Unit 2 Q&A
From NeuroWiki
Q35) ok, i still am just not getting the differences between the phase locking zone, up to 3000hz and above where we cant phase lock. What is going on differently above 3000? you said we can still hear the sounds, but cant distinguish inflections or something... is there any way you can explain this differently because i just dont understand why this is happening at all and what the outcome is.
A35) Not sure, but will try:
A sound < 3000 Hz vibrates basilar membrane. Those hair cells in that part of the membrane depolarize and hyperpolarize in sync with the movement of the membrane, they report to the MSO which establishes position of the sound. The signal is then sent to upwards to the 1° auditory cortex in a tonotopic fashion.
A sound >3000 Hz vibrates the basilar membrane. Those hair cells fire at something less than 3000 Hz. In fact, they fire at a rate that is more consistent with the intensity of the sound rather than the frequency. These report to the LSO to help localise the sound. The signal is then sent to upwards to the 1° auditory cortex in a tonotopic fashion, but in a much more coarse correspondence. The neurons are grouped into those responding to ranges. For example, frequencies from 10,000 to 12,000 Hz report to the 1° auditory cortex in the general 11,0000 Hz zone.
Q34) Is the anterolateral system equivalent to the lateral spinothalamic tract?
A34) Yes.
Q33) I still am having trouble grasping the meaning of referred pain. Can you explain this?
A33) If you have a pain in your toe, a neural pathway reports this to spine which carries the information to the toe portion of the somato-sensory cortex. If you have a pain in your little finger, a neural pathway reports this to spine which carries the information to the little finger portion of the somato-sensory cortex.
If you have a pain in your heart... there is not a corresponding portion of the somato-sensory cortex for the heart(we were behind schedule in the human department, and those uppity trolls in the bat department were all smug about having wings and sonar and such when it looked like we were not even going to have walking online until something after two years! Sheesh. At least we weren't as bad as the platypus folks, tee hee) . So we just wired the heart nociceptive neuron to the arm region of the spine. Pain in the heart is referred to the arm region.
Q32) Not really getting what the deal is with R+G=Y and there not being yellow cones, and then what any of that has to do with blue, other than it is coupled with yellow... Are you saying that if instead of the diagrams from the slides the colors were blue/yellow rather than red/green, we're actually talking about yellow receptors being a combination of red and green cones? Would that then translate into the LGN interpretation of yellow being from a signal from both red and green ganglion cells or is it that signal integrated elsewhere?
A32) Since there are no yellow receptors, the yellow in the surround of the blue-yellow ganglion cell is a product of green and red cones.
Q31) Also, so when you cut the visual path right before the LGN, how is this perceived differently than if you cut the visual pathway between the LGN and V1?
A31) It isn't really. Although the afferents for the LGN are more compact and more likely to be damaged entirely. The optic array going between the LGN and the V1 also carries a lot of efferent information.
Q30)I am unclear on what the difference is between when you hear a sound at lets say 2000Hz vs 500hz? both are under 3000 Hz.
A30) About 1500 Hz. Ar ar ar. Both are phase locked signals generating impulses that are tonotopically mapped to the SO, IC, MGN, and the primary auditory cortex on the temporal lobe. You will hear the different tones because different parts of your cortex will be responding.
Q29) I'm a bit confused on the auditory pathway. In the Bear's book its says that dorsal and ventral cochlear nucleus send signals to the same structures (sup olive to NLL to Inferior colliculus and to MGN), except that the dorsal pathway bypasses the sup olive.
In lecture, I think you said that the Ventral nucleus goes to the Sup olive, and the dorsal nucleus goes to the NLL and it goes the inferior colliculus. And then the info from the inferious colliculus goes the MGN. So does that mean that the ventral pathway doesn't go to the MGN and nor does the doral to NLL pathway?
A29) There is a LOT of cross talk in the auditory system. I tried to simplify it a bit by emphasizing that the primary output from the ventral cochlear nucleus was to the superior olivary complex, while the ventral nucleus sent afferents to the IC and the NLL. However, both have branches to the other nodes (NLL, IC). Everything to the MGN is coming from the IC. The NLL receives only contralateral input.
Q28) What do you mean by green+red=yellow? Is that saying if the two were combined in the center, or??
