Rest in peace, Pieter.
Thank you for everything and for helping me become the neuroscientist I am today.

Pieter had a profound influence on how I investigate the brain.
I’m grateful I stayed in touch during his retirement, where he enjoyed making guitars.

The microscope we used together (pictured below just before his retirement) was where many of these lessons were learned.

He patiently showed me stained brain sections with e.g. Fos, calbindin, mu-opioid receptors. Amazingly, he could even infer corticolimbic inputs from clusters of Fos expression in striatal sections.

I still remember when he asked me to sketch the borders of the nucleus accumbens and justify my choices. “Because it’s in the atlas” wasn’t good enough. He wanted my scientific rationale!

That question led to hours of Socratic dialogue about cell types, neurochemical markers, input-output relationships, and anatomical boundaries.

Pieter taught me how to use the cryostat and dissect brain regions with precision.
But more importantly, he taught me how to think about “What makes a brain area a brain area?”.

My obsession with histology, microscopy, and the medial prefrontal cortex and nucleus accumbens began with him.
It’s something I’ve carried through my postdoc, my time at NIDA, and now as a PI.

As a PhD student, I learned corticostriatal neuroanatomy, histology, and microscopy under his guidance, even though he wasn’t officially my supervisor.
He was just a generous scientist who wanted to help.

Many in behavioural neuroscience will remember Pieter from his influential 2004 Trends in Neurosciences review, which helped shape our understanding of prefrontal–striatal circuitry.

Once again, many thanks to all involved in project! Those on bluesky: @katepeters3.bsky.social‬, ‪@scottkinghorn.bsky.social Finally, special thanks to @moever.bsky.social‬ and Pelle Wilbers at VU Amsterdam for a nice commentary on our article! 🙂https://tinyurl.com/yutzpuv7 14/n‬

Together, impaired neuronal food cue processing from simultaneous prefrontal excitatory 'overdrive' and inhibitory 'underdrive' likely underlies EE's anti-food seeking action, thereby serving as potential neurophysiological targets to develop novel medications that help control food cravings. 13/n

These findings were initially surprising since reduced reward seeking is generally associated with experimental inhibition of PL. But impaired behavioural control is associated with PL hypoactivity. So increased PL excitatory overdrive post-EE may contribute to increased behavioural control. 12/n

So increased gas pedal action might mean decreased braking action? We measured Fos in PL inhibitory interneurons. EE reduced recruitment of cue-reactive, inhibitory interneurons reflecting 'inhibitory underdrive', so decreased braking. 11/n

How does EE impact PL pyramidal cell activity in vivo? We used fibre photometry and measured GCaMP activity and revealed that EE induced a loss of cue specificity and general elevation of PL pyramidal cell activity in vivo during sucrose seeking. So another case of excitatory ‘overdrive’! 😲10/n