The Journal of Neuroscience, May 22, 2019 • 39(21):3995 • 3995

This Week in The Journal

Dopamine Release by median eminence after TIDA neuron Because spike timing is a key determi- Tuberoinfundibular Neurons stimulation, suggesting that DAT does in nant of synaptic plasticity, Yamazaki et al. fact take up at this site. asked whether myelin-induced changes in Stefanos Stagkourakis, Johan Dunevall, Altogether, the results suggest that do- axonal conduction speed influence plas- Zahra Taleat, Andrew G. Ewing, pamine release by TIDA neurons is simi- ticity. Previous work had indicated that and Christian Broberger lar to that of other dopaminergic neurons myelin of CA1 axons in the alveus of in the maximum spike rate achievable mouse hippocampus was depolarized (see pages 4009–4022) without depolarization block, the amount during high-frequency neuronal spiking Release of from the anterior pi- of dopamine released during a burst, and and that this depolarization sped action tuitary is regulated by signaling factors se- the reuptake of the molecule by terminals. potential propagation in underlying ax- creted by hypothalamic neurons into These experiments were performed only ons. Therefore, the authors expressed blood vessels of the median eminence. in male mice, however. Given that TIDA channelrhodopsin or halorhodopsin se- Most of these factors are peptides that in- neurons regulate the release of prolactin, lectively in mature oligodendrocytes, used duce release. A notable excep- the predominant function of which is to light to depolarize or prevent depolariza- tion is dopamine, which is secreted by stimulate lactation, future studies should tion of myelin, and examined the effects of tuberoinfundibular dopamine (TIDA) explore the dynamics of dopamine release these manipulations on synapses between neurons and inhibits the release of prolac- by these neurons in females. CA1 pyramidal cells and postsynaptic tin. This regulatory system also differs neurons in the subiculum. from other in Brief depolarization of oligodendro- which the is released cytes in the alveus transiently narrowed into a narrow synaptic cleft and binds to the width and led to a gradual increase in nearby receptors. Because dopamine se- the amplitude of compound action poten- creted by TIDA neurons diffuses into a tials recorded in CA1 axons at the border much larger space, unique mechanisms of of the subiculum. The depolarization also release and reuptake might be required. increased the conduction speed of the Stagkourakis et al. investigated these longest CA1 axons (those that projected mechanisms by stimulating TIDA neu- to the middle and distal subiculum) and rons in mouse slices and measuring increased the amplitude of evoked EPSCs dopamine levels in the median eminence using fast-scan cyclic voltammetry. in one class of pyramidal cells in the areas Light-mediated activation of channel- targeted by these axons. The effect on EPSC amplitude was apparent 1–3 min af- rhodopsin-expressing TIDA axon termi- Depolarization of myelin (during blue bar) leads to a gradual nals induced dopamine release in the ter oligodendrocyte depolarization and increase in the amplitude of compound action potentials persisted for at least 30 min. Oligodendro- median eminence. The amount of dopa- (CAPs) elicited by CA1 axon stimulation. See Yamazaki et al. cyte depolarization also lowered the mine increased with stimulation frequency for details. up to 10 Hz, after which dopamine release threshold (the number of theta-frequency bursts) required to induce long-term po- declined, because depolarization block Synaptic Effects of Myelin prevented neurons from firing at higher tentiation (LTP) at CA1 synapses in the frequencies. With prolonged stimulation Depolarization middle and distal subiculum. Conversely, (150 s), the maximum spike rate of TIDA inhibiting oligodendrocyte depolariza- Yoshihiko Yamazaki, YoshifumiAbe, neurons dropped to 5 Hz. Notably, dopa- tion during theta-burst stimulation re- Shinsuke Shibata, Tomoko Shindo, duced LTP. Conduction speeds and EPSC mine release was greatest at spike rates sim- Satoshi Fujii, et al. ilar to those exhibited by spontaneously amplitude were not affected for CA1 ax- active TIDA neurons, which fired in bursts (see pages 4036–4050) ons projecting to the proximal subiculum. at ϳ10 Hz or tonically at ϳ5 Hz. These results suggest that myelin depo- Processing of information in the nervous Although TIDA neurons express the larization contributes to LTP induced by system relies on the ability of neurons to in- theta-burst stimulation at some synapses. dopamine transporter (DAT), whether tegrate inputs from multiple sources. This this transporter takes up dopamine re- This effect might stem from the speeding of integration depends on the arrival time action potentials and the synchronization of leased at the median eminence has been of various inputs, which is influenced by questioned, because the neuromodulator spikes across axons. How myelin depolar- presynaptic axon length, diameter, and my- ization induces these effects and how it leads is expected to diffuse quickly away from elination. Neurons work with oligodendro- to persistent increases in synaptic transmis- terminals. To test DAT function, Stagk- cytes to regulate the length and thickness of sion remain to be tested. ourakis et al. applied an inhibitor. The in- their myelin sheaths, thus fine-tuning ac- hibitor slowed the decay and increased the tion potential conduction speed to optimize ThisWeekinTheJournalwaswrittenbyX TeresaEsch,Ph.D. half-width of the dopamine signal in the spike timing at postsynaptic cells. https://doi.org/10.1523/JNEUROSCI.twij.39.21.2019.