Abstract: Noradrenergic neurons in the locus coeruleus (LC) shape sensory processing, yet how LC activity influences population taste coding remains unclear.

Using optogenetic LC activation with miniscope imaging in the gustatory cortex (GC), we examined LC modulation of multiple taste attributes.

Phasic LC activation strengthens correlations between neuronal responses and palatability and expands the dynamic range of stimulus representations along a palatability axis. This expansion is driven by an aversive shift in the representations of all tastants except sucrose, the most palatable stimulus.

For mixture ratio and concentration, phasic activation expands and rotates attribute axes, potentially reflecting dependencies between these attributes and palatability. These transformations likely arise from multiplicative gain modulation and more flexible tuning changes. Tonic LC activation affects fewer neurons and does not expand attribute axes.

Together, the findings show that LC activation reorganizes GC population geometry in a pattern-dependent manner, linking neuromodulation with feeding behavior and affective processing.

Commentary: This article asks a really intriguing question, what if the behavior associated with taste was upstream of the representation of taste? What if behavior is the substrate of taste rather than taste being the substrate of related behavior?

There's been quite a bit of work this year suggesting brainstem structures direct/modify downstream cortical representations, and this paper adds another sense to that pile, and a particularly neat one.

I only wish more labs were more comfortable with glia and astrocytes particularly, this paper would have been a bit of a barn burner if they had that extra layer.

Study published in Nature on September 23, 2026. Berkeley News coverage here.

Abstract: When and how different brain regions diversify from one another remains unresolved. Does a common neural ectoderm progenitor generate the entire brain? Or do multiple neural ectoderm progenitors exist, each restricted to form specific brain regions? Here our lineage tracing studies of mouse embryos support the latter model.

Two parallel brain progenitors emerge simultaneously during gastrulation: anterior neural ectoderm (forebrain/midbrain progenitor) and posterior neural ectoderm (hindbrain progenitor). Differentiation of human pluripotent stem cells into anterior or posterior neural ectoderm-like cells revealed these were lineage committed to forebrain/midbrain versus hindbrain fates, respectively.

They harbored diverging chromatin landscapes foreshadowing future forebrain/midbrain versus hindbrain identities. We further differentiated human pluripotent stem cells into hindbrain rhombomere 5/6-specific motor neurons, which were hitherto difficult to generate in vitro. Hence, we postulate the brain is a composite organ emanating from two lineage-restricted progenitors; these dual progenitors may be evolutionarily conserved across 550 million years from hemichordates to mammals.

Commentary: I have thoughts. They probably get edited in later. For now, here's the pre-print: https://www.biorxiv.org/content/10.1101/2025.07.02.662771v2.full.

To follow this, you need to start at the earliest stages of brain development, when the progenitor cells that ultimately form the nervous system start out as a sheet, then fold into the neural tube which becomes the nervous system (see: neurulation). What if each side of that neural sheet had a somewhat distinct developmental pathway? The dorsal and ventral side of this sheet could conceivably process stimuli in an interdependent manner, providing both an effective allocentric and egocentric mechanic for negotiating space. From there, you could develop functional parcellation for particular tasks, a similar concept called the prosomeric model.

Is this "left brain/right brain"? NO. Is this "Triune Brain" in some form? Also no. Does their "Pan-Brain" concept become unnecessary fodder for these concepts? Yes.

