
PubMed2025

A General Principle of Neuronal Evolution Reveals a Human-Accelerated Neuron Type Potentially Underlying the High Prevalence of Autism in Humans.

The remarkable ability of a single genome sequence to encode a diverse collection of distinct cell types, including the thousands of cell types found in the mammalian brain, is a key characteristic of multicellular life. While it has been observed that some cell types are far more evolutionarily conserved than others, the factors driving these differences in the evolutionary rate remain unknown. Here, we hypothesized that highly abundant neuronal cell types may be under greater selective constraint than rarer neuronal types, leading to variation in their rates of evolution. To test this, we leveraged recently published cross-species single-nucleus RNA-sequencing datasets from three distinct regions of the mammalian neocortex. We found a strikingly consistent relationship where more abundant neuronal subtypes show greater gene expression conservation between species, which replicated across three independent datasets covering >106 neurons from six species. Based on this principle, we discovered that the most abundant type of neocortical neurons-layer 2/3 intratelencephalic excitatory neurons-has evolved exceptionally quickly in the human lineage compared to other apes. Surprisingly, this accelerated evolution was accompanied by the dramatic down-regulation of autism-associated genes, which was likely driven by polygenic positive selection specific to the human lineage. In summary, we introduce a general principle governing neuronal evolution and suggest that the exceptionally high prevalence of autism in humans may be a direct result of natural selection for lower expression of a suite of genes that conferred a fitness benefit to our ancestors while also rendering an abundant class of neurons more sensitive to perturbation.

Humans↗
PubMed1978

Pharmacological and electrophysiological studies of morphine and enkephalin on rat supraspinal neurones and cat spinal neurones.

1 The actions of morphine, methionine and leucine enkephalin, administered electrophoretically, were studied on supraspinal neurones in the cortex and brainstem of the rat anaesthetized with urethane and on spinal Renshaw cells and dorsal horn interneurones in the cat anaesthetized with pentobarbitone.2 The majority of Renshaw cells and cortical and brainstem neurones were excited by all three compounds although some supraspinal neurones were depressed.3 Naloxone reversibly antagonized both excitatory and depressant actions of morphine and enkephalin. Acetylcholine-induced excitation but not amino acid-induced excitation was also antagonized by naloxone.4 Neither morphine nor the enkephalins had any naloxone-reversible action on dorsal horn neurones when ejected from conventional multibarrelled electrodes. However, morphine but not enkephalin, administered into the substantia gelatinosa region of the spinal cord selectively reduced responses to noxious stimuli of neurones in deeper laminae. Naloxone administered into the same region antagonized this action of morphine.5 Intravenous morphine also antagonized responses of dorsal horn neurones to noxious stimuli and subsequent intravenous naloxone reversed this effect.6 It was concluded that the excitatory and inhibitory effects of morphine and enkephalin on central neurones may be mediated by actions on different opiate receptors and that depression of noxious responses of dorsal horn neurones may be relevant to the analgesic action of morphine.

Animals↗
PubMed1976

Metabolic regulations of the rhythmic activity in pacemaker neurons. II. Metabolically induced conversions of beating to bursting pacemaker activity in isolated Aplysia neurons.

In pacemaker neurons of the sea hare Aplysia californica, isolated from their synaptic, ephaptic and humoral inputs, conversion of the regular beating to a bursting discharge pattern can be induced by certain cell metabolites. Administration of the phosphofructokinase (PFK) activator fructose-6-phosphate (F-6-P), or its nonmetabolizable analogue 1-deoxy-F-6-P, induced bursting discharges in R3, R5, R6 and R11 neurons, with spike doublets and triplets appearing transiently in the time pattern. With another PFK activitor, adenosine-5-monophosphate, only double spikes have been noted in R7, R8 and R14 neurons. Burst activity was induced also in the presence of the fructose-1,6-diphosphatase activators, citrate and 3-phosphoglycerate, in R9, R10 and R12 neurons. Cyclic 3',5'-AMP, which also activates the PFK (beside other effects on cellular metabolism), induced bursting discharges in all R3-R14 neurons. In contrast, the inhibitors of the PFK, citrate and ATP, decreased the spike activity of the bursting L3 and L6 neurons, even changing L3 neurons to the regular beating type. Among a variety of cell metabolites tested only pyruvate was able to induce a burst-like tendency in R9 neurons. The characteristic bursting patterns which appeared in the presence of the described metabolic effectors could not be duplicated by low Ca2+ and/or high K+ media nor by artificial shifts in membrane potential triggered by depolarizing and hyperpolarizing currents.

