Gonna make you fall in love with…Spines



The Genius is dead. Genius Re-post:














  1. This has got to be a dumb question, but how can there be more dendrites than axons on a neuron? If every dendrite connects to an axon and vice versa, this would imply equality. Or is it that each axon sends signals to many dendrites in different cells, but each dendrite connects to only one axon? That’s probably it, but I never see it explained. Why not?

  2. Re: Interconnection between axons and dendrites 
    View the dendrites of a neuron as branches of a bush and the axon as the root system. (Some neurons have bushy axon roots; others have one long carrot-like root.) An axon ?root? may pass near the dendrites of thousands of different neurons. Or the axon may pass close to many dendritic branches of the same neuron. Picture a long vine growing through the branches of several neighboring bushes. When an axon and a dendrite branch are sufficiently close a synapse can form. So an axon ?root? could have many connections to the same dendritic branch, could connect to many branches of the same neuron, or could connect to the branches of many different neurons. In a similar manner other neuron axon ?roots? are passing through the same neuron bushes. So a single neuron dendrite branch could pass near the axon ?roots? of many different neurons. 
    Initially, there are a very large number of weak synaptic connections between the axons and dendrites. As the brain matures, a few of the synapses are strengthened while most weaken and disappear, as shown in the images Coffee Mug provided. In a mature human brain, there is an average of 1,000 to 10,000 connections per neuron. 
    The interconnection pattern is different for different neural tissue. Some axons connect nerve centers to distant sensory or motor neurons. Some axons connect different neural layers.

  3. This was a good read. Does this mean if we could find some kind of dendritic spine growth inhibitor (and implement it) FraX would go away? And what is it that the excess spines do to the person exactly? Firing some conflicting impulses?

  4. Shan: ?And what is it that the excess spines do to the person exactly?? 
    At this stage, we only have speculation.  
    I believe that the total connectivity strength of a neuron must be kept within a certain range. Too little or too much and the neuron dies. (A living cell must maintain homeostasis.) As some neurons are strengthened during learning, others should weaken. Thus as a brain matures we should see a few strong synapses rather than many weak synapses. 
    My guess is that the problem isn?t necessarily excess spines. It could be a failure to strengthen synapses which results in the retention of weak synapses. Or it could be a failure to further weaken the weak synapses and so the total connectivity strength isn?t regulated properly. That could lead to inappropriate cell death. 
    (Hopefully Coffee Mug or someone else will correct my mistakes and offer their own conjectures.)

  5. That makes sense, perhaps at an early age our brains are unable to precisely control the impulses released by the neurons, overdoing it could probably damage critical neurons at their most sensitive phase of development.

  6. Opps… 
    “As some neurons are strengthened during learning, others should weaken.” 
    Should read, “As some synapses are strengthened during learning, others should weaken.”

  7. yeah. i don’t think it’s clear what the functional outcome of immature-looking spines is. in a sense, we know what the final outcome is because we know what the symptoms of fragile X syndrome are. on the other hand, the mental retardation could be caused by some other neurological malfunction and the spine morphology is more like a side-effect.  
    if spines can’t be matured you might expect it to be difficult to ever make a secure, permanent synapse. this should in principle make it difficult to learn and maintain information, but only certain types of info are affected, i think. i wonder if the same morphology phenotype is also observed in the cerebellum for instance. searching… i guess so: 
    The fragile X-cerebellum connection. 
    * Huber KM. 
    Center for Basic Neuroscience, Department of Physiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. kimberly.huber@utsouthwestern.edu 
    Fragile X syndrome (FXS) is an inherited form of mental retardation that results from the loss of function of the fragile X mental retardation protein (FMRP). A recent report demonstrated alterations in the structure and plasticity of synapses on cerebellar Purkinje cells in Fmr1 knockout mice, which are a model of FXS. These synaptic alterations are associated with deficits in the cerebellar learning both in the mice and humans with FXS. This work forges an important link between the FMR1 gene, altered synaptic plasticity in the cerebellum and mental retardation. 
    so i guess one can predict global delay in establishing permanency of connection. my question then is, how do the available mechanisms left over provide any permanency? how do fragile X patients learn how to walk or eat? 
    there must be some compensatory mechanism that is doing the job, but not quite..