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"Neurons."
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Governing behavior : how nerve cell dictatorships and democracies control everything we do
\"Everything we and other animals do is caused by electrical signals in nerve cells, or neurons. Neurons are organized into circuits, like the electrical circuits that run electronic devices. This book explores how these circuits function to control behaviors. In some circuits, a single neuron acts like a dictator, gathering information from many sources, making decisions, and issuing commands to produce movements, such as fish and crayfish escape maneuvers. In other circuits, a large population of neurons collectively votes, with no single neuron dominating, mediating color perception, for example, and controlling eye and hand movements to objects of interest. Neural circuits control all behaviors, from the simple and automatic to the complex and deliberative. Some of the most critical circuits generate rhythmic outputs that make an animal breathe, chew, digest, walk, run, swim, or fly. These central nervous system circuits can churn out rhythmic signals on their own, like central government programs, but modify output to match demand, using feedback signals from moving body parts. To select the right behavior for each moment, nervous systems use sophisticated sensory surveillance. For example, owl circuits calculate the precise locations of sound sources to catch mice in the dark. Bats catch flying insects by emitting ultrasonic pulses and using specialized circuits to analyze the echoes, a form of sonar. Central nervous systems keep track of their own movement commands to update the surveillance circuits. Although some neural circuits are innate, others, such as those producing human speech and bird song, depend on learning, even in adulthood.\"-- Provided by publisher.
Book
Correction: Perturbing low dimensional activity manifolds in spiking neuronal networks
[This corrects the article DOI: 10.1371/journal.pcbi.1007074.].
Journal Article
Correction: cGMP dynamics that underlies thermosensation in temperature-sensing neuron regulates thermotaxis behavior in C. elegans
[This corrects the article DOI: 10.1371/journal.pone.0278343.].
Journal Article
Correction: It’s All in Your Mind: Determining Germ Cell Fate by Neuronal IRE-1 in C. elegans
[This corrects the article DOI: 10.1371/journal.pgen.1004747.].[This corrects the article DOI: 10.1371/journal.pgen.1004747.].
Journal Article
Dawn of the neuron : the early struggles to trace the origin of nervous systems
Examines \"the labours and lives of scientists who studied coelenterate nervous systems over several generations, and who approached the puzzling origin of the first nerve cells through the process outlined in evolutionary theory, [and also explores] how these scientists, who were willing to embrace improved and paradigm-changing scientific methods, still revealed their cultural backgrounds, their societal biases, and their attachments to schools of thought and academic traditions while presenting their ground-breaking work\"--Amazon.com.
Book
The Expression and Functionality of CBsub.1R-NMDAR Complexes Are Decreased in A Parkinson’s Disease Model
One of the hallmarks of Parkinson’s disease (PD) is the alteration in the expression and function of NMDA receptor (NMDAR) and cannabinoid receptor 1 (CB[sub.1]R). The presence of CB[sub.1]R-NMDAR complexes has been described in neuronal primary cultures. The activation of CB[sub.1]R in CB[sub.1]R-NMDAR complexes was suggested to counteract the detrimental NMDAR overactivation in an AD mice model. Thus, we aimed to explore the role of this receptor complex in PD. By using Bioluminescence Resonance Energy Transfer (BRET) assay, it was demonstrated that α-synuclein induces a reorganization of the CB[sub.1]R-NMDAR complex in transfected HEK-293T cells. Moreover, α-synuclein treatment induced a decrease in the cAMP and MAP kinase (MAPK) signaling of both CB[sub.1]R and NMDAR not only in transfected cells but also in neuronal primary cultures. Finally, the interaction between CB[sub.1]R and NMDAR was studied by Proximity Ligation Assay (PLA) in neuronal primary cultures, where it was observed that the expression of CB[sub.1]R-NMDAR complexes was decreased upon α-synuclein treatment. These results point to a role of CB[sub.1]R-NMDAR complexes as a new therapeutic target in Parkinson’s disease.
Journal Article