scholarly journals Brain-derived neurotrophic factor differentially modulates excitability of two classes of hippocampal output neurons

2016 ◽  
Vol 116 (2) ◽  
pp. 466-471 ◽  
Author(s):  
A. R. Graves ◽  
S. J. Moore ◽  
N. Spruston ◽  
A. K. Tryba ◽  
C. C. Kaczorowski
Keyword(s):  
Synaptic Plasticity ◽  
Neurotrophic Factor ◽  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Cell Types ◽  
Brain Derived Neurotrophic Factor ◽  
The Other ◽  
Morphological Properties ◽  
Intrinsic Plasticity ◽  
The Brain

Brain-derived neurotrophic factor (BDNF) plays an important role in hippocampus-dependent learning and memory. Canonically, this has been ascribed to an enhancing effect on neuronal excitability and synaptic plasticity in the CA1 region. However, it is the pyramidal neurons in the subiculum that form the primary efferent pathways conveying hippocampal information to other areas of the brain, and yet the effect of BDNF on these neurons has remained unexplored. We present new data that BDNF regulates neuronal excitability and cellular plasticity in a much more complex manner than previously suggested. Subicular pyramidal neurons can be divided into two major classes, which have different electrophysiological and morphological properties, different requirements for the induction of plasticity, and different extrahippocampal projections. We found that BDNF increases excitability in one class of subicular pyramidal neurons yet decreases excitability in the other class. Furthermore, while endogenous BDNF was necessary for the induction of synaptic plasticity in both cell types, BDNF enhanced intrinsic plasticity in one class of pyramidal neurons yet suppressed intrinsic plasticity in the other. Taken together, these data suggest a novel role for BDNF signaling, as it appears to dynamically and bidirectionally regulate the output of hippocampal information to different regions of the brain.

scholarly journals Intrinsic temporal tuning of neurons in the optic tectum is shaped by multisensory experience

2019 ◽  
Author(s):  
Silas E. Busch ◽  
Arseny S. Khakhalin
Keyword(s):  
Neuronal Excitability ◽  
The Other ◽  
Biologically Inspired ◽  
Synaptic Inputs ◽  
Temporal Properties ◽  
Tectal Neurons ◽  
Intrinsic Plasticity ◽  
Future Work ◽  
The Brain ◽  
Light Flashes

AbstractHomeostatic intrinsic plasticity is often described as an adjustment of neuronal excitability to maintain stable spiking output. Here we report that intrinsic plasticity in the tectum of Xenopus tadpoles also supports temporal tuning, wherein neurons independently adjust spiking responses to fast and slow patterns of synaptic activation. Using the dynamic clamp technique, and five different types of visual, acoustic, and multisensory conditioning, we show that in tadpoles exposed to light flashes, tectal neurons became selective for fast synaptic inputs, while neurons exposed to looming and multisensory stimuli remained responsive to longer inputs. We also report a homeostatic co-tuning between synaptic and intrinsic temporal properties in tectal cells, as neurons that naturally received fast synaptic inputs tended to be most responsive to long-lasting synaptic conductances, and the other way around. These results expand our understanding of plasticity in the brain, and inform future work on the mechanisms of sensorimotor transformation.Significance statementWith the recent explosion of work in neural connectivity reconstruction and biologically inspired deep learning, most researchers concentrate on the topology of connections between neurons, rather than on differences in neuronal tuning. Here we show that in a sensory network in Xenopus tadpoles, different neurons are tuned, and respond stronger, to either short or long synaptic inputs. This tuning tended to be opposite to the actual dynamics of synaptic inputs each cell received, such that neurons that normally receive shorter inputs generated stronger spiking in response to longer testing currents, and the other way around. This observation shows that even in networks that don’t generate oscillations, neurons reshape their temporal selectivity, to optimize their impact on distributed calculations.

scholarly journals Bdnf promoter IV-expressing cells in the hippocampus modulate fear expression and hippocampal-prefrontal synchrony in mice

2019 ◽  
Author(s):  
Henry L. Hallock ◽  
Henry M. Quillian ◽  
Yishan Mai ◽  
Kristen R. Maynard ◽  
Julia L. Hill ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Synaptic Plasticity ◽  
Neurotrophic Factor ◽  
Memory Retrieval ◽  
Cell Types ◽  
Fear Memory ◽  
Brain Derived Neurotrophic Factor ◽  
Bdnf Signaling ◽  
Fear Expression

