Are cycles possible in circuits of neurons?

Are cycles possible in circuits of neurons?

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If we consider neurons nodes and connections between them edges, are cycles (from graph theory) are possible in the brain?

To put it another way, would the signal generated fromneuron1be able to travel around in a circuit of other neurons and come back to activateneuron1again? Or is this generally not possible becauseneuron1would still be recovering/re-potentiating?

If yes, as a programmer I would expect this to be the mechanism by which contiguous experience would be possible (ie. the main event loop of an application). Any studies/field/reseachers you could point me to for further research?

There are tons of cycles in the brain. The study of how the brain uses these cycles are used for computation is called Theoretical Neuroscience. Browsing the tag on this website is one way to become introduced to those ideas.

Alternatively, these loops are framed in different ways in "How to Build a Brain" by Chris Eliasmith. Loops involving a population node connecting to itself are considered to be memories. Longer loops, such as the basal-ganglia$ ightarrow$thalamus$ ightarrow$cortex loop could be considered analogous to the "main event loop" of a program, but with a few caveats.

Mirror neuron

A mirror neuron is a neuron that fires both when an animal acts and when the animal observes the same action performed by another. [1] [2] [3] Thus, the neuron "mirrors" the behavior of the other, as though the observer were itself acting. Such neurons have been directly observed in human [4] and primate species, [5] and birds. [6]

In humans, brain activity consistent with that of mirror neurons has been found in the premotor cortex, the supplementary motor area, the primary somatosensory cortex, and the inferior parietal cortex. [7] The function of the mirror system in humans is a subject of much speculation. Birds have been shown to have imitative resonance behaviors and neurological evidence suggests the presence of some form of mirroring system. [5] [8]

To date, no widely accepted neural or computational models have been put forward to describe how mirror neuron activity supports cognitive functions. [9] [10] [11] The subject of mirror neurons continues to generate intense debate. In 2014, Philosophical Transactions of the Royal Society B published a special issue entirely devoted to mirror neuron research. [12]

Some researchers in cognitive neuroscience and cognitive psychology consider that this system provides the physiological mechanism for the perception/action coupling (see the common coding theory). [3] They argue that mirror neurons may be important for understanding the actions of other people, and for learning new skills by imitation. Some researchers speculate that mirror systems may simulate observed actions, and thus contribute to theory of mind skills, [13] [14] while others relate mirror neurons to language abilities. [15] Neuroscientists such as Marco Iacoboni (UCLA) have argued that mirror neuron systems in the human brain help us understand the actions and intentions of other people. In a study published in March 2005 Iacoboni and his colleagues reported that mirror neurons could discern whether another person who was picking up a cup of tea planned to drink from it or clear it from the table. [16] In addition, Iacoboni has argued that mirror neurons are the neural basis of the human capacity for emotions such as empathy. [17]

There are scientists who express skepticism about the theories being advanced to explain the function of mirror neurons. In a 2013 article for Wired, Christian Jarrett cautioned that:

. mirror neurons are an exciting, intriguing discovery – but when you see them mentioned in the media, remember that most of the research on these cells has been conducted in monkeys. Remember too that there are many different types of mirror neuron. And that we're still trying to establish for sure whether they exist in humans, and how they compare with the monkey versions. As for understanding the functional significance of these cells … don't be fooled: that journey has only just begun. [18]

Are cycles possible in circuits of neurons? - Psychology

Advances in neuroscience identified addiction as a chronic brain disease with strong genetic, neurodevelopmental, and sociocultural components. We here discuss the circuit- and cell-level mechanisms of this condition and its co-option of pathways regulating reward, self-control, and affect. Drugs of abuse exert their initial reinforcing effects by triggering supraphysiologic surges of dopamine in the nucleus accumbens that activate the direct striatal pathway via D1 receptors and inhibit the indirect striato-cortical pathway via D2 receptors. Repeated drug administration triggers neuroplastic changes in glutamatergic inputs to the striatum and midbrain dopamine neurons, enhancing the brain’s reactivity to drug cues, reducing the sensitivity to non-drug rewards, weakening self-regulation, and increasing the sensitivity to stressful stimuli and dysphoria. Drug-induced impairments are long lasting thus, interventions designed to mitigate or even reverse them would be beneficial for the treatment of addiction.