Adenosine Monophosphate↗
PubMed1979

Autonomic neurons affected by lipid storage in the spinal cord in Fabry's disease: distribution of autonomic neurons in the sacral cord.

In five patients with Fabry's disease, the distribution of neurons in the spinal cord affected by lipid storage was investigated. Neurons ballooned by lipid storage were located mainly in the thoracolumbar and mid-sacral regions. In the former, they were located exclusively in the intermediolateral nucleus from the first thoracic (or eighth cervical) through the first or second lumbar segments. In the mid-sacral region they were located not only in the intermediolateral nucleus but also in the intermedioventral (Onuf's) nucleus and in the intermediate region of the ventral horn. The affected neurons in the sacral cord are also assumed to be autonomic neurons judging from the selective involvement of known autonomic neurons in the thoracolumbar segments. Based on the distribution of these neurons, it is concluded that autonomic neurons in the human sacral cord from a cell column which differs topographically from that in the thoracolumbar segments. The cell column begins rostrally at the ventral margin of the ventral horn in the second sacral segment as Onuf's nucleus and extends caudally in a dorsolateral direction along the intermediate region to the intermediolateral nucleus in the fourth sacral segment, which forms the caudal part of the cell column.

Adult↗
PubMed1979

Postnatal rat sympathetic neurons in culture. I. A comparison with embryonic neurons.

1. A morphological and physiological comparison was made between embryonically and postnatally derived superior cervical ganglion neurons (SCGN) grown in dissociated cell culture. It was found that while morphologically distinct, the physiological properties of the postnatal neurons were the same as their embryonic counterparts. 2. Intracellular injection of horseradish peroxidase (HPR) demonstrated that SCGN from any age of animal elaborated two basic types of processes, although the pattern of process ramification was unique for each neuron. The two types of proceses were 1) the large, smooth, rapidly tapering; and 2) the thin, nontapering variety, which often contained varicosities along its length. It is suggested that the former are dendritic in function, while the latter act as axons. 3. A difference was noted in somal size and the number of primary processes extended by the embryonic and postnatal neurons, with the latter more closely resembling the in vivo morphology. 4. Resting potentials and action-potential amplitudes of postnatal SCGN were comparable to those found previously for embryonic SCGN in vitro. 5. Iontophoretic application of putative neurotransmitter substances revealed the presence of acetylcholine receptors (AChR) on both embryonic and postnatal SCGN. Picrotoxin-sensitive depolarizing responses to iontophoresed gamma-aminobutyric acid (GABA) was seen on a few embryonic neurons, but not on the older cells. No responses were detected when norepinephrine (NE), glutamate, cAMP, substance P, or dopamine were applied to the SCGN of either age group. 6. Synatpic interaction between postnatal SCGN were found at an earlier in vitro age (12 days) than was the case for embryonic neurons (20 days). 7. Synaptic transmission was found to be chemical in nature. This was shown by 1) a dependence on external Ca2+ concentrations; 2) steplike fluctuations in synpatic potential amplitude, and 3) a variation in potential amplitude with changes in membrane potential. 8. It is concluded that the postnatal SCGN are able to survive in culture even when taken from animals up to 12.5 wk old. The elaboration of processes is in many ways strikingly similar to sympathetic neurons in the animal, and they are able to form functional synaptic interactions.

Age Factors↗
PubMed1976

Metabolic control of respiratory neuronal activity and the accompanying changey-expiratory neurons.

Expiratory-related neurons have been classified according to their phase relation within the respiratory cycle, their response to lung distension and collapse (alpha- and beta-type), and to hyperventilation (tonic firing denoted by "+", cessation of activity by "-"). The dorsal surface of the medulla oblongata was superfused with a metabolite-containing CSF solution and the activity of expiratory (E) and inspiratory-expiratory (IE) neurons was extracellulary recorded. The neuronal sub-types established by their functional behaviour could equally be distinguished by their differential response to one or several metabolites. In contrast to inspiratory (I) neurons, Ealpha- Ebeta-, Ebeta- and IEbeta- neurons are inhibited by 3.5 mM AMP, but are activated by 10 mM citrate (with the exception of Ebeta+ units). Furthermore I cells are activated by ATP, while Ealpha and Ebeta units become inhibited. Vagotomy in some instances affected the response of some IEbeta units. An increase in spike density of IEbeta+ and Ealpha- cells is paralleled by a reduction of both the respiratory rate and the tidal volume, while a lower spike density in IEbeta+, IEbeta- and Ealpha- units is accompanied by increases in respiratory rate and tidal volume. In the case of Ebeta+ and Ebeta- cells lower activity is associated with an increased tidal volume. No metabolite-induced changes could be obtained with cardiovascular or unspecific reticular neurons.

