1-10 of 182 Results



Alexei Verkhratsky

Astrocytes belong to an extended class of astroglia, a class of neural cells of ectodermal, neuroepithelial origin that sustain homeostasis and provide for defense of the brain and the spinal cord. Astroglial cells support homeostasis of the central nervous system at all levels of organization from molecular to organ-wide. Astrocytes cannot generate action potentials, being thus electrically nonexcitable cells. Astrocytic excitability is intracellular, being mediated by associations with spatiotemporal fluctuations of cytoplasmic ions and second messengers in response to chemical or mechanical stimulation. Astrocytes express an extended complement of receptors to neurotransmitters and neurohormones that allow them to coordinate their homeostatic function with neuronal activity. Astrocytic homeostatic responses are primarily mediated by plasmalemmal transporters, which in turn are regulated by cytoplasmic concentration of Na+ ions. Peripheral astrocytic processes, known as leaflets, establish intimate contacts with synapses forming an astroglial synaptic cradle. Astrocytes regulate synaptogenesis, synaptic isolation, synaptic maintenance, and synaptic extinction, thus being fundamental for neuronal plasticity. Loss of astrocytic homeostatic function leads to neuronal damage and is a universal part of pathogenesis of many neurological diseases.


Camillo Golgi  

Paolo Mazzarello

Camillo Golgi (1843–1926), a physician and researcher from Lombardy, was a leading figure in Italian science in the second half of the 19th century. His name is linked to several fundamental contributions: the invention of the “black reaction,” a method that made it possible to highlight, for the first time in history, the fine structure of the central nervous system; the discovery of the Golgi apparatus or complex, one of the fundamental components of the cell; the discovery of the perineural net (an extracellular matrix meshwork that wrap around some neurons with important physiological functions); the identification of the Golgi tendon organ (a proprioceptor that senses tension from the muscle); and the description of the malaria plasmodium cycle in the “tertian” and “quartan” forms of the disease with the identification of the correspondence between the multiplication of the parasite and febrile access (Golgi law). These are major scientific contributions that have profoundly changed basic areas of biology and medicine. To these must be added many other minor contributions that alone could have qualified the reputation of any researcher.


The Medieval Cell Doctrine  

Douglas J. Lanska

The medieval cell doctrine was a series of speculative psychological models derived from ancient Greco-Roman ideas in which cognitive faculties were assigned to “cells,” typically but not exclusively corresponding to the cerebral ventricles. During Late Antiquity and continuing during the Early Middle Ages, Christian philosophers reinterpreted Aristotle’s De Anima, along with later modifications by Herophilos and Galen, in a manner consistent with Christian doctrine. The resulting medieval cell doctrine was formulated by the fathers of the early Christian Church in the 4th and 5th centuries. Illustrations of the medieval cell doctrine were included in manuscripts since at least the 11th century. Printed images of the doctrine appeared in medical, philosophical, and religious works beginning with “graphic incunabula” at the end of the 15th century. Some of these early psychological models assigned various cognitive faculties to different nonoverlapping “cells” within the brain, while others specifically promoted or implied a linear sequence of events. By the 16th century, printed images of the doctrine were usually linear three-cell versions, with few exceptions having four or five cells. These psychological models were based on philosophical speculations rather than clinicopathologic evidence or experimentation. Despite increasingly realistic representations of the cerebral ventricles from the end of the 15th century until the middle of the 16th century, and direct challenges by Massa and Vesalius in the early 16th century and Willis in the 17th century, the doctrine saw its most elaborate formulations in the late 16th and early 17th centuries with illustrations by the Paracelsian physicians Bacci and Fludd. In addition, Descartes reinvigorated the ventricular localization of cerebral faculties in the 17th century beginning with his La Dioptrique (1637) and later with the Latin and French editions of his posthumously published Treatise of Man (1662-1667). Overthrow of the doctrine had to await the development of alternative models of brain function in the 17th and 18th centuries.


