Neuropeptides play essential roles as signaling molecules in the nervous system of animals. Visualization of neuropeptides in experimental settings has advanced through two main approaches: using antibody-based methods and fluorescent protein tagging. These conventional approaches have inherent drawbacks, such as poor antibody specificity and potential functional perturbations due to fusion with bulky, full-length fluorescent proteins. The split GFP system is a versatile tool with broad applications, yet it has been underutilized for neuropeptide labeling. We demonstrate the utility of the split GFP system in the in vivo visualization of two neuropeptides, INS-1 and NLP-40, released from and targeted to neuronal and non-neuronal cells and tissues in C. elegans. Released neuropeptides were successfully visualized by inserting the 16-amino acid GFP11 tag to the sequence of neuropeptides of interest and complementing it with extracellular GFP1–10 fused to a membrane anchor protein,

Insulin-like growth factor (IGF2) in ovaries of Rhipicephalus microplus partially engorged females. Ovaries from females at different feeding stages were used to detect IGF2.

The effects of colchicine on neurosecretory neurons of the rat hypothalamus were studied by immunochemistry, high-resolution radioautography, and conv…

This is a one–year position from April 1st, 2027 on or as soon possible, with possibilities to extend for another two years.

Nearly three decades after the discovery of the orexin (also known as hypocretin) neuropeptides and the identification of orexin deficiency as the cause of narcolepsy type 1,1 orexin 2 receptor (OX2R)...

Proceedings of the National Academy of Sciences, Volume 123, Issue 36, September 2026. SignificanceOxytocin and vasopressin are structurally similar neuropeptides that regulate diverse social behavior and homeostatic processes, often in a sex-dependent manner. Whether such sex-dependent functions arise from fundamental neural circuit ...

The loss of hypothalamic neurons that produce wake-promoting orexin (hypocretin) neuropeptides is responsible for narcolepsy type 1 (NT1). While the number o...

Neuropeptides modulate the Montevideo tree frog love song, according to research in Uruguay.

Nearly three decades after the discovery of the orexin (also known as hypocretin) neuropeptides and the identification of orexin deficiency as the cause of narcolepsy type 1,1 orexin 2 receptor (OX2R)...

Mast cells have been studied extensively for their involvement in allergic reactions, where they secrete numerous powerful mediators in response to immunoglobulin E and specific antigens. However, they are also triggered by neuropeptides, they have been found in close contact with neurons, and they …

Neuropeptides are found in nearly every brain neuron, and can modulate behaviors by regulating neuronal excitability, synaptic transmission, and plasticity. In contrast to the canonical view of neuropeptide release from nerve terminals, we previously reported the somatodendritic release of cholecystokinin (CCK) from ventral tegmental area (VTA) dopamine (DA) neurons. Release of CCK occurs during modest depolarization of VTA DA cells, and by activating CCK2Rs, potentiates synaptic transmission from GABAergic afferents. Here, recording from dopamine neurons in acute midbrain slices from male and female mice, we examined how somatodendritic release of CCK regulates synaptic plasticity and the extent of its influence. Depolarization of a dopamine neuron induced long-term potentiation (LTP) at GABAergic synapses, and in parallel somatodendritic CCK release produced long-term depression (LTD) at glutamatergic synapses. CCK-induced LTP persisted when postsynaptic G protein signaling in dopamine neurons was blocked, suggesting that CCK likely acts at GABAergic presynaptic terminals. Activation of kappa opioid receptors prevented CCK-dependent LTP of GABAergic synapses, indicating interaction between these two neuromodulatory signaling pathways in VTA. Surprisingly, depolarization of one dopamine neuron potentiated synapses onto both the depolarized neuron and neighboring dopamine neurons located up to ∼100 µm away, indicating substantial spread of CCK signaling and synaptic modulation within the VTA region. Taken together, our findings demonstrate that somatodendritic CCK release bidirectionally coordinates synaptic strength across dopamine neurons, identifying a peptide-mediated feedback mechanism that shapes VTA circuit function. Significance Statement Dopamine neurons in the ventral tegmental area (VTA) play central roles in reward, motivation, stress responses, and feeding behavior. While fast synaptic inputs regulate dopamine neuron firing on fast timescales, less is known about how slower neuromodulatory signals shape these circuits. We show that somatodendritic release of the neuropeptide cholecystokinin from dopamine neurons coordinately alters both inhibitory and excitatory synaptic strength and influences neighboring neurons within the VTA. This peptide-mediated feedback mechanism operates over a broader spatial scale than classical synaptic transmission and is regulated by kappa opioid signaling. These findings reveal how local peptide release can reshape dopamine circuit function and may contribute to changes in reward processing and feeding behavior.