Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuronal Connectivity”

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 1,495 records · Page 83Linked to original sources
PubMed2004

Molecular mechanisms of target specificity during synapse formation.

Neurons are connected with a high degree of specificity in neuronal circuits. Axon guidance mechanisms are responsible for directing axons to their approximate target region. It is not well understood how precise synaptic connections form between specific pre- and postsynaptic neurons within the target area. Recent analysis of a group of cell surface proteins in different systems has shed light on the diverse cellular and molecular mechanisms that generate the precise patterns of connectivity.

Animals↗
PubMed1988

[The respiratory center--the regulator of the respiratory system].

The authors consider the respiratory centre to be the regulator of the respiratory system and to consist of 3 main functional blocks: chemoregulator, respiratory rhythm autogenerator and mechanoregulator, functions of which are provided by the neurons of medulla oblongata. The main aim of chemoregulator block is to maintain the level of ventilation volume speed, which is necessary to compensate the difference between the signals of setting and the firing from the chemoreceptors. The main aim of mechanoregulator block is to provide the functioning of the regulation loop of the respiratory muscles comparing the signals which come from the respiratory autogenerator, and the firing of the mechanoreceptors. The generator unit of the respiratory centre is a set of rhythm-forming associations, the system of 4 neurons (early and late inspiratory and expiratory) are typical among them. The neurons are connected by recurrent inhibitory bonds: the neuron of each rhythm-forming group, successively becoming excited, inhibits the two preceding neurons in the cycle; for all this the neuron of the successive group is released from inhibition and in such a way the rhythmogenesis occurs. The respiratory centre forms a common unit for chemo- and mechanoreceptor loops, through which the circuits of feedback for both loops are connected, providing the regulation of breathing.

Animals↗
PubMed1997

Cardiac inhibitory neurons in gastropod snail Achatina fulica.

Two inhibitory heart motor neurons (HI-1, HI-2) were identified in the visceral ganglion of the snail Achatina fulica. Both motor neurons were connected monosynaptically with the myocardium. Irregular action potentials composed a typical pattern of neuronal spontaneous electrical activity. The neurons shared common excitatory synaptic inputs, and were connected through electrical synapses. Neuronal endings of these cells responded to tactile stimulation and to cardiac stretching when the chemical synapses were blocked. HI-1 and HI-2 neurons both elicited inhibitory post synaptic potentials in the myocardium with a constant delay and thereby modulated cardiac spikes frequency and amplitude. Staining with the dye Lucifer yellow revealed that these two neurons were unipolar cells which had dendrites only in the visceral ganglion.

Action Potentials↗
PubMed1988

Lateral hypothalamic area and paraventricular nucleus connections with subfornical organ neurons: an electrophysiological study in the rat.

The neural pathways from the lateral hypothalamic area (LHA) to the hypothalamic paraventricular nucleus (PVN) mediated by subfornical organ (SFO) neurons were examined in urethane-anesthetized male rats in order to determine the excitability of vasopressin (VP)-secreting neurons in the PVN. Microinjection of angiotensin II (AII) into the LHA excited the activity of nearly half (n = 8) of the SFO neurons (n = 18) activated antidromically by electrical stimulation of the PVN. Microinjection of AII into the LHA also caused excitation of approximately one-quarter (n = 11) of putative VP-secreting neurons (n = 45) in the PVN while the excitatory responses of the putative VP-secreting neurons were blocked or attenuated by pretreatment with the AII antagonist, saralasin (Sar), in the SFO. Electrical stimulation of the LHA, on the other hand, produced excitation (n = 17) or inhibition (n = 14) of the putative VP-secreting neurons (n = 52) in the PVN. About half of the excitatory responses to LHA stimulation were blocked or attenuated by pretreatment with Sar in the SFO, whereas the inhibitory responses were not affected. These results show some possible connections between the LHA and PVN, and suggest that AII-sensitive LHA neurons with efferent projections to the SFO may act to enhance the excitability of putative VP-secreting neurons in the PVN via an excitatory influence on the AII-sensitive SFO neurons.

