Researchers exploring risky decision-making in rats found that a specific reward-related neural circuit influences impulsivity and risk-taking in complex ways that depend on timing and biological sex.
Dopamine is often called the brain’s “motivation molecule,” but for me, it represents something deeper, a window into how fragile our neurons can be. The cells that produce dopamine, known as dopaminergic neurons, are among the first to die in Parkinson’s disease, leading to the motor symptoms that gradually rob patients of movement and independence.
To understand what makes these neurons so vulnerable, I used an in-vitro model where I exposed N27 dopaminergic cells to 6-hydroxydopamine (6-OHDA), a toxin that triggers oxidative stress, like what occurs in the Parkinsonian brain. Then, I introduced Selenomethionine (SeMet), an organic form of selenium, to test whether this compound could counteract the damage and help the neurons survive.
Selenium has long intrigued scientists for its paradoxical nature. It is a trace element essential for antioxidant defense, yet in excess it can become toxic. I wanted to see whether a specific range of SeMet concentrations could offer meaningful protection without tipping that balance. My study, carried out at Charles University and the National Institute of Mental Health (NUDZ) in the Czech Republic, set out to define that “safe and effective window.” It is published in the journal In vitro models.
Recent technological advances have opened new possibilities for neuroscience research, allowing researchers to map the brain’s structure and synaptic connectivity (i.e., the junctions via which neurons communicate with each other) with increasing precision.
Despite these developments, most widely employed methods to image synaptic connectivity are slow and fail to precisely record changes in the connections between neurons in vivo, or in other words, while animals are awake and engaging in specific activities.
Two different research groups, one based at Columbia University and UC Berkeley, and the other at the Vision Institute of Sorbonne University in Paris, introduced a promising approach to study synapses in vivo. Their proposed mapping strategies, outlined in two Nature Neuroscience papers, combine holographic optogenetics, a method to selectively and precisely stimulate or silence specific neuron populations, with computational techniques.
In this paper, I explore the limitations of various modern philosophical approaches to Chalmers’ Hard Problem of Consciousness, highlighting how the MVT/absent Primal Eye framework offers a compelling explanation for the qualitative nature of experience. We invite you to read these findings and share your thoughts on this intriguing intersection of philosophy and consciousness.
(https://www.academia.edu/144710257/Problems_with_modern_Philosophical_Solutions_to_Chalmer_s_Hard_Problem_of_Consciousness_and_how_the_loss_of_the_Primal_Eye_in_early_evolution_seemingly_gave_rise_to_waking_and_sleeping_Subjectivity)
Posthuman University Journal, October, 2025.
Materialist reductions fail to bridge the Explanatory Gap, functionalism fails to capture qualia, dissolutionism fails to account for phenomenal reality, and panpsychism collapses under the weight of the Combination Problem. The MVT/ absent Primal Eye philosophical framework seems to successfully explain the qualitative nature of experience without either denying its existence or creating an equally intractable set of metaphysical mysteries.
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What they discovered.
Kampmann’s work, supported by the National Institutes of Science (NIH), maps cellular “decision points” that determine whether brain cells survive or die — laying the groundwork for treatments that intervene before irreversible brain damage occurs.
Using CRISPR-based gene targeting technology that his team helped develop and pioneer the use of in brain cells, Kampmann has identified genes and cellular processes that influence the buildup of amyloid plaque and tau in the brain, two primary contributors to dementia. Thanks to this technology, called CRISPR interference and CRISPR activation, select genes in the laboratory can be turned on or off to protect brain cells from decline.
“We can conduct large-scale experiments that target all the genes in the human genome — 20,000 of them,” said Kampmann, explaining his work after receiving the Byers Award earlier this year. “And that way, we can basically have a little knob on each gene to ask which of all of the genes play a role in a disease.”
People with autism spectrum disorders commonly have difficulty processing sensory information, which can make busy, bright or loud settings—such as schools, airports and restaurants—stressful or even painful. The neurological causes for altered sound processing are complex, and researchers are interested in better understanding them to make life better for people with autism.
In a study that combines behavioral tests, computer models and electrophysiological recordings of neuron activity, researchers have found that hyperactivity of neurons in the auditory cortex and the reaction of these neurons to an unusually broad range of frequencies contribute to this altered sound processing in rat models. The research is published in the journal PLOS Biology.
“One of the things we thought wasn’t being looked at enough was this idea of sensory discrimination: being able to distinguish between different features in our environment,” said Benjamin Auerbach, a professor of molecular and integrative physiology at the University of Illinois Urbana-Champaign.