AbstractBrain-derived neurotrophic factor (BDNF) signaling regulates synaptic plasticity in the hippocampus (HC) and prefrontal cortex (PFC), and has been extensively linked with fear memory expression in rodents. Notably, disrupting BDNF production from promoter IV-derived transcripts enhances fear expression in mice, and decreases fear-associated HC-PFC synchrony, suggesting that Bdnf transcription from promoter IV plays a key role in HC-PFC function during fear memory retrieval. To understand how promoter IV-derived BDNF affects fear expression and HC-PFC connectivity, we generated a viral construct that selectively targets cells expressing promoter IV-derived Bdnf transcripts (“p4-cells”) for tamoxifen-inducible Cre-mediated recombination (AAV8-p4Bdnf-ERT2CreERT2-PEST). Using this construct, we found that ventral (vHC) p4-cells are recruited during fear expression, and that activation of these cells causes exaggerated fear expression that co-occurs with disrupted vHC-PFC synchrony in mice. Our data highlight how this novel construct can be used to interrogate genetically-defined cell types that selectively contribute to BDNF-dependent behaviors.

scholarly journals Changes in the Brain-Derived Neurotrophic Factor Are Associated with Improvements in Diabetes Risk Factors after Exercise Training in Adolescents with Obesity: The HEARTY Randomized Controlled Trial

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Jeremy J. Walsh ◽  
Amedeo D’Angiulli ◽  
Jameason D. Cameron ◽  
Ronald J. Sigal ◽  
Glen P. Kenny ◽  
...  
Keyword(s):  
Risk Factors ◽  
Exercise Training ◽  
Neurotrophic Factor ◽  
Fasting Glucose ◽  
Brain Derived Neurotrophic Factor ◽  
Diabetes Risk ◽  
Model Assessment ◽  
Neurocognitive Deficits ◽  
Diabetes Risk Factors ◽  
The Brain

Obesity in youth increases the risk of type 2 diabetes (T2D), and both are risk factors for neurocognitive deficits. Exercise attenuates the risk of obesity and T2D while improving cognitive function. In adults, these benefits are associated with the actions of the brain-derived neurotrophic factor (BDNF), a protein critical in modulating neuroplasticity, glucose regulation, fat oxidation, and appetite regulation in adults. However, little research exists in youth. This study examined the associations between changes in diabetes risk factors and changes in BDNF levels after 6 months of exercise training in adolescents with obesity. The sample consisted of 202 postpubertal adolescents with obesity (70% females) aged 14–18 years who were randomized to 6 months of aerobic and/or resistance training or nonexercise control. All participants received a healthy eating plan designed to induce a 250/kcal deficit per day. Resting serum BDNF levels and diabetes risk factors, such as fasting glucose, insulin, homeostasis model assessment (HOMA-B—beta cell insulin secretory capacity) and (HOMA-IS—insulin sensitivity), and hemoglobin A1c (HbA1c), were measured after an overnight fast at baseline and 6 months. There were no significant intergroup differences on changes in BDNF or diabetes risk factors. In the exercise group, increases in BDNF were associated with reductions in fasting glucose (β = −6.57, SE = 3.37, p=0.05) and increases in HOMA-B (β = 0.093, SE = 0.03, p=0.004) after controlling for confounders. No associations were found between changes in diabetes risk factors and BDNF in controls. In conclusion, exercise-induced reductions in some diabetes risk factors were associated with increases in BDNF in adolescents with obesity, suggesting that exercise training may be an effective strategy to promote metabolic health and increases in BDNF, a protein favoring neuroplasticity. This trial is registered with ClinicalTrials.gov NCT00195858, September 12, 2005 (funded by the Canadian Institutes of Health Research).

Antiapoptotic activity maintenance of Brain Derived Neurotrophic Factor and the C fragment of the tetanus toxin genetic fusion protein

2008 ◽  
Vol 3 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Jesús Ciriza ◽  
Marcos García-Ojeda ◽  
Inmaculada Martín-Burriel ◽  
Cendra Agulhon ◽  
Francisco Miana-Mena ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Neurotrophic Factor ◽  
Tetanus Toxin ◽  
Brain Derived Neurotrophic Factor ◽  
Trophic Factors ◽  
Low Concentrations ◽  
Neuro2a Cells ◽  
Genetic Fusion ◽  
The Brain ◽  
Lateral Sclerosis

AbstractNeurotrophic factors have been widely suggested as a treatment for multiple diseases including motorneuron pathologies, like Amyotrophic Lateral Sclerosis. However, clinical trials in which growth factors have been systematically administered to Amyotrophic Lateral Sclerosis patients have not been effective, owing in part to the short half-life of these factors and their low concentrations at target sites. A possible strategy is the use of the atoxic C fragment of the tetanus toxin as a neurotrophic factor carrier to the motorneurons. The activity of trophic factors should be tested because their genetic fusion to proteins could alter their folding and conformation, thus undermining their neuroprotective properties. For this purpose, in this paper we explored the Brain Derived Neurotrophic Factor (BDNF) activity maintenance after genetic fusion with the C fragment of the tetanus toxin. We demonstrated that BDNF fused with the C fragment of the tetanus toxin induces the neuronal survival Akt kinase pathway in mouse cortical culture neurons and maintains its antiapoptotic neuronal activity in Neuro2A cells.

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