A 2016 PhD thesis by neuroscientist Nune Martiros at the Massachusetts Institute of Technology has shed fresh light on how the brain encodes and executes well‑practised sequences of actions—a discovery grounded in cutting‑edge electrophysiology, optogenetics and bespoke behavioural assays. Martiros’s work, conducted in MIT ’s Department of Brain and Cognitive Sciences under the supervision of Institute Professor Ann Graybiel , reveals how neurons in the dorsolateral striatum sharply signal the start and end of habitual action “chunks.” The findings carry profound implications for unraveling the neural basis of everyday habits, treating compulsive disorders such as OCD and Tourette ’s, and refining therapies for Parkinson’s disease.
Key findings:
The work, submitted in May 2016 by Nune Martiros to MIT’s Department of Brain and Cognitive Sciences, used a custom behavioural task and cutting‑edge electrophysiology and optogenetics to tease apart how the striatum—a key component of the basal ganglia—supports the seamless chaining of actions into “chunked” habits
.
Novel behavioural paradigm isolates habit signals
Martiros trained rats to execute one of six specific three‑lever‑press sequences, each rewarded only if performed in the correct order. Over 35–40 days, the rodents progressed from chance‑level performance to more than 80 percent accuracy during “in‑the‑zone” sessions, developing tightly stereotyped head‑and‑body movements unique to each individual’s trained sequence.
Crucially, within single training sessions rats oscillated between high‑performance periods, exploratory incorrect sequences and rest. This variability allowed researchers to compare neuronal firing during the exact same motor acts, sometimes rewarded and sometimes not.
“Motor cortex neurons tended to fire consistently with each lever press, regardless of context,” Martiros writes. “But dorsolateral striatal projection neurons responded preferentially at the first and last presses of the learned sequence—absent during incorrect presses or in untrained animals who happened to perform the same motions”
.
Striatal “boundary” signals underpin habit formation
Recording from hundreds of identified striatal neurons, Martiros found that roughly 30 percent of spiny projection neurons (SPNs) activated sharply at sequence onset, and 24 percent at sequence completion. By contrast, only about 10 percent of motor cortex neurons displayed such simple motor‑related activity.
Additional analyses showed that these boundary signals emerged as soon as rats had mastered about 30 correct trials, persisted throughout long‑term training, and were markedly absent when animals performed common but unrewarded incorrect patterns. A subtraction procedure comparing trained versus untrained animals executing the same sequence confirmed that reinforcement history—not mere motor pattern—drives the phenomenon.
The study also implicates fast‑spiking interneurons in sharpening these boundary responses, suggesting a local microcircuit mechanism by which the striatum flags the start and end of habitual action “chunks.”
Dopamine depletion exaggerates normal rhythms
In a second series of experiments, Martiros explored how Parkinson’s‑like dopamine loss alters striatal network activity. Using unilateral dopamine depletion in rats’ dorsolateral striatum, she recorded local field potentials during both rest and task performance.
Against expectations, baseline oscillation strengths remained unchanged. Instead, the normal low‑frequency rhythms associated with task execution were dramatically amplified in the dopamine‑depleted hemisphere—an effect partly reversed by L‑DOPA treatment. These findings hint that Parkinsonian motor deficits may arise not merely from abnormal baseline activity, but from pathologically enhanced task‑dependent signals that disrupt the precision of learned action sequences.
Implications for therapy and beyond
By pinpointing a generalized neural “start‑stop” code for habitual behaviours and demonstrating its modulation by dopamine, this thesis bridges fundamental neuroscience and clinical relevance.
MIT professors praised the rigor and creativity of the work. “Martiros has provided a definitive test for a long‑hypothesized striatal ‘chunking’ signal,” said Dr Ann Graybiel, thesis supervisor and Institute Professor of Brain and Cognitive Sciences. “Her combination of precise behaviour, electrophysiology and optogenetics sets a new standard for dissecting basal ganglia circuits”
.
As neuroscience moves toward circuit‑level understanding of complex behaviours, Martiros’s thesis stands out for its elegant design and translational promise—offering a roadmap for turning fundamental discovery into better outcomes for patients with movement and habit disorders.
'Instant Scholar' is a Times of India initiative to make academic research accessible to a wider audience. If you are a PhD scholar and would like to publish a summary of your research in this section, please share a summary and authorisation to publish it. For submission, and any question on this initiative, write to us at instantscholar@timesgroup.com
Key findings:
- Start‑stop signals: Neurons in the brain’s dorsolateral striatum fire most strongly at the initiation and termination of learned action sequences, but not during the individual movements in between.