Emotion Circuits in the Brain

The field of neuroscience has, after a long period of looking the other way, again embraced emotion as an important research area. Much of the progress has come from studies of fear, and especially fear conditioning. This work has pinpointed the amygdala as an important component of the system involved in the acquisition, storage, and expression of fear memory and has elucidated in detail how stimuli enter, travel through, and exit the amygdala. Some progress has also been made in understanding the cellular and molecular mechanisms that underlie fear conditioning, and recent studies have also shown that the findings from experimental animals apply to the human brain. It is important to remember why this work on emotion succeeded where past efforts failed. It focused on a psychologically well-defined aspect of emotion, avoided vague and poorly defined concepts such as “affect,” “hedonic tone,” or “emotional feelings,” and used a simple and straightforward experimental approach. With so much research being done in this area today, it is important that the mistakes of the past not be made again. It is also time to expand from this foundation into broader aspects of mind and behavior

New material could create 'neurons' and 'synapses' for new computers

Classic computers use binary values (0/1) to perform. By contrast, our brain cells can use more values to operate, making them more energy-efficient than computers. This is why scientists are interested in neuromorphic (brain-like) computing. Physicists from the University of Groningen (the Netherlands) have used a complex oxide to create elements comparable to the neurons and synapses in the brain using spins, a magnetic property of electrons. Their results were published on 18 May in the journal Frontiers in Nanotechnology.

Although computers can do straightforward calculations much faster than humans, our brains outperform silicon machines in tasks like object recognition. Furthermore, our brain uses less energy than computers. Part of this can be explained by the way our brain operates: whereas a computer uses a binary system (with values 0 or 1), brain cells can provide more analogue signals with a range of values.

The operation of our brains can be simulated in computers, but the basic architecture still relies on a binary system. That is why scientist look for ways to expand this, creating hardware that is more brain-like, but will also interface with normal computers. 'One idea is to create magnetic bits that can have intermediate states', says Tamalika Banerjee, Professor of Spintronics of Functional Materials at the Zernike Institute for Advanced Materials, University of Groningen. She works on spintronics, which uses a magnetic property of electrons called 'spin' to transport, manipulate and store information.

In this study, her PhD student Anouk Goossens, first author of the paper, created thin films of a ferromagnetic metal (strontium-ruthenate oxide, SRO) grown on a substrate of strontium titanate oxide. The resulting thin film contained magnetic domains that were perpendicular to the plane of the film. 'These can be switched more efficiently than in-plane magnetic domains', explains Goossens. By adapting the growth conditions, it is possible to control the crystal orientation in the SRO. Previously, out-of-plane magnetic domains have been made using other techniques, but these typically require complex layer structures.

Magnetic anisotropy

The magnetic domains can be switched using a current through a platinum electrode on top of the SRO. Goossens: 'When the magnetic domains are oriented perfectly perpendicular to the film, this switching is deterministic: the entire domain will switch.' However, when the magnetic domains are slightly tilted, the response is probabilistic: not all the domains are the same, and intermediate values occur when only part of the crystals in the domain have switched.

By choosing variants of the substrate on which the SRO is grown, the scientists can control its magnetic anisotropy. This allows them to produce two different spintronic devices. 'This magnetic anisotropy is exactly what we wanted', says Goossens. 'Probabilistic switching compares to how neurons function, while the deterministic switching is more like a synapse.'

The scientists expect that in the future, brain-like computer hardware can be created by combining these different domains in a spintronic device that can be connected to standard silicon-based circuits. Furthermore, probabilistic switching would also allow for stochastic computing, a promising technology which represents continuous values by streams of random bits. Banerjee: 'We have found a way to control intermediate states, not just for memory but also for computing.'

Are cycles possible in circuits of neurons? - Psychology

Previous studies indicated the involvement of cholinergic neurons in seizure however, the specific role of the medial septum (MS)-hippocampus cholinergic circuit in temporal lobe epilepsy (TLE) has not yet been completely elucidated.


In the current study, we used magnetic resonance imaging and diffusion tensor imaging to characterize the pathological change of the MS-hippocampus circuit in 42 patients with TLE compared with 22 healthy volunteers. Using optogenetics and chemogenetics, combined with in vivo or in vitro electrophysiology and retrograde rabies virus tracing, we revealed a direct MS-hippocampus cholinergic circuit that potently attenuates seizure through driving somatostatin inhibition in animal TLE models.


