You’re lying on a sandy beach on a hot sunny afternoon, enjoying a few hours of much needed laziness. As you open your eyes and confront the vastness of the ocean in front of you, light of 600nm wavelength hits your retina, kindling an impossibly long cascade of events in your brain: a molecule called retinal changes shape, neurons fire action potentials down the optic nerve, arrive at the lateral geniculate nucleus deep in the brain causing more action potentials in primary visual cortex in the back of your head, and so on ad infinitum. At some point, the mechanical wonder of 100 billion neurons working together produces something special: your experience of the color blue. What’s special is not that you can discriminate that color from others; nor that you are aware of it and paying attention to it. It is not notable that you can tell us about it, or assign a name to it. It’s that you have a subjective, qualitative experience of the color; there is something it is like to experience the color blue. Some philosophers call these experiences qualia – meaning “what kind” – but it is not important what kind of experience you are having, just that you are having one at all. Modern science hypothesizes that subjective experience is a product of the brain, but has no explanation for it. Continue reading
Study finds that CB1 receptor knockout mice have increased brain inflammation, which leads to earlier cognitive decline.
Brain aging is associated with cognitive decline that is accompanied by progressive neuroinflammatory changes. The endocannabinoid system (ECS) is involved in the regulation of glial activity and influences the progression of age-related learning and memory deficits. Mice lacking the Cnr1 gene (Cnr1?/?), which encodes the cannabinoid receptor 1 (CB1), showed an accelerated age-dependent deficit in spatial learning accompanied by a loss of principal neurons in the hippocampus. The age-dependent decrease in neuronal numbers in Cnr1?/? mice was not related to decreased neurogenesis or to epileptic seizures. However, enhanced neuroinflammation characterized by an increased density of astrocytes and activated microglia as well as an enhanced expression of the inflammatory cytokine IL-6 during aging was present in the hippocampus of Cnr1?/? mice. The ongoing process of pyramidal cell degeneration and neuroinflammation can exacerbate each other and both contribute to the cognitive deficits. Deletion of CB1 receptors from the forebrain GABAergic, but not from the glutamatergic neurons, led to a similar neuronal loss and increased neuroinflammation in the hippocampus as observed in animals lacking CB1 receptors in all cells. Our results suggest that CB1 receptor activity on hippocampal GABAergic neurons protects against age-dependent cognitive decline by reducing pyramidal cell degeneration and neuroinflammation. (via.)