Marijuana affects memory… through astrocytes!

The results of this elegant study published in the recent issue of Cell  are the first to show  that astrocytes play a key role in modulating neuronal activity and working memory.

From medicalnewstoday.com

A major downside of the medical use of marijuana is the drug’s ill effects on working memory, the ability to transiently hold and process information for reasoning, comprehension and learning. Researchers reporting in the March 2 print issue of the Cell Press journal Cell provide new insight into the source of those memory lapses. The answer comes as quite a surprise: Marijuana’s major psychoactive ingredient (THC) impairs memory independently of its direct effects on neurons. The side effects stem instead from the drug’s action on astroglia, passive support cells long believed to play second fiddle to active neurons.

With these experiments in mice, “we have found that the starting point for this phenomenon - the effect of marijuana on working memory - is the astroglial cells,” said Giovanni Marsicano of INSERM in France. 

Read more here: How marijuana makes you forget.

Full article here: CellAcute cannabinoids impair working memory through astroglial CB1 receptor modulation of hippocampal LTD. J. Han et al., 2012.

Tags: astrocytes

adverve:

This is your brain on love.

Got 15 minutes to spare? You probably don’t, but if you do, here’s a chance to witness something beautiful. From curiositycounts:

Stanford neuroscientists host the world’s first love competition, asking contestants between the ages of 10 and 75 to spend 5 minutes in an fMRI machine thinking deeply about the person they love.

Think of it as Eternal Sunshine in reverse. And if you’re into it, swoop up the whole DVD.

biocanvas:

Neurons (in blue to yellow) growing on top of astrocytes (in red, helper cells within the nervous system) in a human stem cell embryoid body (a cluster of differentiating human embryonic stem cells).
Image by Juan Carlos Izpisúa, Center of Regenerative Medicine in Barcelona.

biocanvas:

Neurons (in blue to yellow) growing on top of astrocytes (in red, helper cells within the nervous system) in a human stem cell embryoid body (a cluster of differentiating human embryonic stem cells).

Image by Juan Carlos Izpisúa, Center of Regenerative Medicine in Barcelona.

(via biocanvas)

"Research is to see what everybody else has seen, and to think what nobody else has thought."

— Albert Szent-Györgi (1893-1986) U. S. biochemist

Microglia and Memory

Morphological intricacy of neurons and glia in a mouse hippocampal organotypic slice. Credit to Dr. Chris Henstridge.

Nobel laureate Mario Cappecchi was the first to show a neuro-immune connection in psychiatric diseases. In this provocative and very interesting study Williamson and colleagues make a link between immunity and memory. They report that neonatal bacterial infection can have long-lasting negative effects on learning and memory later in adult life. Here is the abstract of the study published in October in the Journal of Neuroscience.

The proinflammatory cytokine interleukin-1β (IL-1β) is critical for normal hippocampus (HP)-dependent cognition, whereas high levels can disrupt memory and are implicated in neurodegeneration. However, the cellular source of IL-1β during learning has not been shown, and little is known about the risk factors leading to cytokine dysregulation within the HP. We have reported that neonatal bacterial infection in rats leads to marked HP-dependent memory deficits in adulthood. However, deficits are only observed if unmasked by a subsequent immune challenge [lipopolysaccharide (LPS)] around the time of learning. These data implicate a long-term change within the immune system that, upon activation with the “second hit,” LPS, acutely impacts the neural processes underlying memory. Indeed, inhibiting brain IL-1β before the LPS challenge prevents memory impairment in neonatally infected (NI) rats. We aimed to determine the cellular source of IL-1β during normal learning and thereby lend insight into the mechanism by which this cytokine is enduringly altered by early-life infection. We show for the first time that CD11b+ enriched cells are the source of IL-1β during normal HP-dependent learning. CD11b+ cells from NI rats are functionally sensitized within the adult HP and produce exaggerated IL-1β ex vivo compared with controls. However, an exaggerated IL-1β response in vivo requires LPS before learning. Moreover, preventing microglial activation during learning prevents memory impairment in NI rats, even following an LPS challenge. Thus, early-life events can significantly modulate normal learning-dependent cytokine activity within the HP, via a specific, enduring impact on brain microglial function.

Read the full study here 

Redefining the concept of reactive astrocytes

Abstract of the study published by Wilhelmsson et al., in PNAS.

Reactive astrocytes in neurotrauma, stroke, or neurodegeneration are thought to undergo cellular hypertrophy, based on their morphological appearance revealed by immunohistochemical detection of glial fibrillary acidic protein, vimentin, or nestin, all of them forming intermediate filaments, a part of the cytoskeleton. Here, we used a recently established dye-filling method to reveal the full three-dimensional shape of astrocytes assessing the morphology of reactive astrocytes in two neurotrauma models. Both in the denervated hippocampal region and the lesioned cerebral cortex, reactive astrocytes increased the thickness of their main cellular processes but did not extend to occupy a greater volume of tissue than nonreactive astrocytes. Despite this hypertrophy of glial fibrillary acidic protein-containing cellular processes, interdigitation between adjacent hippocampal astrocytes remained minimal. This work helps to redefine the century-old concept of hypertrophy of reactive astrocytes.

Full paper here

fuckyeahnervoussystem:

Rat retina astrocytes and blood vessels [source]

fuckyeahnervoussystem:

Rat retina astrocytes and blood vessels [source]

sciencenote:

“The discovery that 2 percent of T cells can make acetylcholine under the control of nerves gives a new insight into how the nervous system regulates immunity,” said Kevin J. Tracey, MD, president and chief executive officer of The Feinstein Institute for Medical Research, and principal investigator of the study. “The arrival of electrical signals from nerves activates these specialized T cells to produce the acetylcholine necessary to block inflammation, and protect against damage. It is possible to transfer these cells to cross-protect mice from inflammation, and to control these T cells by electrically stimulating the nerves directly.”

Tags: science

psydoctor8:

Growing a Brain in a Dish

That doughnut shape decorated with bright green spots, some connected by red pathways, amidst sky blue neighbors could be an artist’s creation, but is the result of a creative scientific attempt to grow an active brain in a dish, complete with memories. Really.
Researchers at the University of Pittsburgh published this stunning study in the journal Lab on a Chip {the full paper can be accessed here.} When I first learned how to grow cells in a lab, the technique of tissue culture, the idea of even growing brain cells was a far-fetched dream, much less brain cells capable of forming networks, complete with biological signals.

More from Dr. Jeffrey H. Toneye

psydoctor8:

Growing a Brain in a Dish

That doughnut shape decorated with bright green spots, some connected by red pathways, amidst sky blue neighbors could be an artist’s creation, but is the result of a creative scientific attempt to grow an active brain in a dish, complete with memories. Really.

Researchers at the University of Pittsburgh published this stunning study in the journal Lab on a Chip {the full paper can be accessed here.} When I first learned how to grow cells in a lab, the technique of tissue culture, the idea of even growing brain cells was a far-fetched dream, much less brain cells capable of forming networks, complete with biological signals.

More from Dr. Jeffrey H. Toneye

(via houseofmind)