scholarly journals Release of chemical transmitters from cell bodies and dendrites of nerve cells

2015 ◽  
Vol 370 (1672) ◽  
pp. 20140181 ◽  
Author(s):  
Francisco F. De-Miguel ◽  
John G. Nicholls
Keyword(s):  
Action Potentials ◽  
Motor Performance ◽  
Time Course ◽  
Neuronal Cell ◽  
Normal Function ◽  
Snare Proteins ◽  
Signalling Molecules ◽  
Neuronal Cell Bodies ◽  
The Brain

Papers in this issue concern extrasynaptic transmission, namely release of signalling molecules by exocytosis or diffusion from neuronal cell bodies, dendrites, axons and glia. Problems discussed concern the molecules, their secretion and importance for normal function and disease. Molecules secreted extrasynaptically include transmitters, peptides, hormones and nitric oxide. For extrasynaptic secretion, trains of action potentials are required, and the time course of release is slower than at synapses. Questions arise concerning the mechanism of extrasynaptic secretion: how does it differ from the release observed at synaptic terminals and gland cells? What kinds of vesicles take part? Is release accomplished through calcium entry, SNAP and SNARE proteins? A clear difference is in the role of molecules released synaptically and extrasynaptically. After extrasynaptic release, molecules reach distant as well as nearby cells, and thereby produce long-lasting changes over large volumes of brain. Such changes can affect circuits for motor performance and mood states. An example with clinical relevance is dyskinesia of patients treated with l -DOPA for Parkinson's disease. Extrasynaptically released transmitters also evoke responses in glial cells, which in turn release molecules that cause local vasodilatation and enhanced circulation in regions of the brain that are active.

scholarly journals Immunoreactivity of the calbindin D28k in the parahippocampal gyrus of chinchilla

2013 ◽  
Vol 57 (3) ◽  
pp. 387-391
Author(s):  
Radosław Szalak ◽  
Jadwiga Jaworska-Adamu ◽  
Karol Rycerz ◽  
Paweł Kulik ◽  
Marcin Bartłomiej Arciszewski
Keyword(s):  
Brain Area ◽  
Neuronal Cell ◽  
Immunofluorescence Staining ◽  
Parahippocampal Gyrus ◽  
Neuronal Cell Bodies ◽  
Entorhinal Area ◽  
Calbindin D28k ◽  
Retzius Cells ◽  
Species Specific ◽  
The Brain

Abstract Ten adult male chinchillas were used. The localisation of calbindin D28k (CB) was examined with the use of two types of reactions: immunocytochemical peroxidase-antiperoxidase and immunofluorescence staining with a specific monoclonal antibody against CB. Immunocytochemical examination demonstrated the presence of CB-positive neurons in the following layers of all parts the parahippocampal gyrus (PG): marginal, external cellular, middle cellular, and internal cellular, i.e. in entorhinal area, parasubiculum, and presubiculum. Immunofluorescence staining revealed the presence of CB in both Hu C/Dimmunoreactive (IR) neurons and nervous fibers of the PG. CB-IR neuronal cell bodies were moderately numerous (ca. 10% of Hu C/D-IR neurons) and clearly distinguished from the background. Each layer of the brain area consisted of two types of neurons: pyramidal and multiform. Among the second type of neurons, four kinds of morphologically different neuronal subclasses were observed: multipolar, bipolar, round, and Cajal-Retzius cells. It is concluded that the expression of CB in the PG of the chinchilla is species specific and limited to several subclasses of neurons

Role of vasopressin in sympathetic response to paraventricular nucleus stimulation in anesthetized rats

1994 ◽  
Vol 266 (1) ◽  
pp. R228-R236 ◽  
Author(s):  
S. C. Malpas ◽  
J. H. Coote
Keyword(s):  
Paraventricular Nucleus ◽  
Neuronal Cell ◽  
Detection Algorithm ◽  
Homocysteic Acid ◽  
Renal Sympathetic Nerve Activity ◽  
Anesthetized Rats ◽  
Neuronal Cell Bodies ◽  
Peak Detection Algorithm ◽  
Glass Micropipette

