Noninvasive Brain Stimulation Rescues Cocaine-Induced Prefrontal Hypoactivity and Restores Flexible Behavior

West, Elizabeth A.; Niedringhaus, Mark; Ortega, Heather K.; Haake, Rachel M.; Fröhlich, Flavio; Carelli, Regina M.

doi:10.1016/j.biopsych.2020.12.027

Cited by 23 publications

(24 citation statements)

References 64 publications

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“…Of note, the task used by the authors does not probe behavioral flexibility but rather the ability to detect and appropriately "exploit" reward contingencies. This point is of interest since a recent rat study of substance use disorder showed restoration of behavioral flexibility with gamma-tACS, perhaps in contradiction to the reduced learning found here [19]. This further supports the notion that the behavioral effect of tACS (reduced learning) should be counterproductive towards a clinical improvement.…”

Section: Brain Stimulationsupporting

confidence: 76%

Transcranial alternating current stimulation for the treatment of obsessive-compulsive disorder?

2021

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Section: Brain Stimulationsupporting

confidence: 76%

Transcranial alternating current stimulation for the treatment of obsessive-compulsive disorder?

2021

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“…A rodent model of obsessive-compulsive disorder shows elevated PrL neural activity and impairments in reversal learning [57]. Our current findings taken with animal models of neuropsychiatric disease suggest that PrL neural activity may need to be optimally dynamic for flexible behavior as impaired behavior has also been reported when PrL neural activity is dampened [14, 51] or heightened [57]. Finally, it would be interesting if rats with one of the distinct phenotypes are more susceptible to drug seeking or more vulnerable to stressors given that rats that show deficits in behavioral flexibility measured by probabilistic reversal learning are more likely to escalate drug seeking [6].…”

Section: Discussionmentioning

confidence: 90%

“…PrL neural encoding dynamically updates outcome value during set-shifting in real-time where the outcomes are delivered through the session [19, 20], supporting its potential role in flexibility with feedback. We previously have shown that PrL neural encoding throughout learning predicts how well rats are able to suppress their behavior post-devaluation [14]. Here, we aimed to determine how the PrL encodes information related to reward predictive cues after the expected outcome value of those cues has been decreased, i.e., when the animals alter their behavior in real-time to adjust to those expected outcome values compared to when the animals experience the updated outcome value within the session.…”

Section: Introductionmentioning

confidence: 99%

Prelimbic cortex neural encoding dynamically tracks expected outcome value

Niedringhaus

West

2022

Preprint

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Animals must modify their behavior based on updated expected outcomes in a changing environment. Prelimbic cortex (PrL) neural encoding during learning predicts and is necessary for appropriately altering behavior based on new expected outcome value following devaluation. We aimed to determine how PrL neural activity encodes reward predictive cues after the expected outcome value of those cues is decreased following conditioned taste aversion. In one post- devaluation session, rats were tested under extinction to determine their ability alter their behavior to the expected outcome values (i.e., extinction test). In a second post-devaluation session, rats were tested with the newly devalued outcome delivered so that the rats experienced the updated outcome value within the session (i.e., re-exposure test). We found that PrL neural encoding to the cue associated with the devalued reward predicted the ability of rats to suppress behavior in the extinction test session, but not in the re-exposure test session. While all rats were able to successfully devalue the outcome during conditioned taste aversion, a subset of rats continued to consume the devalued outcome in the re-exposure test session. We found differential patterns of PrL neural encoding in the population of rats that did not avoid the devalued outcome during the re-exposure test compared to the rats that successfully avoided the devalued outcome. Our findings suggest that PrL neural encoding dynamically tracks expected outcome values, and differential neural encoding in the PrL to reward predictive cues following expected outcome value changes may contribute to distinct behavioral phenotypes.

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“…This effect may be mediated by increased inhibitory input to PrL pyramidal neurons, as suggested by a larger number of PFC c-fos+ GABAergic cells after acute clozapine treatment (45) and rescue of PCPinduced decrease in GAD67 and PV expression in PV+ neurons after chronic exposure (15). It will be of interest to learn whether the induction or reversal of changes in transmitter identity contributes to the therapeutic effect of transcranial magnetic stimulation (46)(47)(48)(49)(50) and other forms of non-invasive manipulation of neuronal activity (51).…”

Section: Discussionmentioning

confidence: 99%

Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits

Pratelli

Thaker

et al. 2022

Preprint

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Decreased cognitive ability is a major consequence of exposure to drugs of abuse, but the underlying neuroplastic changes have been elusive. We show that both phencyclidine and methamphetamine cause a population of prelimbic pyramidal neurons to switch from a glutamatergic to a GABAergic phenotype. Overriding the gain of GABA with RNA-interference prevents drug-induced cognitive deficits and locomotor sensitization, connecting the change in neurotransmitter identity with altered behavior. Chemogenetic suppression of drug-induced hyperactivity also prevents the change in transmitter phenotype or reverses it after it has occurred, preventing or rescuing the associated behavioral changes. These findings may provide therapeutic opportunities to mitigate drug-induced cognitive deficits by manipulating electrical activity in the prelimbic cortex.

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Noninvasive Brain Stimulation Rescues Cocaine-Induced Prefrontal Hypoactivity and Restores Flexible Behavior

Cited by 23 publications

References 64 publications

Transcranial alternating current stimulation for the treatment of obsessive-compulsive disorder?

Transcranial alternating current stimulation for the treatment of obsessive-compulsive disorder?

Prelimbic cortex neural encoding dynamically tracks expected outcome value

Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits

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