scholarly journals How recent learning shapes the brain: Memory-dependent functional reconfiguration of brain circuits

NeuroImage ◽  
2021 ◽  
Vol 245 ◽  
pp. 118636
Author(s):  
Roberta Passiatore ◽  
Linda A. Antonucci ◽  
Sabine Bierstedt ◽  
Manojkumar Saranathan ◽  
Alessandro Bertolino ◽  
...  
Keyword(s):  
1997 ◽  
Vol 3 (2) ◽  
pp. 79-85 ◽  
Author(s):  
David Nutt ◽  
Caroline Bell

Anxiety is a very common and disabling condition which has serious consequences for patients, their families and society in general. The past decade has witnessed an increase in the recognition and understanding of the problem but considerable confusion and debate remains over attitudes towards treatment. The background to this controversy dates from the late 1980s when widespread and vehement criticism of doctors and drug companies over the use of benzodiazepines began. Although the litigation was unsuccessful, it resulted in a pervading feeling of uncertainty (both within the medical profession and among patients) about prescribing or taking any drug as a treatment for anxiety. The situation has been further confounded by the split that has occurred between the proponents of pharmacological and psychological approaches to management. These controversies have left the practising clinician in an unenviable position, with few practical or relevant guidelines to follow. Developments over recent years, however, should put an end to this confusion; new pharmacotherapies such as the selective serotonin reuptake inhibitors (SSRIs) and buspirone, and older ones such as the tricyclic antidepressants (TCAs), have emerged as effective alternatives to the benzodiazepines and have been paralleled by a similar growth in effective and available psychological treatments, particularly cognitive and cognitive–behavioural therapy. This progress seems set to continue with the rapid expansion of knowledge about the brain circuits and transmitters regulating anxiety that is now emerging from imaging studies.


Author(s):  
Oscar Herreras ◽  
Julia Makarova ◽  
José Manuel Ibarz

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.


Science ◽  
2017 ◽  
Vol 357 (6347) ◽  
pp. 159.3-159
Author(s):  
Peter Stern
Keyword(s):  

2020 ◽  
Vol 2 (2) ◽  
pp. 58-70
Author(s):  
Zorisadday Gonzalez ◽  
Richard W. McCallum

The pathophysiology of nausea and vomiting in gastroparesis is complicated and multifaceted involving the collaboration of both the peripheral and central nervous systems. Most treatment strategies and studies performed in gastroparesis have focused largely on the peripheral effects of this disease, while our understanding of the central nervous system mechanisms of nausea in this entity is still evolving. The ability to view the brain with different neuroimaging techniques has enabled significant advances in our understanding of the central emetic reflex response. However, not enough studies have been performed to further explore the brain–gut mechanisms involved in nausea and vomiting in patients with gastroparesis. The purpose of this review article is to assess the current status of brain imaging and summarize the theories about our present understanding on the central mechanisms involved in nausea and vomiting (N/V) in patients with gastroparesis. Gaining a better understanding of the complex brain circuits involved in the pathogenesis of gastroparesis will allow for the development of better antiemetic prophylactic and treatment strategies.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Mehmet S. Ozdas ◽  
Aagam S. Shah ◽  
Paul M. Johnson ◽  
Nisheet Patel ◽  
Markus Marks ◽  
...  

Abstract Non-invasive, molecularly-specific, focal modulation of brain circuits with low off-target effects can lead to breakthroughs in treatments of brain disorders. We systemically inject engineered ultrasound-controllable drug carriers and subsequently apply a novel two-component Aggregation and Uncaging Focused Ultrasound Sequence (AU-FUS) at the desired targets inside the brain. The first sequence aggregates drug carriers with millimeter-precision by orders of magnitude. The second sequence uncages the carrier’s cargo locally to achieve high target specificity without compromising the blood-brain barrier (BBB). Upon release from the carriers, drugs locally cross the intact BBB. We show circuit-specific manipulation of sensory signaling in motor cortex in rats by locally concentrating and releasing a GABAA receptor agonist from ultrasound-controlled carriers. Our approach uses orders of magnitude (1300x) less drug than is otherwise required by systemic injection and requires very low ultrasound pressures (20-fold below FDA safety limits for diagnostic imaging). We show that the BBB remains intact using passive cavitation detection (PCD), MRI-contrast agents and, importantly, also by sensitive fluorescent dye extravasation and immunohistochemistry.


eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Ting-hao Huang ◽  
Peter Niesman ◽  
Deepshika Arasu ◽  
Donghyung Lee ◽  
Aubrie L De La Cruz ◽  
...  