We found that patients with TLE with hippocampal sclerosis showed a decrease of neuronal fiber connectivity of the MS-hippocampus compared with healthy people. In the mouse TLE model, MS cholinergic neurons ceased firing during hippocampal seizures. Optogenetic and chemogenetic activation of MS cholinergic neurons (but not glutamatergic or GABAergic [gamma-aminobutyric acidergic] neurons) significantly attenuated hippocampal seizures, while specific inhibition promoted hippocampal seizures. Electrophysiology combined with modified rabies virus tracing studies showed that direct (but not indirect) MS-hippocampal cholinergic projections mediated the antiseizure effect by preferentially targeting hippocampal GABAergic neurons. Furthermore, chemogenetic inhibition of hippocampal somatostatin-positive (rather than parvalbumin-positive) subtype of GABAergic neurons reversed the antiseizure effect of the MS-hippocampus cholinergic circuit, which was mimicked by activating somatostatin-positive neurons.


These findings underscore the notable antiseizure role of the direct cholinergic MS-hippocampus circuit in TLE through driving the downstream somatostatin effector. This may provide a better understanding of the changes of the seizure circuit and the precise spatiotemporal control of epilepsy.

Neurotransmitters and Receptors: Dopamine

Horizontal Cells

Horizontal cells mediate lateral inhibition and synaptic feedback to photoreceptor cells. Different horizontal cell subtypes couple together through gap junctions to form networks. In retinas of both mammalian and nonmammalian vertebrates, the activation of D1-like receptors uncouples the horizontal cells, narrowing their receptive fields. The activation of dopamine D1 receptors in dark-adapted retinas depolarizes horizontal cells and reduces responses to flickering lights. The depolarization is due to the cAMP-dependent enhancement of glutamate-gated currents through α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA)/kainate glutamate receptors in the horizontal cell membrane other voltage-gated channels may also be involved.

Handbook of Mammalian Vocalization

Steven M. Barlow , . Arlette Kolta Radder , in Handbook of Behavioral Neuroscience , 2010

V. Neurochemical modulation of central pattern generator activity

Central pattern generators are subject to extensive neuromodulation. This generates flexibility in the rhythmic outputs of these neural networks and ultimately results in behavioral flexibility through an expanded motor repertoire. Neuromodulators exert two basic effects on CPGs, including alteration to intrinsic membrane properties and modulation of the strength of synaptic interactions among members of the pattern generating circuit. Combinations of these effects, with each modulator affecting a select subset of CPG neurons, account for many of the observed effects of neuromodulators. Furthermore, the combination of two or more neuromodulators may interact to cause more complex or different effects than they do when released independently ( Dickinson, 2006 ).

Changes in the pattern of neurotransmitter release and in the relative concentrations of neuromodulators can have profound effects on the operational dynamics of a CPG. A clever set of experiments in the crab have demonstrated systematic fractionation of pyloric CPGs with changes in neuromodulator type and its concentration levels. Neuromodulatory substances can alter the cellular and synaptic properties of neurons in CPG pathways ( Swensen and Marder, 2001 ) to regulate phase switching, reflex reversal and reflex gain.

The effects of neuromodulators may also interact with one another, and even modulatory neurons are often subject to modulation, enabling higher order control and indirect interactions among central pattern generators ( Dickinson, 2006 ). In addition, modulators often directly mediate the interactions between functionally-related CPGs. This enabling feature of CPG control has special relevance for the diverse repertoire of ororhythmic outputs and resulting motor behavior.

The generator in the respiratory system, like other CPGs, is subjected to modulation by several different amines and peptides, including 5HT ( Pena and Ramirez, 2002 see also review by Dickinson, 2006 ), substance P ( Pena and Ramirez, 2004 Del Negro et al., 2005 ), norepinephrine ( Viemari and Ramirez, 2006 ) and acetylcholine (ACh) functioning via muscarinic acetylcholine receptors (mAChRs) ( Shao and Feldman, 2005 ). Each modulator affects the pacemaker types and other neurons differentially, so that, for example, the relative contributions of cadmium (Cd)-sensitive pacemakers might increase in the presence of substance P, whereas other modulators (e.g., 5HT) enhance the contributions of the non-Cd-sensitive pacemakers ( Pena and Ramirez, 2002 Tryba et al., 2006 ). The important role of neuromodulation in the respiratory pattern was recently shown in a series of experiments examining the role of 5HT2A receptors. This is the same receptor type that is considered crucial in the spinal locomotor CPG function in mammals. Blocking 5HT2A receptors significantly reduced eupneic activity, but did not eliminate it ( Pena and Ramirez, 2002 Tryba et al., 2006 ). Thus, multiple pacemaker neuron types in the pre-Botzinger complex (pre-BotC) of the respiratory system interact to produce rhythmic output ( Dickinson, 2006 ). Neuromodulators provide a mechanism to alter the relative contributions of the different pacemakers, leading to substantial changes in motor output and to different forms of respiratory behavior.

