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A fracture in the compound eye of a housefly, showing the interior structure of the ommatidia.
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Scanning electron micrographs of diatoms, microscopic algae that form the base of the food chain and produce 20% of Earth’s oxygen.
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Amphipod exoskeleton structures.
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(Source: hecticity, via the-hanged-hermit)
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The Spinal Cord
A bundle of nerve fibers
Myelinated Axons
Cells of the choroid plexus, which produce cerebral-spinal fluid.
A neuron and blood cells.
Freeze fracture of a neuronMicroscopic images of the nervous system.
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(Source: weheartit.com, via guysinsuits)
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![neurolove:
Neurotransmitter action
I mentioned in a previous post that neurotransmitters can act by opening a ligand-gated ion channel, which can let a specific ion into the cell/neuron. Neurotransmitters can have more complicated actions by acting on G-protein coupled receptors (shown in the image above).
When a neutrotransmitter binds to a G-protein coupled receptor, ions do not pass through- instead, the receptor undergoes a conformational (shape) change that “activates” the G-protein. Depending on the type of G-protein that is associated with that receptor, it can have different downstream effects. Essentially, once that G-protein has been activated, it can activate or shut down different molecules inside the cell, which will then have their own actions on other molecules, through a whole cascade of events.
Compared to a ligand-gated ion channel, the actions through a G-protein coupled receptor are slow, but they can be much further reaching. For instance, through that cascade, different molecules can be activated that may activate certain genes that change the way the cell/neuron will act in the future. Note that of course, like many other things I talk about, this is all a simplified explanation of what is going on, but will help you understand the basic principles.
To make it a bit more complicated, for example… One major effector of G-protein coupled signaling is the cAMP (cyclic adenosine monophosphate- often said as cyclic A-M-P), which can have big effects with calcium pathways and protein kinase A (PKA). For an example of a faster effect, one thing that this pathway does is open HCN and KCNQ channels, which cause a current leak in a dendrite, by letting out potassium. This can then “shunt” a signal coming in with sodium, such that the neuron would be less likely to build to a action potential. I’ll mention here that at Yale, Amy Arnsten’s lab has done some fabulous work to look at how this process may act in prefrontal cortex (http://www.ncbi.nlm.nih.gov/pubmed/17448997).
[Image Source]](http://24.media.tumblr.com/b8db04c5a157e738839a9e3d89042024/tumblr_mkl261gsbv1qb6etto1_500.jpg)
Neurotransmitter action
I mentioned in a previous post that neurotransmitters can act by opening a ligand-gated ion channel, which can let a specific ion into the cell/neuron. Neurotransmitters can have more complicated actions by acting on G-protein coupled receptors (shown in the image above).
When a neutrotransmitter binds to a G-protein coupled receptor, ions do not pass through- instead, the receptor undergoes a conformational (shape) change that “activates” the G-protein. Depending on the type of G-protein that is associated with that receptor, it can have different downstream effects. Essentially, once that G-protein has been activated, it can activate or shut down different molecules inside the cell, which will then have their own actions on other molecules, through a whole cascade of events.
Compared to a ligand-gated ion channel, the actions through a G-protein coupled receptor are slow, but they can be much further reaching. For instance, through that cascade, different molecules can be activated that may activate certain genes that change the way the cell/neuron will act in the future. Note that of course, like many other things I talk about, this is all a simplified explanation of what is going on, but will help you understand the basic principles.
To make it a bit more complicated, for example… One major effector of G-protein coupled signaling is the cAMP (cyclic adenosine monophosphate- often said as cyclic A-M-P), which can have big effects with calcium pathways and protein kinase A (PKA). For an example of a faster effect, one thing that this pathway does is open HCN and KCNQ channels, which cause a current leak in a dendrite, by letting out potassium. This can then “shunt” a signal coming in with sodium, such that the neuron would be less likely to build to a action potential. I’ll mention here that at Yale, Amy Arnsten’s lab has done some fabulous work to look at how this process may act in prefrontal cortex (http://www.ncbi.nlm.nih.gov/pubmed/17448997).
[Image Source]
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Dean Blunt ‘The Redeemer’ out May 1st .
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(Source: embodyperfection, via guysinsuits)
