In May 2016, thirteen dogs housed in backyards within a single neighborhood were reported to have developed convulsions and died within a 24 h period. An investigation of the scene by law enforcement resulted in submission of eight dogs for postmortem examination. It was suspected that a rapid acting toxin was the cause of death. A gas chromatography-mass spectrophotometry (GC-MS) protocol combined with thin-layer chromatography that allows screening for common convulsants failed to identify a toxin in either pooled gastric content or liver samples from select cases. After consultation with a veterinary toxicologist, sodium fluoroacetate poisoning was investigated. Sodium fluoroacetate, also known as 1080, is a pesticide that was available in the United States from the 1940's to the 1970's, but since 1972 has been banned or under EPA restricted use. When gastric content was re-tested using a GC-MS protocol with selective fluoroacetate ion monitoring and carbon 14 radiolabeling to facilitate quantification, 379 ppb sodium fluoroacetate was detected in a pooled gastric content sample. In spite of its banned status, sodium fluoroacetate remains a rarely reported cause of malicious poisoning in domestic dogs in the United Sates. This compound is highly toxic and is capable of causing death in dogs, humans, other mammals, and insects in ingested quantities as small as a few droplets. Even when geographic or historical proximity to a source is not evident, this intoxication should be considered in dogs exhibiting compatible clinical signs.

Neural oscillations, or brain rhythms, fluctuate in a manner reflecting ongoing behavior. Whether these fluctuations are instrumental or epiphenomenal to the behavior remains elusive. Attempts to experimentally manipulate neural oscillations exogenously using noninvasive brain stimulation have shown some promise, but difficulty with tailoring stimulation parameters to individuals has hindered progress in this field. We demonstrate here using electroencephalography (EEG) neurofeedback in a brain-computer interface that human participants (n = 44) learned over multiple sessions across a 6-day period to self-regulate their Beta rhythm (13-20 Hz), either up or down, over the right inferior frontal cortex. Training to downregulate Beta was more effective than training to upregulate Beta. The modulation was evident only during neurofeedback task performance but did not lead to offline alteration of Beta rhythm characteristics at rest, nor to changes in subsequent cognitive behavior. Likewise, a control group (n = 38) who underwent training to up or downregulate the Alpha rhythm (8-12 Hz) did not exhibit behavioral changes. Although the right frontal Beta rhythm has been repeatedly implicated as a key component of the brain's inhibitory control system, the present data suggest that its manipulation offline prior to cognitive task performance does not result in behavioral change in healthy individuals. Whether this form of neurofeedback training could serve as a useful therapeutic target for disorders with dysfunctional inhibitory control as their basis remains to be tested in a context where performance is abnormally poor and neural dynamics are different. K E Y W O R D S alpha oscillations, beta oscillations, brain-computer interface, inhibitory control, neurofeedback, stop signal task [Correction added on June 11, 2022, after first online publication: DOI number was updated in 2.5 section instead of the text '[URL to be inserted after acceptance]'].

Neural oscillations, or brain rhythms, fluctuate in a manner reflecting ongoing behavior. Whether these fluctuations are instrumental or epiphenomenal to the behavior remains elusive. Attempts to experimentally manipulate neural oscillations exogenously using non-invasive brain stimulation have shown some promise, but difficulty with tailoring stimulation parameters to individuals has hindered progress in this field. We demonstrate here using electroencephalography (EEG) neurofeedback in a brain-computer interface that human participants (n=44) learned over multiple sessions across a 6-day period to self-regulate their Beta rhythm (13-20 Hz) over the right inferior frontal cortex (rIFC). This Beta modulation had observable consequences on cognitive behavior: changes in an individual's inhibitory control performance before and after training were predicted by the magnitude of their training-related change in Beta over rIFC. This was not the case for a control group (n=38) who underwent training of their Alpha rhythm (8-12 Hz). The present data support the view that the right frontal Beta rhythm is a key component of the brain's inhibitory control system. Most importantly, we introduce causality to this relationship for the first time, as experimental modulation of rIFC Beta activity had a measurable impact upon behavior.