Information flow in neurons proceeds by integrating inputs in dendrites, generating action potentials near the soma, and releasing neurotransmitters from nerve terminals in the axon. We found that in the striatum, acetylcholine-releasing neurons induce action potential firing in distal dopamine axons. Spontaneous activity of cholinergic neurons produced dopamine release that extended beyond acetylcholine-signaling domains, and traveling action potentials were readily recorded from dopamine axons in response to cholinergic activation. In freely moving mice, dopamine and acetylcholine covaried with movement direction. Local inhibition of nicotinic acetylcholine receptors impaired dopamine dynamics and affected movement. Our findings uncover an endogenous mechanism for action potential initiation independent of somatodendritic integration and establish that this mechanism segregates the control of dopamine signaling between axons and somata.

The brain's response to sensory input is strikingly modulated by behavioral state. Notably, the visual response of mouse primary visual cortex (V1) is enhanced by locomotion, a tractable and accessible example of a time-locked change in cortical state. The neural circuits that transmit behavioral state to sensory cortex to produce this modulation are unknown. In vivo calcium imaging of behaving animals revealed that locomotion activates vasoactive intestinal peptide (VIP)-positive neurons in mouse V1 independent of visual stimulation and largely through nicotinic inputs from basal forebrain. Optogenetic activation of VIP neurons increased V1 visual responses in stationary awake mice, artificially mimicking the effect of locomotion, and photolytic damage of VIP neurons abolished the enhancement of V1 responses by locomotion. These findings establish a cortical circuit for the enhancement of visual response by locomotion and provide a potential common circuit for the modulation of sensory processing by behavioral state.

Transmission from striatal cholinergic interneurons (CINs) controls dopamine release through nicotinic acetylcholine receptors (nAChRs) on dopaminergic axons. Anatomical studies suggest that cholinergic terminals signal predominantly through non-synaptic volume transmission. However, the influence of cholinergic transmission on electrical signaling in axons remains unclear. We examined axo-axonal transmission from CINs onto dopaminergic axons using perforated-patch recordings, which revealed rapid spontaneous EPSPs with properties characteristic of fast synapses. Pharmacology showed that axonal EPSPs (axEPSPs) were mediated primarily by high-affinity α6-containing receptors. Remarkably, axEPSPs triggered spontaneous action potentials, suggesting that these axons perform integration to convert synaptic input into spiking, a function associated with somatodendritic compartments. We investigated the cross-species validity of cholinergic axo-axonal transmission by recording dopaminergic axons in macaque putamen and found similar axEPSPs. Thus, we reveal that synaptic-like neurotransmission underlies cholinergic signaling onto dopaminergic axons, supporting the idea that striatal dopamine release can occur independently of somatic firing to provide distinct signaling.

Recent advances in the field of Voltage Imaging, with a special focus on new constructs and novel implementations.

Basal Ganglia Advances is a collection highlighting research on the structure, function, and disorders of the basal ganglia. It features studies spanning neuroscience, clinical insights, and computational models, serving as a hub for advances in movement, cognition, and behavior.

Work related to place tuning, spatial navigation, orientation and direction. Mainly includes articles on connectivity in the hippocampus, retrosplenial cortex, and related areas.

This brief review summarizes the most recent progress in in vivo voltage imaging in the neurosciences, as an extension to the work presented at the voltage imaging session of the 2025 FENS regional meeting in Oslo. First, we outline the latest advances in genetically encoded voltage indicators. Next, we examine technical innovations that have reshaped imaging platforms and lay the groundwork to investigate neural activity in real time across large fields of view and in deep tissue. Finally, we highlight a selection of compelling applications that have emerged over the past 5 years, illustrating how voltage imaging evolved from a proof of concept to being deployed to answer pending neuroscientific questions.

Activity of the mesolimbic dopamine system has long been implicated in encoding primary rewards and contributing to the addictive properties of drugs of abuse. Dopamine neurons in the ventral tegmental area (VTA) of the midbrain typically show patterns of spontaneous burst activity that align with the onset of salient events or rewarding stimuli, resulting in phasic dopamine release in the nucleus accumbens (NAc). Fiber photometry is increasingly being used as an accessible technique to quantify neural activity with high temporal resolution at sensors offering signal specificity in stable recordings over extended periods of time. It has been well established by multiple techniques that opioids increase mesolimbic dopamine activity, likely through disinhibition of VTA neurons. Here we used fiber photometry to compare sub-second transient events from VTA neurons with GCaMP6f and dopamine release in the lateral shell of the NAc with dLight1.3b and GRABDA2h in response to morphine treatment. In weekly sessions, one dose of morphine was administered in escalating order (2.5, 5,7.5, and 10 mg/kg, intraperitoneal). Consistent with prior literature, both GCaMP6f in VTA neurons and dLight1.3b in NAc showed patterns of increased signal following morphine treatment. In contrast, morphine suppressed transient activity at GRABDA2h sensors. Further analyses of whole signal streams from each sensor showed a generalized increase, but reduction in variability of the GRABDA2h signal, consistent with the interpretation of sensor saturation. Such results emphasize the importance of the inclusion of appropriate controls to contextualize the interpretation of biosensor responses, particularly in response to pharmacological treatment.

CD30 is a pivotal immunohistochemical marker for the diagnosis of selected lymphoid neoplasms and an important biomarker that informs clinical consideration of CD30-targeted therapy. With the expanding clinical application of brentuximab vedotin (BV) and BV-based regimens in classical Hodgkin lymphoma, peripheral T-cell lymphoma, primary cutaneous CD30-positive T-cell lymphoproliferative disorders, and relapsed/refractory diffuse large B-cell lymphoma, the clinical role of CD30 testing has evolved beyond conventional diagnostic classification to encompass therapeutic decision-making and laboratory quality management. This review integrates the 5th edition of the WHO classification of haematolymphoid tumours (WHO-HAEM5), the International Consensus Classification (ICC, 2022), pivotal clinical trials, and recent international consensus recommendations to summarize the expression patterns of CD30 across different lymphoma subtypes, principles for immunohistochemical interpretation, standardized pathology reporting, evidence supporting CD30-targeted therapy, and key quality assurance requirements for laboratory practice. Particular emphasis is placed on the following concepts: immunohistochemistry remains the preferred method for CD30 assessment; pathology reports should adopt a descriptive approach that documents the localization, staining intensity, proportion, and distribution pattern of CD30-positive tumor cells; the clinical benefit of brentuximab vedotin is not simply correlated with the level of CD30 expression, as some patients with low-level expression or even no detectable CD30 expression by visual assessment of conventional immunohistochemistry may still derive therapeutic benefit; and standardized pre-analytical handling, quality control, interpretation criteria, review procedures, and recognition of intratumoral heterogeneity should be incorporated into routine laboratory practice. Practical recommendations regarding CD30 testing workflows, quality assurance, common diagnostic pitfalls, and pathology reporting are also provided to facilitate standardized pathology practice, laboratory quality management, and multidisciplinary clinical decision-making.