Lifeboat Foundation

Previous studies have shown that AgRP neurons in the arcuate nucleus (ARC) respond to energy deficits and play a key role in the control of feeding behavior and metabolism. Here, we demonstrate that chronic unpredictable stress, an animal model of depression, decreases spontaneous firing rates, increases firing irregularity and alters the firing properties of AgRP neurons in both male and female mice. These changes are associated with enhanced inhibitory synaptic transmission and reduced intrinsic neuronal excitability. Chemogenetic inhibition of AgRP neurons increases susceptibility to subthreshold unpredictable stress. Conversely, chemogenetic activation of AgRP neurons completely reverses anhedonic and despair behaviors induced by chronic unpredictable stress.

What if our bodies kept evolving? And are there body parts that will disappear one day?
The First 1000 people to click this link get a FREE SKILLSHARE PREMIUM MEMBERSHIP: https://skl.sh/asapscience01211

Our backs hurt, ankles break and feet are busted! Not to mention having a baby is dangerous and our eyes are built backwards. There is a lot that doesn’t work in our bodies, so today we are going to explain the perfectly evolved human. Evolutionary biologists have been battling this scenario for years so we explain it all. Including the need for ostrich feet, bipedal bodies, bilateral symmetry, rewiring neurons in the eye and having dog ears! Let us know if you would want this body!?

Continue reading “This Is The Perfectly Evolved Human” »

A neurscience/neurogenesis link.

~~~

Natural compounds found in apples and other fruits may help stimulate the production of new brain cells, which may have implications for learning and memory, according to a new study in mice published in Stem Cell Reports.

Cell-Intrinsic Learning And Memory Storage Dynamics — Dr. David Glanzman Ph.D., Professor, in the Department Integrative Biology and Physiology, at UCLA College of the Life Sciences.

Dr. David Glanzman is Professor, in the Department Integrative Biology and Physiology, at UCLA College of the Life Sciences, Professor in the Department of Neurobiology in the David Geffen School of Medicine, and Member, Brain Research Institute.

Continue reading “Dr. David Glanzman Ph.D. — UCLA — Studying Cell-Intrinsic Learning And Memory Storage Dynamics” »

After tracing the origins of schizophrenia to genes expressed in the placenta while in utero, scientists have now zeroed in on the combination of risk factors that could predict which infants are at greatest risk of developing the condition later in life.

The findings reinforce an emerging picture of schizophrenia as a genetic disorder, with a fate determined by complications that can arise during pregnancy.

Researchers from the Lieber Institute for Brain Development at Johns Hopkins University and the University of North Carolina in the US analysed the relationship between key genes and cognitive development in the first few years after birth.

Although wireless optogenetic technologies enable brain circuit investigation in freely moving animals, existing devices have limited their full potential, requiring special power setups. Here, the authors report fully implantable optogenetic systems that allow intervention-free wireless charging and controls for operation in any environment.

Recordings of cells in the human dorsomedial prefrontal cortex identify a population of neurons that encode information about others’ beliefs and distinguish them from self-belief-related representations, providing insight into cellular-level processing underlying human theory of mind.

Despite great advances in the field of intensive care, when patients survive a severe.

Brain injury but remain in a chronic Vegetative State (VS) or Minimally Conscious.

State (MCS) (i.e., a disorder of consciousness; DOC), little can be done to promote.

Continue reading “Ultrasonic thalamic stimulation in chronic disorders of consciousness” »

Circulating branched-chain amino acids (BCAAs) are elevated in obesity and diabetes, and recent studies support a causal role for BCAAs in insulin resistance and defective glycemic control. The physiological mechanisms underlying BCAA regulation are poorly understood. Here we show that insulin signaling in the mediobasal hypothalamus (MBH) of rats is mandatory for lowering plasma BCAAs, most probably by inducing hepatic BCAA catabolism. Insulin receptor deletion only in agouti-related protein (AgRP)–expressing neurons (AgRP neurons) in the MBH impaired hepatic BCAA breakdown and suppression of plasma BCAAs during hyperinsulinemic clamps in mice. In support of this, chemogenetic stimulation of AgRP neurons in the absence of food significantly raised plasma BCAAs and impaired hepatic BCAA degradation.