Motivation & Behavior
The neural circuit mechanism of object craving and hunting
Animals continuously interact with objects to acquire useful resources for their survival. It has been unknown as to how the brain yields the motivation toward objects. Researchers at KAIST reveal that a specific group of neurons in the medial preoptic area (MPA) induce hunting-like behavior to acquire target objects. Photostimulation of these neurons induces chasing, holding, biting, and retrieving target toys in mice. When exposed to crickets, these mice show predatory actions to catch and kill the prey. This finding strongly suggests that the biological meaning of playing with object is associated with hunting behavior. Inspired by this object-carving mechanism, researchers developed a new technology called by MIDAS (MPA-induced drive assisted steering). During photostimulation of the MPA circuit, mice chase a head mounted object swung around by computer program wirelessly in the front of head. The MIDAS mice navigate pathways along the programmed route in a complex maze with avoiding obstacles. This finding and the MIDAS technology will be useful for understanding and modulating of foraging behaviors and related human disorders such as object hoarding disorders and shopping addiction.
The thalamic mechanism of motor behavior
Parkinson’s disease (PD) is a debilitating movement disorder that affects more than 10 million people worldwide. Although it is known that PD is caused by a lack of the brain neuromodulator dopamine, it is unknown how this disease causes the debilitating motor abnormalities, such as tremor and loss of voluntary movement, that plague PD patients. Research published in the journal Neuron on 30 August, by a research team led by Dr. Daesoo Kim of the Department of Biological Sciences at Korea Advanced Science & Technology (KAIST) has identified a new mechanism that underlies Parkinson disease. This discovery may help to alleviate the motor problems suffered by Parkinson patients. The basal ganglia are a brain structure that controls complex movements. During low dopamine states, such as PD, the basal ganglia more strongly inhibit their target neurons. For the past three decades, scientists have assumed that this stronger inhibition caused the motor problems of PD patients. To test this assumption, the researchers used optogenetic technology to directly activate basal ganglia inhibitory output and then examined the response of target neurons in the thalamus, a part of the brain also involved in movement. Surprisingly, the target neurons in the thalamus exhibited a paradoxical increase in activity in response to the inhibition. This rebound excitation produced aberrant muscular rigidity and tremor that is very similar to the symptoms of PD patients. Eliminating this rebound firing caused the motor symptoms to be completed cured in an animal model of PD, proving that the rebound firing causes the motor problems experienced by PD patients.
Dr. Daesoo Kim said: "This study overturns three decades of consensus on the provenance of Parkinsonian symptoms.” Dr. Jeongjin Kim, the lead researcher on the project, remarked: “The therapeutic implications of this study for treatment of Parkinsonian symptoms are profound. It may soon become possible to remedy movement disorders without using dopamine.”
Dr. George Augustine at NTU and Duke university added “Our findings are a breakthrough, both for understanding how the brain normally controls movement of our body and for understanding how this control goes awry during PD and related dopamine-deficiency disorders. Most importantly, our work opens up promising new avenues for alleviating the suffering of PD patients”.