Action Potentials↗
PubMed1990

Scanning electron-microscope observations of the perikaryal projections of rabbit spinal ganglion neurons after enzymatic removal of connective tissue and satellite cells.

The true surface of rabbit spinal ganglion neurons has been made directly accessible to scanning electron-microscope observation after removal of both the connective tissue and satellite cells that normally cover it. The neuronal surface is characterized by a profusion of slender projections whose shapes have been determined and whose length and width have been quantified. Controls carried out with transmission electron microscopy demonstrate that the procedure employed in this study satisfactorily preserves neuronal structure.

Animals↗
PubMedDate not supplied

[Conditioned reflex changes in the functional connections between adjacent and remote cortical neurons].

A motor conditioned reflex to sound was elaborated in cats with electrodes (nichrome wire dia 50 mcm) chronically implanted in the auditory cortex. Multineuronal activity preceding by 30 s the conditioned signal was analysed. Impulse activity of two to three neurones was isolated from every record by means of an amplitude discriminator. Dependence between impulse series isolated either from one record or from records obtained with two electrodes placed at a distance of up to 200 mcm from one another, was estimated by crossover interval histograms. Consequently functional connections between neurones were defined by the dependence of impulse series. In the process of conditioning dynamic reorganization of interneuronal connections was revealed. With a stable reflex, the number of connections both between neurons in the microregion and between neurones of neighbouring microregions considerably increased due to an increased number of excitatory connections. After extinction of the reflex, the number of connections between adjacent neurons increased still more, though due to enhancement of the inhibitory type connections. Nonetheless, excitatory connections kept dominating. At the same time, the number of connections between neurons of the neighbouring microsystems sharply decreased.

Animals↗
PubMedDate not supplied

Trophic factor-induced plasticity of synaptic connections between identified Lymnaea neurons.

Neurotrophic factors participate in both developmental and adult synaptic plasticity; however, the underlying mechanisms remain unknown. Using soma-soma synapses between the identified Lymnaea neurons, we demonstrate that the brain conditioned medium (CM)-derived trophic factors are required for the formation of excitatory but not the inhibitory synapse. Specifically, identified presynaptic [right pedal dorsal 1 (RPeD1) and visceral dorsal 4 (VD4)] and postsynaptic [visceral dorsal 2/3 (VD2/3) and left pedal dorsal 1 (LPeD1)] neurons were soma-soma paired either in the absence or presence of CM. We show that in defined medium (DM-does not contain extrinsic trophic factors), appropriate excitatory synapses failed to develop between RPeD1 and VD2/3. Instead, inappropriate inhibitory synapses formed between VD2/3 and RPeD1. Similarly, mutual inhibitory synapses developed between VD4 and LPeD1 in DM. These inhibitory synapses were termed novel because they do not exist in the intact brain. To test whether DM-induced, inappropriate inhibitory synapses could be corrected by the addition of CM, cells were first paired in DM for an initial period of 12 hr. DM was then replaced with CM, and simultaneous intracellular recordings were made from paired cells after 6-12 hr of CM substitution. Not only did CM induce the formation of appropriate excitatory synapses between both cell pairs, but it also reduced the incidence of inappropriate inhibitory synapse formation. The CM-induced plasticity of synaptic connections involved new protein synthesis and transcription and was mediated via receptor tyrosine kinases. Taken together, our data provide the first direct insight into the cellular mechanism underlying trophic factor-induced specificity and plasticity of synaptic connections between soma-soma paired Lymnaea neurons.

Animals↗
PubMed1977

[Characteristics of neuronal structure and afferent connections of the central gray matter of cat's brain stem].