Vasopressin may play an extrahypothalamic role in the central control of the cardiovascular system, specifically acting as a spinal neurotransmitter in the pathway where the paraventricular nucleus (PVN) alters sympathetic outflow. In this study, the effect of stimulating neuronal cell bodies in the PVN on renal sympathetic nerve activity (RSNA) and the possible involvement of vasopressin in the pathway was investigated in anesthetized rats. The PVN was stimulated by microinjection with 0.2 M D,L-homocysteic acid via a glass micropipette, and the hemodynamic and sympathetic responses were recorded. A computerized sympathetic peak-detection algorithm was applied to recordings of sympathetic discharges to retrieve information about the characteristics of RSNA during PVN stimulation. The algorithm scanned the series of RSNA voltages for significant increases followed by significant decreases in a small cluster of voltage values. Once each synchronized RSNA peak had been detected, its corresponding amplitude and peak-to-peak interval were calculated. PVN stimulation consistently increased the amplitude of RSNA (mean 30 +/- 5.6% over control), arterial pressure, and the peak-to-peak interval of discharges. A V1 vasopressin antagonist intrathecally administered as a 500-pmol dose was subsequently able to completely block the hemodynamic response (blood pressure increase of 14 +/- 5%) and a 35 +/- 6% increase in RSNA in response to PVN stimulation and intrathecal vasopressin. Thus spinal vasopressin is likely to be a neurotransmitter involved in the cardiovascular regulation involving the PVN.

Forward Dendritic Spikes

2011 ◽  
pp. 42-59
Author(s):  
Oscar Herreras ◽  
Julia Makarova ◽  
José Manuel Ibarz
Keyword(s):  
Action Potentials ◽  
Remarkable Property ◽  
Synaptic Inputs ◽  
Brain Circuits ◽  
Voltage Dependent ◽  
Dendritic Spikes ◽  
Underlying Mechanisms ◽  
The Brain ◽  
Made In

Neurons send trains of action potentials to communicate each other. Different messages are issued according to varying inputs, but they can also mix them up in a multiplexed language transmitted through a single cable, the axon. This remarkable property arises from the capability of dendritic domains to work semi autonomously and even decide output. We review the underlying mechanisms and theoretical implications of the role of voltage-dependent dendritic currents on the forward transmission of synaptic inputs, with special emphasis in the initiation, integration and forward conduction of dendritic spikes. When these spikes reach the axon, output decision was made in one of many parallel dendritic substations. When failed, they still serve as an internal language to transfer information between dendritic domains. This notion brakes with the classic view of neurons as the elementary units of the brain and attributes them computational/storage capabilities earlier billed to complex brain circuits.

Contributions of nerves and metabolites to exercise vasodilation: a unifying hypothesis

1979 ◽  
Vol 236 (5) ◽  
pp. H705-H719 ◽  
Author(s):  
C. R. Honig
Keyword(s):  
Skeletal Muscle ◽  
Local Anesthetics ◽  
Time Course ◽  
Striated Muscle ◽  
Neuronal Cell ◽  
Half Time ◽  
Phasic Contraction ◽  
Dose Time ◽  
Intrinsic Nerves ◽  
Neuronal Cell Bodies

Neuronal cell bodies exist in arterioles of skeletal muscle and appear to initiate vasodilation during phasic contraction. The following findings indicate that intrinsic nerves rather than metabolites maintain vasodilation during sustained phasic contraction with free flow. 1) Under certain conditions maximal vasodilation can occur without detectable release of metabolites. 2) When metabolites are released during exercise, their concentrations in blood or tissue do not always determine the extent of vasodilation. 3) Vasodilation during sustained contraction can be partly blocked by local anesthetics. The extent of block is inversely proportional to the concentration of metabolites. Dose, time course of block, and other tests of specificity indicate that local anesthetics act on the intrinsic nerves rather than smooth or striated muscle. When contraction stops, neurogenic vasodilation decays rapidly (half time less than 1 min). Sustained vasodilation during recovery is therefore fully accounted for by metabolites. A hypothesis is suggested that integrates the roles of extrinsic nerves, intrinsic nerves, and metabolites in support of muscle contraction.

