Summary
A bioRxiv preprint reports that ventral tegmental area dopamine activity drives bursting in basal forebrain neurons in rats and mice. The researchers measured a roughly 10-millisecond delay and used optogenetic manipulations to test the connection.
A bioRxiv preprint posted on October 2, 2026, reports that activity in dopamine neurons in the ventral tegmental area (VTA) rapidly drives bursting in noncholinergic neurons in the basal forebrain (BF). In recordings from freely moving rats, VTA dopamine activity preceded BF activity by about 10 milliseconds. Experiments in rats and genetically targeted mice also let the researchers test whether this fast coordination reflected a direct causal connection.
The findings suggest a route by which reward-related signals can pass quickly between two distinct brain systems. The work is an animal study and is currently presented as a preprint.
Recording and testing the connection
The researchers recorded activity from putative dopamine neurons and BF bursting neurons in freely moving rats. Across individual trials, the two populations were closely coordinated in both response size and spike timing. Dopamine activity came first by approximately 10 milliseconds during well-trained behaviour, during learning, and even outside obvious task events.
To test causality, the team used optogenetics—light-based control of genetically targeted neurons—in DAT-Cre mice. Activating VTA dopamine neurons rapidly recruited BF bursting neurons, with response delays matching those seen in the rat recordings. Stimulating dopamine-neuron terminals in the BF produced responses at shorter latencies, consistent with a local pathway in that region.
The researchers also inhibited dopamine neurons or their BF terminals. This reduced cue-evoked responses and ongoing activity in a substantial subset of BF bursting neurons. Together, the activation and inhibition experiments support a causal contribution from dopamine neurons to BF activity, rather than a correlation produced only by a shared upstream signal.
A fast signal with a possible second transmitter
The rapid BF responses persisted after the researchers blocked D1 and D2 dopamine receptors. Anatomical tracing also identified glutamatergic synapses from dopamine neurons to the BF. The authors propose glutamate co-release as a candidate explanation for the speed of the connection: dopamine neurons may influence BF neurons through a fast glutamatergic signal as well as through dopamine signalling. The findings support this mechanism as a possibility, rather than establishing it as the sole explanation.
The study adds a direct link between reward-prediction activity in VTA dopamine neurons and bursting in BF neurons. Its animal experiments show that this link can operate on a millisecond timescale and can influence activity beyond individual reward cues. Whether the same circuit dynamics operate in humans, and how they affect behaviour, will require further research.