The central grey matter was studied in kittens and adult cats by Golgi method after destruction of the reticular formation. Two types of neurons have been shown. One of them--similar to those of the reticular formation--from the external two thirds of the substance. Others--similar to neuroblasts--lie near the wall of the aqueduct of Sylvius. Afferent fibres running to neurons of the vertebral and lateral parts of the external zone of the central grey matter from the reticular formation zone adjacent to nuclei of the spinal pathway of the trigeminal nerve and from the caudal reticular nucleus of the pons were detected. The neurons of the internal, parietal zone of the substance are considered as haemoreceptors of the liquid cerebral medium. The material is discussed from the viewpoint of participation of the structures in question in the functional system controlling behavior of man and animals during starvation.

Animals↗
PubMed2004

The focality of the global Alzheimer brain process: is the selective vulnerability of neurons a specific phenomenon of primary neuronal pathobiology?

A focality in the development of a global series of predisposing factors that conditions a progressiveness in the neurodegenerative process of Alzheimer type would appear to arise as a specific lesion of the neuron. Such a neuronal lesion would perhaps disrupt functional connectivity of neuronal networks in a process involving loss of neuronal viability. Indeed, a strict concept of selective vulnerability of neurons in the Alzheimer brain might be simply a preconditioning by microenvironmental factors that interacts with the individual neuron in terms of cellular component depletion or in terms of plasmalemmal disruption. In a final analysis, perhaps, the individual neuron would appear as the essential focus of a process that would account for a conditioning globality of the Alzheimer process that promotes both progressiveness and irreversibility of the brain pathology.

Alzheimer Disease↗
PubMed2001

Electrical activity and development of neural circuits.

A distinct feature of the nervous system is the intricate network of synaptic connections among neurons of diverse phenotypes. Although initial connections are formed largely through molecular mechanisms that depend on intrinsic developmental programs, spontaneous and experience-driven electrical activities in the developing brain exert critical epigenetic influence on synaptic maturation and refinement of neural circuits. Selective findings discussed here illustrate some of our current understanding of the effects of electrical activity on circuit development and highlight areas that await further study.

Action Potentials↗
PubMed2004

Trophic support delays but does not prevent cell-intrinsic degeneration of neurons deficient for munc18-1.

The stability of neuronal networks is thought to depend on synaptic transmission which provides activity-dependent maintenance signals for both synapses and neurons. Here, we tested the relationship between presynaptic secretion and neuronal maintenance using munc18-1-null mutant mice as a model. These mutants have a specific defect in secretion from synaptic and large dense-cored vesicles [Verhage et al. (2000), Science, 287, 864-869; Voets et al. (2001), Neuron, 31, 581-591]. Neuronal networks in these mutants develop normally up to synapse formation but eventually degenerate. The proposed relationship between secretion and neuronal maintenance was tested in low-density and organotypic cultures and, in vivo, by conditional cell-specific inactivation of the munc18-1 gene. Dissociated munc18-1-deficient neurons died within 4 days in vitro (DIV). Application of trophic factors, insulin or BDNF delayed degeneration up to 7 DIV. In organotypic cultures, munc18-1-deficient neurons survived until 9 DIV. On glial feeders, these neurons survived up to 10 DIV and 14 DIV when insulin was applied. Co-culturing dissociated mutant neurons with wild-type neurons did not prolong survival beyond 4 DIV, but coculturing mutant slices with wild-type slices prolonged survival up to 19 DIV. Cell-specific deletion of munc18-1 expression in cerebellar Purkinje cells in vivo resulted in the specific loss of these neurons without affecting connected or surrounding neurons. Together, these data allow three conclusions. First, the lack of synaptic activity cannot explain the degeneration in munc18-1-null mutants. Second, trophic support delays but cannot prevent degeneration. Third, a cell-intrinsic yet unknown function of munc18-1 is essential for prolonged survival.

Action Potentials↗
PubMed1990

Neuronal development in vitamin B6 deficiency.