Low-affinity sulfonylurea binding sites reside on neuronal cell bodies in the brain

1997 ◽  
Vol 745 (1-2) ◽  
pp. 1-9 ◽  
Author(s):  
Ambrose A Dunn-Meynell ◽  
Vanessa H. Routh ◽  
Joseph J McArdle ◽  
Barry E Levin
Keyword(s):  
Binding Sites ◽  
Neuronal Cell ◽  
Neuronal Cell Bodies ◽  
The Brain

scholarly journals The central role of mitochondria in axonal degeneration in multiple sclerosis

2014 ◽  
Vol 20 (14) ◽  
pp. 1806-1813 ◽  
Author(s):  
Graham R Campbell ◽  
Joseph T Worrall ◽  
Don J Mahad
Keyword(s):  
Multiple Sclerosis ◽  
Axonal Degeneration ◽  
Neuronal Cell ◽  
Mitochondrial Respiratory Chain ◽  
Respiratory Chain Complexes ◽  
Autoimmune Encephalomyelitis ◽  
Mitochondrial Abnormalities ◽  
Neuronal Cell Bodies ◽  
Chain Complexes

Neurodegeneration in multiple sclerosis (MS) is related to inflammation and demyelination. In acute MS lesions and experimental autoimmune encephalomyelitis focal immune attacks damage axons by injuring axonal mitochondria. In progressive MS, however, axonal damage occurs in chronically demyelinated regions, myelinated regions and also at the active edge of slowly expanding chronic lesions. How axonal energy failure occurs in progressive MS is incompletely understood. Recent studies show that oligodendrocytes supply lactate to myelinated axons as a metabolic substrate for mitochondria to generate ATP, a process which will be altered upon demyelination. In addition, a number of studies have identified mitochondrial abnormalities within neuronal cell bodies in progressive MS, leading to a deficiency of mitochondrial respiratory chain complexes or enzymes. Here, we summarise the mitochondrial abnormalities evident within neurons and discuss how these grey matter mitochondrial abnormalities may increase the vulnerability of axons to degeneration in progressive MS. Although neuronal mitochondrial abnormalities will culminate in axonal degeneration, understanding the different contributions of mitochondria to the degeneration of myelinated and demyelinated axons is an important step towards identifying potential therapeutic targets for progressive MS.

scholarly journals Adaptive behaviour and learning in slime moulds: the role of oscillations

2021 ◽  
Vol 376 (1820) ◽  
pp. 20190757 ◽  
Author(s):  
Aurèle Boussard ◽  
Adrian Fessel ◽  
Christina Oettmeier ◽  
Léa Briard ◽  
Hans-Günther Döbereiner ◽  
...  
Keyword(s):  
Information Processing ◽  
Adaptive Behaviour ◽  
Learning Abilities ◽  
Slime Mould ◽  
Signalling Molecules ◽  
Slime Moulds ◽  
Wave Patterns ◽  
Spatio Temporal ◽  
The Brain

The slime mould Physarum polycephalum , an aneural organism, uses information from previous experiences to adjust its behaviour, but the mechanisms by which this is accomplished remain unknown. This article examines the possible role of oscillations in learning and memory in slime moulds. Slime moulds share surprising similarities with the network of synaptic connections in animal brains. First, their topology derives from a network of interconnected, vein-like tubes in which signalling molecules are transported. Second, network motility, which generates slime mould behaviour, is driven by distinct oscillations that organize into spatio-temporal wave patterns. Likewise, neural activity in the brain is organized in a variety of oscillations characterized by different frequencies. Interestingly, the oscillating networks of slime moulds are not precursors of nervous systems but, rather, an alternative architecture. Here, we argue that comparable information-processing operations can be realized on different architectures sharing similar oscillatory properties. After describing learning abilities and oscillatory activities of P. polycephalum , we explore the relation between network oscillations and learning, and evaluate the organism's global architecture with respect to information-processing potential. We hypothesize that, as in the brain, modulation of spontaneous oscillations may sustain learning in slime mould. This article is part of the theme issue ‘Basal cognition: conceptual tools and the view from the single cell’.

scholarly journals Deletion of the voltage-gated calcium channel, CaV1.3, causes deficits in motor performance and associative learning

2020 ◽  
Author(s):  
Marisol Lauffer ◽  
Hsiang Wen ◽  
Bryn Myers ◽  
Ashley Plumb ◽  
Krystal Parker ◽  
...  
Keyword(s):  
Motor Learning ◽  
Associative Learning ◽  
Motor Performance ◽  
Social Preference ◽  
Neural Circuits ◽  
Social Deficits ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
The Brain