Witten grew up in Princeton, New Jersey, where her parents were both professors at Princeton University. [1] Her father, Edward Witten, was a theoretical physicist and professor of mathematics at Princeton University, and her mother, Chiara Nappi was a professor of physics. [1] Witten attended Princeton High School in her hometown and then stayed close to home attending Princeton University for her undergraduate education. [1] Witten's sister, Daniela Witten pursued an undergraduate degree in Math and Biology at Stanford University. [2]

At Princeton, Witten majored in physics, but it was during her undergraduate degree that she became fascinated by biology, specifically neuroscience. [1] During her first year at Princeton, Witten worked as a research assistant in the lab of Lee Merrill Silver, studying molecular biology and genetics. [3] Later in her undergraduate degree, Witten joined the lab of Michael J. Berry, where she conducted research towards her undergraduate thesis in computational neuroscience. [4] Her undergraduate honors thesis was titled “Testing for Metabolic Efficiency in the Neural Code of the Retina” and was awarded by the department of physics. [4] Witten graduated from Princeton with an A.B. in Physics in 2002. [1]

Inspired by her undergraduate research experiences, Witten pursued her graduate education in neuroscience at Stanford University in 2003. [5] Under the mentorship of Eric Knudsen, Witten explored the neurobiological mechanisms of attention and strategies of information processing in the central nervous system of owls. [6]

Sensory Information Processing in Barn Owls Edit

Prediction is a fundamental neural computation performed by the brain to mediate appropriate behavioral responses to changing and uncertain environments. [7] In Witten's early graduate work, she explored how a specific neural circuit in the barn owl predicts the location of motion auditory stimuli. [7] The optical tectum is an area of the barn owl brain that helps to orient an owls gaze towards an auditory stimulus, and this is enabled by neurons encoding information from the auditory system to make a topographic map of auditory space. [7] Witten wanted to understand how this topographic map changes when auditory stimuli are moving. [7] She found that auditory receptive fields both sharpen and shift with stimulus position, showing that auditory fields make predictive shifts to track the location of auditory stimuli. [7]

Witten then became interested in exploring how the brain detects a singular object when it must integrate a variety of sensory stimuli and information from various channels. [8] Using a Hebbian Plasticity model, Witten proposed that the synaptic plasticity underlying object detection and representation in the brain results from the difference in spatial representations of one type of input relative to that of another. [8] She found that the amount of plasticity for each channel of sensory input depended on the strength and the width of the receptive field for that channel. [8] With stronger inputs guiding plasticity, this could account for the development and maintenance of aligned sensory representations in the brain. [8]

Using Optogenetics to Dissect Reward Circuits Edit

After defending her PhD in 2008, Witten stayed at Stanford to conduct her postdoctoral studies in the lab of Karl Deisseroth. [1] Under Deisseroth's mentorship, Witten learned how to use optogenetic technologies to dissect genetically defined cell types within neural circuits, and Witten's particular interest was cholinergic neurons in the brain's reward circuitry. [9] In a first author paper in Science, published in 2010, Witten dissected the role of cholinergic neurons in the nucleus accumbens which, although they make up only 1% of the local neurons, play significant roles in modulating circuitry and driving behavior. [9] She further found that these cholinergic interneurons were activated by cocaine administration, yet silencing them lead to increased medium spiny neuron activity in the NaC and prevented cocaine conditioning in mice. [9] Witten's finding highlighted the critical role such a small population of neurons can play in mediating behavioral outcomes. [8]

Since inhibition of cholinergic interneurons in the striatum ameliorated drug-induced conditioning, Witten and Deisseroth filed a patent for the use of optogenetic technologies in cholinergic interneurons in the NAc or striatum. [10] They proposed to first use the technology to better understand reward behaviors and addiction in rodent models, and later to target specific neural circuits in the treatment of addiction disorders in humans through the administration of opsin encoding polynucleotides into the striatum. [10] Through optical or electrical stimulation, this technology would enable temporally-precise treatment strategies for those suffering from addiction. [10]