Adenosine Monophosphate↗
PubMed1979

Neurogenesis and neuron regeneration in the olfactory system of mammals. I. Morphological aspects of differentiation and structural organization of the olfactory sensory neurons.

The neurogenetic process leading to the formation of primary sensory neurons persists into adult life in the olfactory epithelium of mammals. The morphological stages of maturation and ageing of this exceptional neuron have been described both at light and electron microscopical levels. For descriptive purposes the neural elements have been classified as: (1) basal cells proper, (2) globose basal cells, and (3) neurons. Intermediate stages, however, have been identified. Autoradiographic observations complement the morphological studies and provide a time sequence of the morphological stages leading to the mature neurons. A typical columnar arrangement of the sensory neurons has been described. Furthermore, active and quiescent zones have been recognized in the neuroepithelium. In the active zones the neurogenetic process is vigorous, and the zones are characterized by the presence of immature elements. However, in the quiescent zones there exists a population of mature elements while immature neurons are sparse.

Animals↗
PubMed1979

The spontaneous firing patterns of forebrain neurons. IV. Effects of bilateral and unilateral frontal cortical ablations on firing of caudate, globus pallidus and thalamic neurons.

To assess the effects of partial deafferentation of the neostriatum on spontaneous neuronal activity in the basal ganglia and related thalamic nuclei, ablations of frontal cortex were carried out in adult cats. Postoperative measures of interspike intervals of single neurons in the caudate nucleus, globus pallidus and ventral anterior-ventral lateral complex of the thalamus revealed a slowing of neuronal firing in these structures as compared with non-lesioned controls. The fact that deafferentation by cortical damage produces changes in neuronal firing in target neurons of the striatum (globus pallidus) and in thalamic neurons at least two synapses removed from the striatum is noteworthy. The possible extent to which these results might have been influenced by reduction of cortical inputs to or denervation of the thalamus is discussed.

Afferent Pathways↗
PubMed1979

Vestibular neuronal function during ischemia. Response of vestibular neurons to vertebral and carotid artery occlusion in rabbits.

The relation between ischemia experimentally produced by occlusion of arteries injecting to the brain and the changes in vestibular excitability was examined in 102 rabbit vestibular neurons responding to sinusoidal rotation. During occlusion of ipsilateral and/or contralateral vertebral and common carotid arteries, the neuronal activity took on three different patterns with respect to the frequency of neuronal discharge. The incidence of alteration of neuronal activities reflected vestibular excitability dependent on hemodynamic changes due to occlusion of the ipsilateral vertebral artery rather than due to occlusion of the contralateral artery. Occlusion of common carotid arteries caused no significant difference between the right and left vessels in the resultant change of the neuronal activity, and differed little, either, from occlusion of vertebral arteries in the incidence of the changes. A supplementary experiment, in which the four arteries were only partially occluded, clearly showed that the resultant changes in neuronal activity reflect the role of Willis' circle in the maintenance of blood flow to vestibular nuclei.

Animals↗
PubMed1976

Metabolic control of respiratory neuronal activity and the accompanying changes in breathing movements of the rabbit. III. Phase shifts in respiratory neurons induced by inflation and collapse of the lung, hyperventilation, or metabolic modifiers.

Phase shifts between inspiratory-related and expiratory-related discharge patterns can be reversibly induced in respiratory neurons following volume changes of the lung, hypocapnic apnea as a result of hyperventilation, or superfusion with certain metabolic modifiers. Phase-spanning expiratory-inspiratory or inspiratory-expiratory discharges are frequently induced in those neurons which are activated either by pulmonary stretch receptors or collapse afferents. The same is true for regulatory effectors which activate key steps of the neuronal metabolism such as ADP, 3-phosphoglycerate, L-glutamine, fructose-6-phosphate and fructose-1,6-diphosphate. In contrast, inhibitory vagal inputs or superfusion with citrate, an inhibitory metabolic modifier, revert preexisting expiratory-inspiratory discharges into a phase-coupled inspiratory pattern. It is postulated that the respiratory neuronal networks represents a time-optimal control system which strives to adjust to a new equilibrium value in a minimum of time, following a given mechanical or chemical perturbation. Following the hypothesis advanced by Cohen (1974) that the phase-spanning units modulate the activity of the in-phase neurons, it is suggested that the additional recruitment of expiratory-inspiratory and inspiratory-expiratory units provides a measure of the quality of time-optimal control and hence a performance index of the system.

Animals↗