Understanding the computations that take place in brain circuits requires identifying how neurons in those circuits are connected to one another. We describe a technique called TRACT (TRAnsneuronal Control of Transcription) based on ligand-induced intramembrane proteolysis to reveal monosynaptic connections arising from genetically labeled neurons of interest. In this strategy, neurons expressing an artificial ligand (‘donor’ neurons) bind to and activate a genetically-engineered artificial receptor on their synaptic partners (‘receiver’ neurons). Upon ligand-receptor binding at synapses the receptor is cleaved in its transmembrane domain and releases a protein fragment that activates transcription in the synaptic partners. Using TRACT in Drosophila we have confirmed the connectivity between olfactory receptor neurons and their postsynaptic targets, and have discovered potential new connections between neurons in the circadian circuit. Our results demonstrate that the TRACT method can be used to investigate the connectivity of neuronal circuits in the brain.


2007 ◽  
Vol 292 (3) ◽  
pp. R1338-R1348 ◽  
Author(s):  
Joel C. Geerling ◽  
Arthur D. Loewy

Thirst and sodium appetite are both critical for restoring blood volume. Because these two behavioral drives can arise under similar physiological conditions, some of the brain sensory sites that stimulate thirst may also drive sodium appetite. However, the physiological and temporal dynamics of these two appetites exhibit clear differences, suggesting that they involve separate brain circuits. Unlike thirst-associated sensory neurons in the hypothalamus, the 11-β-hydroxysteroid dehydrogenase type 2 (HSD2) neurons in the rat nucleus tractus solitarius (NTS) are activated in close association with sodium appetite ( 16 ). Here, we tested whether the HSD2 neurons are also activated in response to either of the two physiological stimuli for thirst: hyperosmolarity and hypovolemia. Hyperosmolarity, produced by intraperitoneal injection of hypertonic saline, stimulated a large increase in water intake and a substantial increase in immunoreactivity for the neuronal activity marker c-Fos within the medial NTS, but not in the HSD2 neurons. Hypovolemia, produced by subcutaneous injection of hyperoncotic polyethylene glycol (PEG), stimulated an increase in water intake within 1–4 h without elevating c-Fos expression in the HSD2 neurons. The HSD2 neurons were, however, activated by prolonged hypovolemia, which also stimulated sodium appetite. Twelve hours after PEG was injected in rats that had been sodium deprived for 4 days, the HSD2 neurons showed a consistent increase in c-Fos immunoreactivity. In summary, the HSD2 neurons are activated specifically in association with sodium appetite and appear not to function in thirst.


2021 ◽  
Author(s):  
Robert Kozol ◽  
David James ◽  
Ivan Varela ◽  
Sureni Sumathipala ◽  
Stephan Züchner ◽  
...  

Abstract People with Phelan-McDermid Syndrome, caused by mutations in the SHANK3 gene, commonly present with symptoms of sensory hyporeactivity. To investigate how shank3 mutations impact brain circuits and contribute to sensory hyporeactivity, we generated two shank3 zebrafish mutant models. These shank3 mutant models both exhibit hyporeactivity to visual stimuli. Using whole-brain activity mapping, we show that light receptive brain nuclei show normal levels of activity while sensorimotor integration and motor regions are less active in shank3-/- mutants. Specifically rescuing Shank3 in a sensorimotor nucleus of the rostral brainstem is sufficient to rescue shank3-/- mutant hyporeactivity. In summary, reduced sensory responsiveness in shank3-/- mutant is associated with reduced activity across the brain and can be rescued by restoring Shank3 function in the rostral brainstem.


2019 ◽  
Author(s):  
Haojiang Luan ◽  
Alexander Kuzin ◽  
Ward F. Odenwald ◽  
Benjamin H. White

Summary:Genetic methods for targeting small numbers of neurons of a specific type are critical for mapping the brain circuits underlying behavior. Existing methods can provide exquisite targeting precision in favorable cases, but for many cases alternative techniques will be required. Here, we introduce a new step-wise combinatorial method for sequentially refining neuronal targeting: Depending on the restriction achieved at the first step, a second step can be easily implemented to further refine expression. For both steps, the new method relies on two independent intersections. The primary intersection targets neurons based on their developmental origins (i.e. lineage) and terminal identities, while the second intersection limits the number of lineages represented in the primary intersection by selecting lineages with overlapping activity of two distinct enhancers during neurogenesis. Our method relies critically on two libraries of 134 transgenic fly lines that express fragments of a split Cre recombinase under the control of distinct neuroblast enhancers. The split Cre fragments are fused to non-interacting pairs of split inteins, which ensure reconstitution of full-length and active Cre when all fragments are expressed in the same cell. Our split Cre system, together with its open source libraries, represent off-the-shelf components that should facilitate the targeting and characterization of brain circuits in Drosophila. Our methodology may also prove useful in other genetic model organisms.


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