The longer I’m in this forum the more I realise how ignorant I am, and the more I wonder how much is yet to be discovered. I’d never heard of these cilia on neurons nor of the Arc gene protein vesicles discussed in another thread – thanks to
Wolfhnd and
Zetrique respectively.
Whilst perusing this thread I was tending to agree with
Biowizard, who said in one post –
“Especially for a cell that is crowded by other cells and can’t have enough access to the surrounding biochemical environment to sense it. Kind of like a submarine’s periscope”, and in a later post –
“I don't know. But if these cilia exist in a lot of other cell types, I am less inclined to think that neuron's co-opting them for their own use marks a first-event in the evolutionary timeline”, and of
Asparagus who said –
“That central body is isolated from the rest of the body by the blood/brain barrier. It has its own immune system. The little cilia appear to be part of a theme.”And
Bangstrom, I see where you have changed from your position of their origin being a result of symbiogenesis with bacteria. It was because of that position I did some research this arvo.
I may as well post it anyhow.
My impression is that these cilia have been around for quite a long time on the evolutionary scale. A couple of these references suggest that their absence results in the loss of some vital functions. If they were just ‘recently’-acquired appendages from an evolutionary point of view, one would expect that their absence would not have such marked effects.
The author (Laura Sanders) of the Science News article that was posted in the OP, cited the first three of the following.
1. Mice without normal cilia in parts of their brain had trouble remembering a painful shock and recognizing familiar objects -
http://journals.plos.org/plosone/articl ... ne.0106576 . The title of the paper was
Hippocampal and Cortical Primary Cilia Are Required for Aversive Memory in Mice (by Malarky et al) -
“we specifically disrupted ciliogenesis in the cortex and hippocampus of mice through conditional deletion of the Intraflagellar Transport 88 (Ift88) gene. The effects on learning and memory were analyzed using both Morris Water Maze and fear conditioning paradigms. In comparison to wild type controls, cilia mutants displayed deficits in aversive learning and memory and novel object recognition.” These seem to me to be important survival requirements for mammals at least.
2.
"Impaired signalling from the primary cilia of MC4R neurons is a common pathway underlying genetic causes of obesity of humans. The authors demonstrated that MC4R colocalises with adenylyl cyclase 3 (ADCY3) at the primary cilia of a subset of hypothalamic neurons, that obesity-associated MC4R mutations impair ciliary localisation and that impairment of adenylyl cyclase signalling at the primary cilia of these neurons increases body weight -
http://www.nature.com/articles/s41588-0 ... cenews.org This article was presented as a PDF; I couldn't copy and paste so retyped the above part Abstract.
3. In an article titled
C. elegans Ciliated Sensory Neurons Release Extracellular Vesicles that Function in Animal Communication by Wang et al – see
https://www.sciencedirect.com/science/a ... 2214000037 - the authors made certain claims as shown in this part of their summary -
“We show here that specific Caenorhabdidits elegans ciliated sensory neurons shed and release extracellular vesicles (ECVs) containing GFP-tagged polycystins LOV-1 and PKD-2. These ECVs are also abundant in the lumen surrounding the cilium. Electron tomography and genetic analysis indicate that ECV biogenesis occurs via budding from the plasma membrane at the ciliary base and not via fusion of multivesicular bodies. Intraflagellar transport and kinesin-3 KLP-6 are required for environmental release of PKD-2::GFP-containing ECVs. ECVs isolated from wild-type animals induce male tail-chasing behavior, while ECVs isolated from klp-6 animals and lacking PKD-2::GFP do not. We conclude that environmentally released ECVs play a role in animal communication and mating-related behaviors.”
You’ll note that the first two studies involve hippocampus and hypothalamus neurons, the former being involved in emotional responses, and the latter with the autonomic nervous system.
4. This article -
http://www.sciencedirect.com/science/ar ... 6803002419 -
The neuronal primary cilium—an extrasynaptic signaling device by JF Whitfield, indicates that these cilia are also present on retinal rods and cones as well as on kidney cells. The fact that their disablement causes polycystic kidney disease indicates that they have a
vital rather than minor function.
Abstract"Many, but likely most, neurons in the central nervous system have a nonmotile “primary” cilium extending like an antenna or finger from one of the pair of centrioles in the cell's centrosome into the extracellular space. Since their discovery over 100 years ago, these organelles have been either dismissed as functionless relicts of a bygone era or more often simply ignored. However, it has long been known that the photoreceptor-bearing outer segments of retinal rods and cones are modified primary cilia and it has recently been found that kidney cells' primary cilia are sensitive flowmeters the disabling of which causes polycystic kidney disease. It has also been recently shown that somatostatin sst3 receptors and serotonin 5-HT6 receptors are selectively sited on neurons in various parts of the rat brain. It seems likely that these selectively-receptored neuronal primary cilia will turn out to be the forerunners of a family of cell-signaling devices that help drive various brain functions by sending signals into their own cells and into adjacent cells through gap junctions and via conventional chemical synapses."In view of the nature of the effects of interfering with the function of these cilia, I imagine that they have been around virtually since the origins of specialised cells. The serious studies on them seem to be relatively recent.
Cilia in the brain
by wolfhnd on January 19th, 2018, 9:28 pm
