Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA; Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA; Neuroscience Graduate Program, University of California, San Francisco, San Francisco, CA 94158, USA.
Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA; Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA.
Neuron. 2017 Dec 20;96(6):1272-1281.e4. doi: 10.1016/j.neuron.2017.11.041.
The brain transforms the need for water into the desire to drink, but how this transformation is performed remains unknown. Here we describe the motivational mechanism by which the forebrain thirst circuit drives drinking. We show that thirst-promoting subfornical organ neurons are negatively reinforcing and that this negative-valence signal is transmitted along projections to the organum vasculosum of the lamina terminalis (OVLT) and median preoptic nucleus (MnPO). We then identify molecularly defined cell types within the OVLT and MnPO that are activated by fluid imbalance and show that stimulation of these neurons is sufficient to drive drinking, cardiovascular responses, and negative reinforcement. Finally, we demonstrate that the thirst signal exits these regions through at least three parallel pathways and show that these projections dissociate the cardiovascular and behavioral responses to fluid imbalance. These findings reveal a distributed thirst circuit that motivates drinking by the common mechanism of drive reduction.
大脑将对水的需求转化为饮水的欲望，但这种转化是如何发生的仍不清楚。在这里，我们描述了前脑口渴回路驱动饮水的动机机制。我们表明，促进口渴的穹窿下器官神经元具有负强化作用，这种负效价信号沿投射传递到终板血管器（OVLT）和中脑前视核（MnPO）。然后，我们在 OVLT 和 MnPO 中鉴定了分子定义的细胞类型，这些细胞类型对流体失衡激活，并表明刺激这些神经元足以驱动饮水、心血管反应和负强化。最后，我们证明，口渴信号通过至少三条平行通路离开这些区域，并表明这些投射将对流体失衡的心血管和行为反应分开。这些发现揭示了一个分布式口渴回路，通过减少驱动力的共同机制来激励饮水。