The morphological changes observed in developing brain regions associated with maternal vitamin B6 deficits are summarized in Table 4. Brain development is a complex and orderly process consisting of cell division, proliferation, migration, and maturation. In the rat, vitamin B6 deficits imposed in utero and up to 30 days postnatal interfere with this orderly process. Deficits of the vitamin imposed in utero have been associated with reduced numbers of total and normal neurons in neocortex and with increased shrunken neurons (700-1500% of controls) in this region. These changes reflect the critical role of vitamin B6 in both neurogenesis and neuron longevity in neocortex. Postnatal cellular events in the neocortex, that is, neuron differentiation and synaptogenesis, were also altered by vitamin B6 deficits; higher order dendrites were reduced on stellate neurons in Layer II and on pyramidal neurons in Layer V. Synaptic density was less in the neutrophil of neocortex and in caudate/putamen, but structural integrity of the synapse was maintained. In cerebellum, both the molecular and granular areas were reduced, the monolayer organization of Purkinje cells was disrupted, and dendritic arborization of the cells was decreased. The number of myelinated axons, as determined by electron microscopy, was decreased in the mediodorsal portion of the pyramidal tract in the medulla oblongata as well as the specific activity of myelination of the total brain. Thus the functional consequences of vitamin B6 deficits during neuronal development may be through reduced connections among neurons and decreased myelination, which alter the rate and magnitude of transmission of nerve impulses.

Animals↗
PubMed1995

Modulation of an inhibitory interneuron in the neural circuitry for the tail withdrawal reflex of Aplysia.

1. Serotonin (5-HT), small cardioactive peptide B (SCPB) and FMRFamide have well-established facilitatory and inhibitory effects on sensory neurons and their connections with motor neurons mediating withdrawal reflexes in Aplysia. Little is known, however, about their effects on interneurons contributing to those reflexes. As a first step, we examined the effects of these three transmitters on the identified inhibitory interneuron RP14 in isolated pleural-pedal ganglia. 2. Bath application of 5-HT hyperpolarized RP14, inhibited its spontaneous activity and decreased its excitability. In addition, 5-HT decreased the amplitude of inhibitory postsynaptic potentials produced by RP14 in tail sensory and motor neurons. 3. In contrast, bath application of SCPB increased spontaneous activity in RP14. Subsequent application of 5-HT to the bath, which still contained SCPB, inhibited RP14. Therefore, the effects of SCPB were essentially opposite to those of 5-HT on this inhibitory interneuron. 4. FMRFamide had little effect on RP14. It did not produce an obvious change in its resting membrane potential and produced only a transient increase in its spontaneous activity. 5. These results suggest that various neuromodulators have differential effects on elements of the neuronal circuit underlying the tail-withdrawal reflex of Aplysia. Differential modulation may determine the overall behavioral manifestations associated with sensitization.

Action Potentials↗
PubMed1998

Changes in membrane and synaptic properties of thalamocortical circuitry caused by hydrogen peroxide.

Free radical (FR) production was linked to the generation of epileptiform activity. We performed electrophysiological recordings in rat thalamocortical slices to investigate the effects of FRs on the intrinsic and synaptic properties of thalamic and cortical neurons. Whole cell recordings from identified cortical pyramidal neurons and thalamic neurons of the ventrobasal nucleus revealed that exposure to the FR-forming agent H2O2 (2.5 mM) decreased gamma-aminobutyric acid-A- and gamma-aminobutyric acid-B-mediated inhibition to 35.3 +/- 13.4% and 13.7 +/- 4.4% (means +/- SE) of control in cortical neurons and to 41.8 +/- 14.8% and 33.6 +/- 11.6% of control in thalamic neurons. H2O2 application increased excitatory transmission in thalamic neurons to 162.9 +/- 29.6% of control but caused no change in cortical neurons. H2O2 altered significantly the characteristic low-pass filter behavior of cortical and thalamic cells as determined by their input impedances. After 35 min of superfusion, the impedance of cortical neurons decreased by 67.0 +/- 14.5%, and thalamic decreased by 76.3 +/- 2.7% for the frequencies in the range 1-50 Hz while remaining constant for frequencies > 200 Hz. Neuronal hyperexcitability was manifested during H2O2 exposure by continuous firing and long depolarizing shifts in response to extracellular stimulation in both thalamocortical and cortical neurons only in slices preserving thalamocortical connections. In slices with severed thalamocortical connections, cortical neurons did not show signs of hyperexcitability. These observations indicate that FRs could promote hyperexcitability of thalamocortical circuits by altering the balance between excitation and inhibition and by transforming the characteristic low-pass filter behavior into a flat band-pass filter.