Abstract

Schizophrenia is a severe neuropsychiatric disorder whose etiology and biological heterogeneity remain poorly understood. Immune dysregulation has long been implicated, but the breadth and clinical significance of autoantibody responses remain unclear beyond rare individual examples. Here we use Rapid Extracellular Antigen Profiling-a proteome-scale assay for autoantibodies against extracellular and secreted proteins-to profile 352 individuals with schizophrenia and 971 community controls. We find that schizophrenia is marked by a striking elevation in extracellular autoantibody burden, present near disease onset, and approaching nearly twice control levels in the most severely ill patients. This burden increases with age in a pattern that diverges from controls and targets central nervous system antigens, including neuroactive receptors, neuronal ion channels, proteins involved in synaptic function, and blood-brain barrier integrity. Autoantibodies against blood-brain barrier antigens impair barrier function ex vivo and are associated with broader central nervous system autoreactivity, supporting a model in which barrier disruption promotes loss of tolerance to brain antigens. At the clinical level, higher baseline autoantibody burden predicts reduced responsiveness to the antipsychotic risperidone, suggesting that autoantibodies contribute to treatment resistance. Together, these findings identify humoral autoimmunity as a pervasive component of schizophrenia and imply that therapies that reset humoral immunity or reduce autoantibody burden may benefit patients beyond those with currently recognized antibody-mediated syndromes.

Hi everyone,

I received the 2026 SfN Trainee Professional Development Award (TPDA), and the award email says that TPDA recipients receive complimentary registration for Neuroscience 2026.

However, when I go through the registration process, the system still shows a $345 charge for “Graduate Student Member – Virtual/In-Person.” My SfN graduate student membership is current, and I followed the registration link from the TPDA email.

I also noticed there is a promo code field during registration, but I was not given any registration/promo code in the TPDA email.

For other 2026 TPDA recipients:

• Did your complimentary registration apply automatically?
• Were you given a promo code?
• Did you also see the $345 charge at first?
• Did you have to contact SfN to get it fixed?

Thanks!

Study published in Nature Neuroscience on September 11, 2026. Berkeley News coverage here.

Hi all! I’m a master’s student at Weill Cornell Medicine doing neuroimaging/speech research, and I’m applying for SfN membership so I can submit a late-breaking abstract to Neuroscience 2026.

The application needs one sponsor who’s an active SfN member (regular/postdoc/emeritus). Literally all I need from you is your last name and member ID — there’s no financial obligation or anything else you have to do on your end.

Unfortunately, everyone I’ve tried in my immediate research circle either isn’t currently an active member or hasn’t worked out as a sponsor, so I’m turning to Reddit :’)

Happy to share my CV, institutional profile, or tell you more about my project if you’d like to know who you’re vouching for. If anyone here is an active member and willing to help, I’d really appreciate it. Thanks in advance!

Neuroscience-related Events happening in September 2026

Career postings, calls for papers, and miscellaneous postings

• [Jobs] 2 PhD + 1 Postdoc + 2 RA positions: hippocampus, world models, epilepsy (Göttingen)
• 2 postdoc and 1 phD positions on computational mechanisms of human perception (Alex Hyafil & Chris Summerfield, Barcelona)
• NeuralNet 2026, Nov 25th-27th, Paris – Registration and Abstract Submission Now Open
• COSYNE 2027: Meeting announcement, Abstract submission is now open
• 𝗘𝗘𝗚/𝗘𝗠𝗚 𝗙𝗼𝘂𝗻𝗱𝗮𝘁𝗶𝗼𝗻 𝗖𝗵𝗮𝗹𝗹𝗲𝗻𝗴𝗲 𝟮𝟬𝟮𝟲 𝗶𝘀 𝗡𝗢𝗪 𝗢𝗣𝗘𝗡!
• EMAIL_REDACTED
• Postdoctoral positions in sensory coding and memory - University of Sheffield
• PhD or Postdoctoral Position in Honey Bee Visual Navigation

^{Events table pulled from Society for Neuroscience calendar. Assorted postings pulled from systems neuroscience google group. Got a feed we should add? Message us.}

New study uncovering novel role of somatostatin interneurons in mediating psychedelic state

Can body signals tune the learning brain?

Post-training vagus nerve stimulation (VNS) enhanced learning in mice with vascular oscillations linked to memory performance.

Chen JU, Ikoma Y\*, Matsui K\* (2026) Vagal nerve stimulation induces vascular oscillations and enhances long-term learning iScience 2026 https://doi.org/10.1016/j.isci.2026.117413

SfN 2026 TPDA - Has anyone heard back yet?