Behavioral, Cognitive, and Neural Mechanisms of Human Social Interaction  

Antonia F. de C. Hamilton

Social interaction is a fundamental part of what makes humans human and draws on a wide range of neural and cognitive mechanisms. This review summarizes research in terms of four suggested brain networks. First, the social perception network responds selectively to viewing and interpreting other people’s faces and bodies. Second, the theory of mind network is engaged when people think about other people’s beliefs and knowledge states. Third, the mirror neuron network has a role in understanding and imitating actions. Fourth, the emotion network shows some selective responses to emotional facial expressions and when people empathize with other’s pain. The role of these four networks in dynamic social interactions and real-world communication is also considered.


Jean-René Cruchet (1875–1959)  

Olivier Walusinski

Jean-René Cruchet (1875–1959) was a French physician from Bordeaux, where he practiced for the entirety of his career. His notoriety resulted from his publication of the first cases of the encephalitis lethargica epidemic in World War I soldiers in 1917, a few days before Constantin von Economo reported his cases. Cruchet developed an interest in abnormal movements, notably tics and dystonia, for which he primarily saw a psychological cause, to be treated rigorously with good habits and repressive precepts. He wrote prolifically about his areas of interest, also focusing on parkinsonian syndromes and the treatment of hysterics, notably soldiers with camptocormia. One of the first physicians to also be an aviator, Cruchet was a pioneer in the study of autonomic modifications caused by flying and pressure variations, which he referred to as aviator’s disease. As a personality with an outsized ego, he imagined that he would remain as famous after his death as Jean-Martin Charcot or Louis Pasteur.


Transcriptional Regulation Underlying Long-Term Sensitization in Aplysia  

Robert J. Calin-Jageman, Theresa Wilsterman, and Irina E. Calin-Jageman

The induction of a long-term memory requires both transcriptional change and neural plasticity. Many of the links between transcription and memory have been revealed through the study of long-term sensitization in the Aplysia genus of marine mollusks. Sensitization is a conserved, non-associative form of pain memory in which a painful stimulus produces an increase in arousal and defensive behavior. The neural circuits that help encode sensitization memory are well characterized, and sensitization can be simulated in neuronal cell cultures. One feature of sensitization in Aplysia is that only some training protocols initiate transcription and produce long-term memory; others produce only short-term memories. This occurs because the induction of long-term sensitization requires the activation of two signal-transduction pathways that regulate transcription: (a) a fast but transient activation of the cAMP/PKA pathway that activates the transcription factor CREB1 and (b) a delayed activation of the ERK isoform of MAPK that deactivates the transcriptional repressor CREB2. The effectiveness of different training protocols is based on the synchronization of these pathways. The cAMP/PKA and MAPK pathways are complex, involving extracellular and trans-synaptic signaling, feedback loops, and crosstalk. It has proven possible to model transcriptional activation with enough fidelity to generate in silico predictions for optimized learning, which has been validated in cell cultures and intact animals. Training protocols that successfully activate CREB1 while deactivating CREB2 produce a complex transcriptional cascade that helps encode long-term sensitization memory. The transcriptional cascade involves a focused wave of immediate-early transcriptional activations. This includes the activation of additional transcription factors, such as C/EBP, as well as effectors such as uch, sensorin, and tolloid/BMP-1. These early transcriptional changes close feedback loops that help extend and stabilize the early wave of transcriptional changes, triggering a broader late wave of transcriptional changes likely to alter neural signaling, increase protein production, transport mRNAs, and induce meta-plasticity. A small set of transcripts participate in both the early and late waves, and several of these (CREB1, synataxin, eIF4) play essential roles in completing the induction of long-term sensitization. Most transcriptional changes fade as sensitization memory is forgotten, but some changes persist beyond forgetting, including a long-lasting up-regulation of an inhibitory peptide transmitter that could foster forgetting. The maintenance of long-term sensitization may involve self-sustaining transcriptional feedback loops. In particular, CREB1 binds to its own promoter, producing a long-lasting increase in CREB1 mRNA, protein, and gene activation that is essential for sustaining cellular correlates of sensitization for at least 1 day after induction. Many aspects of the induction, stabilization, and maintenance of sensitization memory in Aplysia are conserved, suggesting that it will continue to be a fruitful, simpler system for understanding the physical basis of lasting memory.