AbstractL-type voltage-gated calcium channels (LVGCCs) are important regulators of neuronal activity and are widely expressed throughout the brain. One of the major LVGCC isoforms in the brain is CaV1.3. Mice lacking CaV1.3 (CaV1.3 KO) have impairments in fear conditioning and depressive-like behaviors, which have been linked to the role of CaV1.3 in hippocampal and amygdala function. Genetic variation in CaV1.3 has been linked to a variety of psychiatric disorders, including autism and schizophrenia, which are associated with motor, learning, and social deficits. Here, we explored whether CaV1.3 plays a role in these behaviors. We found that CaV1.3 KO mice have deficits in rotarod learning despite normal locomotor function. Deletion of CaV1.3 is also associated with impaired associative learning on the Erasmus Ladder. We did not observe any impairments in CaV1.3 KO mice on assays of anxiety-like, depression-like, or social preference behaviors. Our results suggest an important role for CaV1.3 in neural circuits involved in motor learning and concur with previous data showing its involvement in associative learning.

scholarly journals The prion protein gene: a role in mouse embryogenesis?

Development ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 117-122 ◽  
Author(s):  
J. Manson ◽  
J.D. West ◽  
V. Thomson ◽  
P. McBride ◽  
M.H. Kaufman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nervous System ◽  
Prion Protein ◽  
In Situ Hybridisation ◽  
Neuronal Cell ◽  
Normal Function ◽  
Cell Populations ◽  
Specific Expression ◽  
The Brain ◽  
Prp Gene

The neural membrane glycoprotein PrP (prion protein) has a key role in the development of scrapie and related neurodegenerative diseases. During pathogenesis, PrP accumulates in and around cells of the brain from which it can be isolated in a disease-specific, protease-resistant form. Although the involvement of PrP in the pathology of these diseases has long been known, the normal function of PrP remains unknown. Previous studies have shown that the PrP gene is expressed tissue specifically in adult animals, the highest levels in the brain, with intermediate levels in heart and lung and low levels in spleen. Prenatally, PrP mRNA has been detected in the brain of rat and hamster just prior to birth. In this study we have examined the expression of the PrP gene during mouse embryonic development by in situ hybridisation and observed dramatic regional and temporal gene expression in the embryo. Transcripts were detected in developing brain and spinal cord by 13.5 days. In addition, PrP gene expression was detected in the peripheral nervous system, in ganglia and nerve trunks of the sympathetic nervous system and neural cell populations of sensory organs. Expression of the PrP gene was not limited to neuronal cells, but was also detected in specific non-neuronal cell populations of the 13.5 and 16.5 day embryos and in extra-embryonic tissues from 6.5 days. This cell-specific expression suggests a pleiotropic role for PrP during development.

scholarly journals Molecular and Cellular Impact of Inflammatory Extracellular Vesicles (EVs) Derived from M1 and M2 Macrophages on Neural Action Potentials

2020 ◽  
Vol 10 (7) ◽  
pp. 424
Author(s):  
Sarah Vakili ◽  
Taha Mohseni Ahooyi ◽  
Shadan S. Yarandi ◽  
Martina Donadoni ◽  
Jay Rappaport ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Immune Cells ◽  
Action Potentials ◽  
M2 Macrophage ◽  
M2 Macrophages ◽  
Neuronal Functions ◽  
The Brain ◽  
Macrophage Subtypes ◽  
M1 And M2 Macrophages

Several factors can contribute to neuroinflammatory disorders, such as cytokine and chemokines that are produced and released from peripherally derived immune cells or from locally activated cells such as microglia and perivascular macrophages in the brain. The primary function of these cells is to clear inflammation; however, following inflammation, circulating monocytes are recruited to the central nervous system (CNS). Monocyte-derived macrophages in the CNS play pivotal roles in mediating neuroinflammatory responses. Macrophages are heterogeneous both in normal and in pathological conditions due to their plasticity, and they are classified in two main subsets, classically activated (M1) or alternatively activated (M2). There is accumulating evidence suggesting that extracellular vesicles (EVs) released from activated immune cells may play crucial roles in mediating inflammation. However, a possible role of EVs released from immune cells such as M1 and M2 macrophages on neuronal functions in the brain is not known. In order to investigate the molecular and cellular impacts of macrophages and EVs released from macrophage subtypes on neuronal functions, we used a recently established in vitro M1 and M2 macrophage culture model and isolated and characterized EVs from these macrophage subtypes, treated primary neurons with M1 or M2 EVs, and analyzed the extracellular action potentials of neurons with microelectrode array studies (MEA). Our results introduce evidence on the interfering role of inflammatory EVs released from macrophages in interneuronal signal transmission processes, with implications in the pathogenesis of neuroinflammatory diseases induced by a variety of inflammatory insults.

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