• Please review the updated member agreement. Included is a new statement supporting the scientific method and evidence-based medicine. Claims or statements about disease processes should reference widely accepted scientific resources. Theoretical medical speculation is encouraged as part of the overall scientific process. However, unscientific statements that promote unfounded ideological positions or agendas may be removed.
  • Free admissions webinar for pre-vets! “Apply Smarter” Webinar

futuredoctor10

10+ Year Member
Jan 25, 2007
1,625
19
Status
Resident [Any Field]
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?
 

thatscorrect7

10+ Year Member
Aug 8, 2007
71
0
Status
Pre-Medical
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.
 

Attachments

futuredoctor10

10+ Year Member
Jan 25, 2007
1,625
19
Status
Resident [Any Field]
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?
 
About the Ads

futuredoctor10

10+ Year Member
Jan 25, 2007
1,625
19
Status
Resident [Any Field]
ok cool.

by "on" and "off"
you mean depolarized = inactive rhodopsin and hyper = active "on" rhodopsin right?
 
About the Ads