2-Amino-5-phosphonovalerate↗
PubMed1992

Neuronal excitability: voltage-dependent currents and synaptic transmission.

Neuronal membrane excitability and the synaptic connections among neurons produce behavior and cognition. The intracellular compartment of neurons is negatively charged relative to the extracellular space, and this charge, as well as current flow, is produced by ions. From the perspective of charged ions, the lipid bilayer of the neuronal membrane acts as a capacitor, and transmembrane glycoprotein pores or channels act as resistors. The open and closed states of ionic channels determine the membrane potential. At equilibrium, the lowest resistance or greatest permeability is for potassium, and the resting membrane potential is close to the equilibrium potential for potassium. When a channel is opened, permeable ions diffuse down their electrochemical gradients and the membrane potential is changed. Channels are gated (opened or closed) by voltage, neurotransmitters, and second messengers. The neuron integrates synaptic potentials produced by transmitter-gated channel activity and either generates a subthreshold potential, or a suprathreshold depolarization that generates an action potential or a burst of action potentials. Action potential generation is mediated by a large, brief sodium influx that is followed by activation of a voltage-dependent potassium eflux. The pattern of action potential firing is dependent on the interaction of a repertoire of voltage-dependent ion conductances. The action potential is the main signaling mechanism to activate synaptic transmission at axon terminals. Synaptic transmission is graded depending on the amount of calcium entering the presynaptic terminal. The number of action potentials, or the shape of the action potential, will determine the amount of calcium entering the terminal and the efficacy of synaptic transmission. Presynaptic ion channels may also be controlled by neurotransmitters or modulators and affect synaptic transmission by altering the amount of calcium influx.

Animals↗
PubMed1993

How independent are the messages carried by adjacent inferior temporal cortical neurons?

There are at least three possibilities for encoding information in a small area of cortex. First, neurons could have identical characteristics, thus conveying redundant information; second, neurons could give different responses to the same stimuli, thus conveying independent information; or third, neurons could cooperate with each other to encode more information jointly than they do separately, that is, synergistically. We recorded from 28 pairs of neurons in inferior temporal cortex of behaving rhesus monkeys. Each pair was recorded from a single microelectrode. Both the magnitude and the temporal modulation of the responses were quantified. We separated the responses into signal (average response to each stimulus) and noise (deviation of each response from the average). Linear regression showed that an average of only 18.7% of the magnitude of the signal carried by one neuron could be predicted from the magnitude of the other, and only 22.0% could be predicted by including the temporal modulation. For the noise, the figures were 5.5% and 6.3%, respectively, even less than for the signal. Information theoretic analysis shows that the pairs of neurons we studied carried an average of 20% redundant information. However, even this relatively small amount of redundancy places a severe upper limit on the information that can be transmitted by a neuronal pool. A pool of neurons for which each pair is mutually redundant to extent y can only carry a maximum of 1/y, here five times, as much information as one neuron alone. Information theoretic analysis gave no evidence for the presence of information as a function of both neurons considered together, that is, synergistic codes. Cross-correlation showed that at least 61% of the neuronal pairs shared connections in some manner. Given these shared connections, if adjacent neurons had had identical characteristics, then the noise on the outputs of these neurons would have been highly correlated, and it would not be possible to separate the signal and noise. The severe impact of correlated noise and information redundancy leads us to propose that the processing carried out by these neurons evolved both to provide a rich description of many stimulus properties and simultaneously to minimize the redundancy in a local group of neurons. These two principles appear to be a major constraint on the organization of inferior temporal, and possibly all, cortex.

Animals↗