Combining Anterograde Tracing and Immunohistochemistry to Define Neuronal Synaptic Circuits

2016 ◽  
pp. 63-80
Author(s):  
Dusica Bajic
Keyword(s):  
Anterograde Tracing ◽  
Synaptic Circuits

scholarly journals Phagocytic glial cells: sculpting synaptic circuits in the developing nervous system

2013 ◽  
Vol 23 (6) ◽  
pp. 1034-1040 ◽  
Author(s):  
Dorothy P. Schafer ◽  
Beth Stevens
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Synaptic Circuits ◽  
Developing Nervous System

Pattern of retinal projections in the California ground squirrel (Spermophilus beecheyi): Anterograde tracing study using cholera toxin

2003 ◽  
Vol 463 (3) ◽  
pp. 317-340 ◽  
Author(s):  
Daniel E. Major ◽  
Hillary R. Rodman ◽  
Camilo Libedinsky ◽  
Harvey J. Karten
Keyword(s):  
Cholera Toxin ◽  
Ground Squirrel ◽  
Anterograde Tracing ◽  
Spermophilus Beecheyi ◽  
California Ground Squirrel ◽  
Retinal Projections

scholarly journals Efferent projections of the retrorubral nucleus to the substantia nigra and ventral tegmental area in cats as shown by anterograde tracing

1996 ◽  
Vol 40 (3) ◽  
pp. 219-228 ◽  
Author(s):  
M.P.M. Arts ◽  
H.J. Groenewegen ◽  
J.G. Veening ◽  
A.R. Cools
Keyword(s):  
Substantia Nigra ◽  
Ventral Tegmental Area ◽  
Anterograde Tracing ◽  
Efferent Projections ◽  
Ventral Tegmental

scholarly journals Rapid Neuronal Ultrastructure Disruption and Recovery during Spreading Depolarization-Induced Cytotoxic Edema

2020 ◽  
Vol 30 (10) ◽  
pp. 5517-5531 ◽  
Author(s):  
Sergei A Kirov ◽  
Ioulia V Fomitcheva ◽  
Jeremy Sword
Keyword(s):  
Tissue Perfusion ◽  
Ultrastructural Level ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Structural Basis ◽  
Cytotoxic Edema ◽  
Spreading Depolarization ◽  
Synaptic Circuits ◽  
Common Carotid Artery Occlusion

Abstract Two major pathogenic events that cause acute brain damage during neurologic emergencies of stroke, head trauma, and cardiac arrest are spreading depolarizing waves and the associated brain edema that course across the cortex injuring brain cells. Virtually nothing is known about how spreading depolarization (SD)-induced cytotoxic edema evolves at the ultrastructural level immediately after insult and during recovery. In vivo 2-photon imaging followed by quantitative serial section electron microscopy was used to assess synaptic circuit integrity in the neocortex of urethane-anesthetized male and female mice during and after SD evoked by transient bilateral common carotid artery occlusion. SD triggered a rapid fragmentation of dendritic mitochondria. A large increase in the density of synapses on swollen dendritic shafts implies that some dendritic spines were overwhelmed by swelling or merely retracted. The overall synaptic density was unchanged. The postsynaptic dendritic membranes remained attached to axonal boutons, providing a structural basis for the recovery of synaptic circuits. Upon immediate reperfusion, cytotoxic edema mainly subsides as affirmed by a recovery of dendritic ultrastructure. Dendritic recuperation from swelling and reversibility of mitochondrial fragmentation suggests that neurointensive care to improve tissue perfusion should be paralleled by treatments targeting mitochondrial recovery and minimizing the occurrence of SDs.

scholarly journals N-cadherin regulates molecular organization of excitatory and inhibitory synaptic circuits in adult hippocampus in vivo

Hippocampus ◽  
2014 ◽  
Vol 24 (8) ◽  
pp. 943-962 ◽  
Author(s):  
Jessica S. Nikitczuk ◽  
Shekhar B. Patil ◽  
Bridget A. Matikainen-Ankney ◽  
Joseph Scarpa ◽  
Matthew L. Shapiro ◽  
...  
Keyword(s):  
Molecular Organization ◽  
Synaptic Circuits ◽  
Adult Hippocampus

Cholecystokinin-8s excites identified rat pancreatic-projecting vagal motoneurons

2007 ◽  
Vol 293 (2) ◽  
pp. G484-G492 ◽  
Author(s):  
Shuxia Wan ◽  
F. Holly Coleman ◽  
R. Alberto Travagli
Keyword(s):  
Brain Stem ◽  
Pancreatic Polypeptide ◽  
Potassium Conductance ◽  
Input Resistance ◽  
Exocrine Secretion ◽  
Motor Nucleus ◽  
Pancreatic Exocrine Secretion ◽  
Calcium Dependent ◽  
Synaptic Circuits ◽  
Pancreatic Exocrine

It is known that cholecystokinin (CCK) acts in a paracrine fashion to increase pancreatic exocrine secretion via vagal circuits. Recent evidence, however, suggests that CCK-8s actions are not restricted to afferent vagal fibers, but also affect brain stem structures directly. Within the brain stem, preganglionic neurons of the dorsal motor nucleus of the vagus (DMV) send efferent fibers to subdiaphragmatic viscera, including the pancreas. Our aims were to investigate whether DMV neurons responded to exogenously applied CCK-8s and, if so, the mechanism of action. Using whole cell patch-clamp recordings we show that perfusion with CCK-8s induced a concentration-dependent excitation in ∼60% of identified pancreas-projecting DMV neurons. The depolarization was significantly reduced by tetrodotoxin, suggesting both direct (on the DMV membrane) and indirect (on local synaptic circuits) effects. Indeed, CCK-8s increased the frequency of miniature excitatory currents onto DMV neurons. The CCK-A antagonist, lorglumide, prevented the CCK-8s-mediated excitation whereas the CCK-B preferring agonist, CCK-nonsulfated, had no effect, suggesting the involvement of CCK-A receptors only. In voltage clamp, the CCK-8s-induced inward current reversed at −106 ± 3 mV and the input resistance increased by 150 ± 15%, suggesting an effect mediated by the closure of a potassium conductance. Indeed, CCK-8s reduced both the amplitude and the time constant of decay of a calcium-dependent potassium conductance. When tested with pancreatic polypeptide (which reduces pancreatic exocrine secretion), cells that responded to CCK-8s with an excitation were, instead, inhibited by pancreatic polypeptide. These data indicate that CCK-8s may control pancreas-exocrine secretion also via an effect on pancreas-projecting DMV neurons.

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