Glenn M Toney
Texas A&M University-College Station, TX·Neuroscience
A small brain region called the paraventricular nucleus of the hypothalamus (PVN or PVH) helps control breathing, stress responses and the sympathetic nervous system, which raises heart rate and blood pressure. Both projects ask how signaling inside this hub goes wrong in disease.
- Fields
Neuroscience
Physiology
Pharmacology
- Topics
paraventricular nucleus
hypothalamus
oxytocin
- Grants
- 2 known grants, through May 2029
What they work on
- Test whether raising the brain's own opioids in the PVH of normal mice reproduces the heightened opioid-induced respiratory depression seen in mice exposed to chronic intermittent hypercapnic hypoxia, a model of sleep apnea.
- Determine how oxytocin receptor signaling blocks fentanyl's inhibition of breathing neurons, and whether PVH opioid receptor blockade normalizes overdose hypersensitivity in sleep apnea model mice.
- Use optogenetic and chemogenetic excitation and inhibition of PVH oxytocin neurons to test whether they can produce exaggerated OIRD in normal mice and reduce it in sleep apnea model mice.
- Measure the speed, sensitivity and strength of glutamate-GABA strengthening at single pre-sympathetic neurons in a new horizontal brain slice, using optogenetic activation of glutamate inputs from the median preoptic nucleus.
- Raise and lower the glutamate transporter EAAT3 in GABA inputs to the PVN, and knock down vGlut2, to test how these changes alter sympathetic responses to angiotensin II, hyperosmolality, water deprivation and high salt.
More about the research
One asks why people with sleep apnea are especially vulnerable to opioid overdose. The other asks how the region's sympathetic-driving neurons are normally kept quiet, and how that restraint fails in cardiovascular and metabolic disease.
Why it matters
Sleep apnea patients are among those most likely to die from opioid overdose. Identifying the oxytocin circuit that fails in them could reveal targets for drugs that protect breathing without blocking pain relief or triggering withdrawal. Separately, understanding how inhibition normally keeps sympathetic-driving neurons quiet could guide efforts to prevent or reverse the chronically elevated sympathetic activity seen in major cardiovascular and metabolic diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Brian Ruyle
Washington University in St Louis, MO·Neuroscience·Early-career
Determine whether fentanyl acts before or after the synapse in the nucleus of the solitary tract, using a new transgenic MOR-Cre rat line with chemogenetics, optogenetics and fiber photometry to manipulate and record mu-opioid-receptor-expressing cells.
Xiaoting Wu
Icahn School of Medicine at Mount Sinai, NY·Neuroscience
Identify neuromodulatory inputs to ventral CA1 (vCA1), a hippocampal region, that drive positive social memories, using optogenetics in Cre-driver mice, fiber photometry during social interactions, and conditional deletion of neuromodulators.
Teresa A Milner
Weill Medical College of Cornell University, NY·Neuroscience
Test whether altered GluA1 signaling in PVN neurons contributes to angiotensin II-induced hypertension in post-AOF mice. GluA1 is part of AMPA glutamate receptors, which relay fast excitatory signals between neurons.
The school
Texas A&M University-College Station: 23 labs on PI Pages, $1.4B a year on research, 768 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.