- Task specificity: The same neurons remain quiet when animals perform incorrect or unreinforced movement patterns, demonstrating that this “boundary” signal reflects learned programs rather than simple motor actions.
- Dopamine’s dual role: In models of Parkinson’s‑like dopamine depletion, normal task‑related brain rhythms are exaggerated—suggesting new avenues for understanding motor symptoms and refining treatments such as L‑DOPA.
The work, submitted in May 2016 by Nune Martiros to MIT’s Department of Brain and Cognitive Sciences, used a custom behavioural task and cutting‑edge electrophysiology and optogenetics to tease apart how the striatum—a key component of the basal ganglia—supports the seamless chaining of actions into “chunked” habits
.
Novel behavioural paradigm isolates habit signals
Martiros trained rats to execute one of six specific three‑lever‑press sequences, each rewarded only if performed in the correct order. Over 35–40 days, the rodents progressed from chance‑level performance to more than 80 percent accuracy during “in‑the‑zone” sessions, developing tightly stereotyped head‑and‑body movements unique to each individual’s trained sequence.
Crucially, within single training sessions rats oscillated between high‑performance periods, exploratory incorrect sequences and rest. This variability allowed researchers to compare neuronal firing during the exact same motor acts, sometimes rewarded and sometimes not.
“Motor cortex neurons tended to fire consistently with each lever press, regardless of context,” Martiros writes. “But dorsolateral striatal projection neurons responded preferentially at the first and last presses of the learned sequence—absent during incorrect presses or in untrained animals who happened to perform the same motions”
.
Striatal “boundary” signals underpin habit formation
Recording from hundreds of identified striatal neurons, Martiros found that roughly 30 percent of spiny projection neurons (SPNs) activated sharply at sequence onset, and 24 percent at sequence completion. By contrast, only about 10 percent of motor cortex neurons displayed such simple motor‑related activity.
Additional analyses showed that these boundary signals emerged as soon as rats had mastered about 30 correct trials, persisted throughout long‑term training, and were markedly absent when animals performed common but unrewarded incorrect patterns. A subtraction procedure comparing trained versus untrained animals executing the same sequence confirmed that reinforcement history—not mere motor pattern—drives the phenomenon.
The study also implicates fast‑spiking interneurons in sharpening these boundary responses, suggesting a local microcircuit mechanism by which the striatum flags the start and end of habitual action “chunks.”
Dopamine depletion exaggerates normal rhythms
In a second series of experiments, Martiros explored how Parkinson’s‑like dopamine loss alters striatal network activity. Using unilateral dopamine depletion in rats’ dorsolateral striatum, she recorded local field potentials during both rest and task performance.
Against expectations, baseline oscillation strengths remained unchanged. Instead, the normal low‑frequency rhythms associated with task execution were dramatically amplified in the dopamine‑depleted hemisphere—an effect partly reversed by L‑DOPA treatment. These findings hint that Parkinsonian motor deficits may arise not merely from abnormal baseline activity, but from pathologically enhanced task‑dependent signals that disrupt the precision of learned action sequences.
Implications for therapy and beyond
By pinpointing a generalized neural “start‑stop” code for habitual behaviours and demonstrating its modulation by dopamine, this thesis bridges fundamental neuroscience and clinical relevance.
- Parkinson’s disease: Targeting excessive task‑related oscillations may refine neuromodulation strategies such as deep brain stimulation or tailored pharmacotherapy, improving motor control.
- Compulsive disorders: Conditions like obsessive‑compulsive disorder and Tourette syndrome, marked by overlearned or maladaptive action patterns, could be better understood—and treated—by modulating the same striatal circuitry.
- Rehabilitation and habit change: Insights into how habits are neurally “chunked” may inform behavioural therapies and technologies aimed at replacing harmful routines with healthier ones.
MIT professors praised the rigor and creativity of the work. “Martiros has provided a definitive test for a long‑hypothesized striatal ‘chunking’ signal,” said Dr Ann Graybiel, thesis supervisor and Institute Professor of Brain and Cognitive Sciences. “Her combination of precise behaviour, electrophysiology and optogenetics sets a new standard for dissecting basal ganglia circuits”
.
As neuroscience moves toward circuit‑level understanding of complex behaviours, Martiros’s thesis stands out for its elegant design and translational promise—offering a roadmap for turning fundamental discovery into better outcomes for patients with movement and habit disorders.
'Instant Scholar' is a Times of India initiative to make academic research accessible to a wider audience. If you are a PhD scholar and would like to publish a summary of your research in this section, please share a summary and authorisation to publish it. For submission, and any question on this initiative, write to us at instantscholar@timesgroup.com
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