Witten then wanted to apply optogenetics to rat models to explore neural reward circuitry, so she created Th::Cre and Chat::Cre driver lines in rats. [11] With these novel driver lines, Witten injected viruses to express Cre-dependent opsins in the rat brain to clarify the causal relationship between dopamine neuron firing and positive reinforcement in her novel rate driver lines. [11] Witten did confirm that stimulating Ventral Tegmental Area Dopamine neurons in Th::Cre rats did produce intracranial self-stimulation which highlighted the power of her tool for dissecting specific neural circuits in rats using optogenetics, which was previously not possible. [11]

Witten continued to explore cholinergic circuits in the striatum and the role of dopamine neurons in driving reward behaviors throughout her time in the Deisseroth Lab and became co-author on many papers during her four-year tenure in the lab. [12]

After a successful postdoctoral experience in the Deisseroth Lab, Witten was recruited to Princeton University, her alma mater, in 2012 to become an Assistant Professor in of Psychology and Neuroscience within the Princeton Neuroscience Institute and Department of Psychology. [1] Witten started her lab at Princeton and was dedicated to exploring the neural circuits driving reward learning and decision making in rodent models. [5] Through the use of techniques like optogenetics, rodent behavior, electrophysiology, imaging, and computational modeling, Witten and her team are able to discover novel mechanisms by which striatal and other reward circuitry drive behaviors. [5] In 2018, Ilana was promoted to Associate Professor and granted tenure at Princeton University. [13]

In addition to her role as a principal investigator, Witten is a member of the committee for PNI graduate student admissions, a member of committee to select URMs for PNI summer program, a member of the committee for redesigning the graduate student curriculum, as well as many other committee roles to support her Princeton neuroscience community. [5] Witten also teaches many classes at Princeton and is a member of BRAIN CoGS (Circuits of Cognitive Systems), a 7-lab NIH funded project to understand how working memory function underlies decision making. [14]

Dissecting Reward Circuitry Edit

In 2016, Witten and her team at Princeton published a paper looking at the distinct functions of different populations of midbrain dopamine neurons defined by their striatal target region. [15] They found that dopamine neurons that project to the ventral striatum have stronger responses to reward consumption and reward predicting cues where as the dopamine neurons that project to the dorsomedial striatum respond robustly to contralateral choices. [15] Though both subpopulations displayed reward-prediction error, Witten's findings show that distinct dopamine terminal input locations support specialization of function in the striatum. [15]

Continuing to study striatal neurons implicated in reward learning, Witten returned to findings from her postdoctoral work on cholinergic striatal interneurons to probe the connection between their activity profiles, synaptic plasticity, and reward learning. [16] Witten and her team found that activity of cholinergic neurons regulates extinction learned cocaine-context associations. [16] Further, cholinergic neurons mediate a sustained reduction in presynaptic glutamatergic input into the medium spiny neurons of the striatum. [16] This work highlighted, for the first time, the modulatory role of cholinergic interneurons in the striatum. [16]

Circuits Encoding Social and Spatial Information Edit

Since social interaction is intrinsically rewarding, Witten became interested in shaping part of her research program around understanding social information processing within the dopaminergic reward system. In 2017, Witten and her team explored a unique subset of prelimbic (PL) cortical neurons implicated in social behavior that project to the nucleus accumbens (NAc), amygdala, and ventral tegmental area. [17] Interestingly, activation of the PL-NAc projection lead to decreased social preference, so Witten and her team sought to understand what information this projection was conveying. [17] They found that it conveyed both spatial and social information that allowed the formation of social-spatial associations to guide social behavior. [17]

Diverse Dopamine Neuron Encoding Edit

Witten and her colleagues then dissecting the dopaminergic neurons in the VTA more rigorously. [18] Though these neurons are canonically associated with reward circuitry, they have been implicated in various other behavioral variables, so Witten was interested in looking at their ability to encode reward, reward predicting cues, reward history, spatial position, kinematics, and behavioral choice. [18] Through in vivo calcium imaging, Witten and her team found functional clusters of VTA DA neurons associated with both reward associated and non-reward associated variables, and these neurons were also spatially clustered within the VTA. [18]

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Dr. Mike Klaybor

Dr. Mike Klaybor brings thirty years of experience in practicing counseling psychology with individuals and couples. His approach is cognitive behavioral therapy or CBT. Specific specialties include anxiety and stress management, chronic pain & chronic illness management, depression, substance abuse evaluations, employee assistance and executive coaching for workplace performance and leadership.

Watch the video: Πώς μπορούμε να αναπτύξουμε νέους νευρώνες στον εγκέφαλο. TED (August 2022).