N2A: a computational tool for modeling from neurons to algorithms

Rothganger, Fredrick; Warrender, Christina E.; Trumbo, Derek; Aimone, James B.

doi:10.3389/fncir.2014.00001

Cited by 67 publications

(73 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In teleost hindbrain and spinal cord, most gap junctions represent heterologous couplings of axon terminals onto somata and “somatic dendrites” of unlike neurons (Diamond and Huxley, 1968), including sensory neurons coupled to motor neurons (this report) and interneurons coupled to principal or projection neurons (Maler et al, 1981; Serrano-Vélez et al, 2014). This widespread heterologous coupling is in contrast with the often, though not exclusive, homologous coupling found at dendro-dendritic, presumably “purely electrical” synapses in mammalian CNS (Kosaka, 1983; Kosaka and Hama, 1985; Fukuda and Kosaka, 2000a; Kosaka and Kosaka, 2004; Kosaka and Kosaka, 2005; Fukuda et al, 2006).…”

Section: Discussionmentioning

confidence: 97%

Heterotypic gap junctions at glutamatergic mixed synapses are abundant in goldfish brain

et al. 2015

View full text Add to dashboard Cite

Gap junctions provide for direct intercellular electrical and metabolic coupling. The abundance of gap junctions at “large myelinated club ending” synapses on Mauthner cells of the teleost brain provided a convenient model to correlate anatomical and physiological properties of electrical synapses. There, presynaptic action potentials were found to evoke short-latency electrical “pre-potentials” immediately preceding their accompanying glutamate-induced depolarizations, making these the first unambiguously identified “mixed” (i.e., chemical plus electrical) synapses in the vertebrate CNS. We recently showed that gap junctions at these synapses exhibit asymmetric electrical resistance (i.e., electrical rectification), which we correlated with total molecular asymmetry of connexin composition in their apposing gap junction hemiplaques, with Cx35 restricted to axon terminal hemiplaques and Cx34.7 restricted to apposing Mauthner cell plasma membranes. We now show that similarly heterotypic neuronal gap junctions are abundant throughout goldfish brain, with labeling exclusively for Cx35 in presynaptic hemiplaques and exclusively for Cx34.7 in postsynaptic hemiplaques. Moreover, the vast majority of these asymmetric gap junctions occur at glutamatergic axon terminals. The widespread distribution of heterotypic gap junctions at glutamatergic mixed synapses throughout goldfish brain and spinal cord implies that pre- vs. postsynaptic asymmetry at electrical synapses evolved early in the chordate lineage. We propose that the advantages of the molecular and functional asymmetry of connexins at electrical synapses that are so prominently expressed in the teleost CNS are unlikely to have been abandoned in higher vertebrates. However, to create asymmetric coupling in mammals, where most gap junctions are composed of Cx36 on both sides, would require some other mechanism, such as differential phosphorylation of connexins on opposite sides of the same gap junction or on asymmetric differences in the complement of their scaffolding and regulatory proteins.

show abstract

Section: Discussionmentioning

confidence: 97%

Heterotypic gap junctions at glutamatergic mixed synapses are abundant in goldfish brain

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Although the thalamus receives strong driver inputs from the peripheral whisker sensors via the brainstem, the majority of the synapses on thalamic neurons originate in cortex (Varela, 2014). In addition, recent evidence has shown that direct corticothalamic feedback onto VPm neurons can lead to a sustained depolarization of the baseline membrane potential (Crandall et al, 2015; McCormick and von Krosigk, 1992; Mease et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Information Coding through Adaptive Gating of Synchronized Thalamic Bursting

et al. 2016

View full text Add to dashboard Cite

Summary It has been posited that the regulation of burst/tonic firing in the thalamus could function as a mechanism for controlling not only how much, but what kind of information is conveyed to downstream cortical targets. Yet how this gating mechanism is adaptively modulated on fast time scales by ongoing sensory inputs in rich sensory environments remains unknown. Using single unit recordings in the rat vibrissa thalamus (VPm), we found that the degree of bottom-up adaptation modulated thalamic burst/tonic firing as well as the synchronization of bursting across the thalamic population along a continuum for which the extremes facilitate detection or discrimination of sensory inputs. Optogenetic control of baseline membrane potential in thalamus further suggests that this regulation may result from an interplay between adaptive changes in thalamic membrane potential and synaptic drive from inputs to thalamus, setting the stage for an intricate control strategy upon which cortical computation is built.

show abstract

“…As major nodes of the “salience network,” these regions are strongly modulated by DA and NE (Chandler et al, 2014; Cole et al, 2013; Hermans et al, 2011; Seeley et al, 2007) and are amenable to the influence of MPH. Indeed, previous studies have shown that MPH attenuates dACC/insular activity in the context of surprise or error.…”

Section: Discussionmentioning

confidence: 99%

The effects of methylphenidate on cerebral responses to conflict anticipation and unsigned prediction error in a stop-signal task

Manza

Ide

et al. 2016

J Psychopharmacol

View full text Add to dashboard Cite

To adapt flexibly to a rapidly changing environment, humans must anticipate conflict and respond to surprising, unexpected events. To this end, the brain estimates upcoming conflict on the basis of prior experience and computes unsigned prediction error (UPE). Although much work implicates catecholamines in cognitive control, little is known about how pharmacological manipulation of catecholamines affects the neural processes underlying conflict anticipation and UPE computation. We addressed this issue by imaging 24 healthy young adults who received a 45 mg oral dose of methylphenidate (MPH) and 62 matched controls who did not receive MPH prior to performing the stop-signal task. We used a Bayesian Dynamic Belief Model to make trial-by-trial estimates of conflict and UPE during task performance. Replicating previous research, the control group showed anticipation-related activation in the presupplementary motor area and deactivation in the ventromedial prefrontal cortex and parahippocampal gyrus, as well as UPE-related activations in the dorsal anterior cingulate, insula, and inferior parietal lobule. In group comparison, MPH increased anticipation activity in the bilateral caudate head and decreased UPE activity in each of the aforementioned regions. These findings highlight distinct effects of catecholamines on the neural mechanisms underlying conflict anticipation and UPE, signals critical to learning and adaptive behavior.

show abstract

N2A: a computational tool for modeling from neurons to algorithms

Cited by 67 publications

References 32 publications

Heterotypic gap junctions at glutamatergic mixed synapses are abundant in goldfish brain

Heterotypic gap junctions at glutamatergic mixed synapses are abundant in goldfish brain

Information Coding through Adaptive Gating of Synchronized Thalamic Bursting

The effects of methylphenidate on cerebral responses to conflict anticipation and unsigned prediction error in a stop-signal task

Contact Info

Product

Resources

About