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The Eye, Rod Cells, and Polarization

Discussion in 'MCAT Study Question Q&A' started by futuredoctor10, Jan 2, 2009.

  1. futuredoctor10

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    EK Biology Chapter 4:

    Rhodopsin is made of a protein bound to a prosthetic group called retinal.
    The photon isomerizes retinal causing the membrane of the rod cell to become less permeable to sodium ions and hyperpolarize.
    Hyperpolarization is transduced to an action potential and the signal is sent to the brain.

    Picture on p.97

    Dark / rod cell depolarized: ·. .Na+ channels open, . .inactive rhodopsin,. .glutamate released
    ·. .bipolar cell either inhibited or excited, depending on glutamate receptors

    Light / rod cell hyperpolarized:
    ·. .Na+ channels close,. .active rhodopsin, ..bipolar cell either released from inhibition or suppressed, depending on glutamate receptors


    I do not fully understand.

    What I gather:
    If light is present, photons isomerize retinal.
    This makes the membrane of the rod cell less permeable to sodium ions.
    Na+ channels close.
    Hyperpolarization occurs.

    So how does rhodopsin get activated when Na+ channels close?
    Where are glutamate (and glutamate receptors) involved?
     
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  3. thatscorrect7

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    What's happening is that like most neurotransmitters, it depends on what kind of glu receptors are on the bipolar cells.

    It happens that each rod cell is connected to two bipolar cells.

    It is correct that in hyperpolarization, action potential is inhibited so then no glutamate is released. But think about it this way.

    The visual field is kind of like a pixel on your screens. I've attached a picture on .doc

    Ex. There are bipolar cells A and B.
    A: once glutamate binds, it is inhibitory on this bipolar cell. this is the on-center bipolar cell. QUICK REVIEW: ok so the light was on right, so then for this ON-center cell, the LACK of glutamate means excitation (inhibition of inhibitory neuron) - so then the on-center bipolar talks to the ganglion cell to go to the LGN in the thalamus.

    B: once glutamate binds, it's excitatory on this bipolar cell. This is the OFF-center bipolar cell. when the light is OFF (glutamate is released) then this cell is excited.

    The eye tends to see by a rule of contrasts.
    rhodopsin activation is independent of sodium.
    light changes the conformation from cis to trans and then something called transducin is involved which then works through some G protein pathway.

    Then if hyperpolarized (light on) no glu is released. Excitation (no inhibition) of on-center bipolar cell, tells brain (via ganglion) that this on-center rod cell is on.
    If depolarized (light off) glu released. Excitation of the off-center bipolar, tells brain that off center is on.
     

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  4. futuredoctor10

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    Thanks for the doc and explanation. Lots of details... should we know this for the MCAT? What is the "take-home" concept we should know for the MCAT?
     
  5. thatscorrect7

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    just remember hyper-on , de-off

    thats all.
     
  6. futuredoctor10

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    ok cool.

    by "on" and "off"
    you mean depolarized = inactive rhodopsin and hyper = active "on" rhodopsin right?
     
  7. thatscorrect7

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    or like

    light on - hyperpolarized
    light off - depol.
     
  8. futuredoctor10

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    Haha whoops I was making things complicated. Got it now, gracias!
     

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