Crossmodal Plasticity, Sensory Experience, and Cognition  

Valeria Vinogradova and Velia Cardin

Crossmodal plasticity occurs when sensory regions of the brain adapt to process sensory inputs from different modalities. This is seen in cases of congenital and early deafness and blindness, where, in the absence of their typical inputs, auditory and visual cortices respond to other sensory information. Crossmodal plasticity in deaf and blind individuals impacts several cognitive processes, including working memory, attention, switching, numerical cognition, and language. Crossmodal plasticity in cognitive domains demonstrates that brain function and cognition are shaped by the interplay between structural connectivity, computational capacities, and early sensory experience.


Jean-Martin Charcot (1825–1893)  

Olivier Walusinski

Jean-Martin Charcot (1825–1893), son of a Parisian craftsman, went on to a brilliant university career and worked his way to the top of the hospital hierarchy. Becoming a resident in 1858 at the women’s nursing home and asylum at La Salpêtrière Hospital, he returned there in 1868 as chief physician. Observing more than 2,000 elderly women, he first worked as a geriatrician–internist, leading him to describe thyroid pathology, cruoric pulmonary embolism, and so forth. To deal with the numerous nervous system pathologies, he applied the anatomoclinical method with the addition of microscopy. In less than around 10 years, his perspicacious clinical eye enabled him to describe Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, and tabetic arthropathy and to identify medullary localizations, for example. Already aware of functional neurological disorders, at that time referred to as hysteria and frequent to this day, Charcot used hypnosis to try to decipher the pathophysiology. His thinking gradually evolved from looking for lesions to recognizing triggering psychological trauma. This prolonged search, misinterpreted for years, opened the way to fine, precise clinical semiology, specific to neurology and psychosomatic medicine. Charcot knew how to surround himself with a cohort of brilliant clinicians, who often became as famous as he was, notably Pierre Marie (1853–1940), Georges Gilles de la Tourette (1857–1904), Joseph Babiński (1857–1932), and Pierre Janet (1859–1947). This cohort and the breadth of Charcot’s innovative work define what is now classically called the “Salpêtrière School.”


Diagnosis and Treatment of Gambling Addiction  

Gemma Mestre-Bach and Marc N. Potenza

Gambling disorder (GD) is a relatively rare psychiatric concern that may carry substantial individual, familial, and societal harms. GD often presents complex challenges, with high prevalence in adolescents and young adults. GD often co-occurs with other psychiatric disorders, complicating treatment. GD has multiple biopsychosocial contributions, with genetic, environmental, and psychological factors implicated. Advances in neuroimaging and neurochemistry offer insights into the neurobiology of GD. GD diagnostic criteria have evolved, although identification often remains challenging given shame, stigma, ambivalence regarding treatment and limited screening. Because many people with GD do not receive treatment, identification (screening and treatment outreach) and therapeutic (behavioral, neuromodulatory, and pharmacological) approaches warrant increased consideration and development..


The Natural Scene Network  

Diane Beck and Dirk B. Walther

Interest in the neural representations of scenes centered first on the idea that the primate visual system evolved in the context of natural scene statistics, but with the advent of functional magnetic resonance imaging, interest turned to scenes as a category of visual representation distinct from that of objects, faces, or bodies. Research comparing such categories revealed a scene network comprised of the parahippocampal place area, the medial place area, and the occipital place area. The network has been linked to a variety of functions, including navigation, categorization, and contextual processing. Moreover, much is known about both the visual representations of scenes within the network as well as its role in and connections to the brain’s semantic system. To fully understand the scene network, however, more work is needed to both break it down into its constituent parts and integrate what is known into a coherent system or systems.