A28) We have ganglion cells that are R+G-, and G+R-, and B+Y- . But no yellow cones. The inhibitory yellow in the surround is a circuit that combines red and green receptors. (So it is really B+G-R-, just to make things worse.)
Q27) Also, which two models of horizontal cells are you referring to?
A27) Horizontal cells can synapse onto either receptor cells or bipolar cells.
Q26) I don’t fully understand end-stopped cells, how exactly do they determine length? If complex cells are determining movement and it’s direction how is that information used by end-stopped cells to determine length? It’d seem to me the information from simple cells would be better to determine length of a bar from. Is it that there is an array of complex cells and those that have no change in their firing rate (or those that are changing their firing rate) are determining the length or am I just not even close?
A26) I agree. It seems that using simple cells as afferents to hypercomplex cells would be a good way to go.
Q25) Is loss of sensation/numbness synonymous to loss of pain or loss of discriminative touch?
A24) Depends upon the damage. You can have pain, but loss of discriminative touch. The skin feels numb.
Q23) Can damage at higher level orders, such as the thalamus, lead to pain loss as well?
A23) Sure. And cortical damage as well.
Q22) Does color loss necessarily have to do with problems in Parvocellular layers of the LGN or does it have to do more with injury to the V4 or blobs?
A22) This depends upon whether it is one eye only. Also, how would you affect just the blobs and not the cells in between?
Q21) Also, since motion/edge detection can occur at numerous places(konicellular layers, ganglion receptive fields, MT) how would you localize where an injury was if someone lacked motion detection?
A21) Konicellular layers would be field/eye specific. Ganglion cells would be a portion of the field and more than motion would be affected. MT would be for everything. A total loss.
Q20) Near the oval window, the basilar membrane is wide and thick. This point processes high frequency tones and is less flexible because it receives higher energy signals since it's closer to the oval window. Farther away from it, the membrane is more narrow and thinner. This area receives low frequency tones, and is more flexible since the signal is weaker.
A20) Almost. Near the oval window the membrane is narrow and thick. More distal it is wide and thin. This is counter-intuitive because of the shape of the cochlea, but that is how it is.
Q19a) Are there two MSO's (right and left) because in the review it was said that Damage to the Left MSO means you cant hear on the right side. We understand how the coincidence detection works, we dont see how specific damage affects which side of the hearing. So for example, If you can't hear on the right side--> we know the Left MSO is damage, what is wrong with the LSO then? Only the L LSO? Or both?
A19a) First off- yes, there are two MSO's. A left and, well... a right. What we saw was only a model of what is theorized to happen. Each MSO receives input from both ears with coincidence detection being the prime model. However, in reality, it is a little different from this. The MSO neurons respond best to contralateral input, therefore the right MSO is signaling the location of sounds on the left side. If this R-MSO is damaged, you will still be able to detect the Interaural Time Differences (ITDs) for sounds on the right side.
Q19b) "If this R-LSO is damaged, you will still be able to detect the Interaural Time Differences (ITDs) for sounds on the right side." Did you mean the R-MSO?
A19b) oops. Yes, ok.. I corrected it. Hmm, now to re-read the question. Ah, the circumstance given in the original question (from an old exam) made a distinction between high and low frequency sounds. We were interested in low frequency sounds only.
Q18) For the gate theory principle of rubbing to inhibit pain- you said that the mechanoreceptor neuron also activates the secondary nociceptive neuron, but in the Purves textbook, this doesn't happen. could you clarify?
A18) Yes, Purves simplifies this circuit (Figure 10.8b) to make their point of how moderate mechanoreception can inhibit nociception. I went step further to point out that extreme mechanoreception will override this inhibition and lead to mechanoreceptor-induced pain. So, there are three phases.
Q17) What senses/sensory areas are present on both hemispheres of the brain? For example, is smell on both hemispheres in approximately the same region? What about the others?
A17) First order sensation is nearly always bi-lateral for all senses. Other forms of perception such as motion and language are unilateral.
Q16) Is the form and function of the basilar membrance similar to a reed in certain musical instruments?
A16) Yes. Very much so.
Q15) Also, is it possible to use drugs (actual and theoretical) to change vision and hearing in a way to improve things like music and movies, such as making standard definition seem like high definition? I've been "told" that recreational drugs can make movies trippy, so I figure other positive things can be induced.
A15) Hmm, How to answer this. I also have been told that this is true. Certainly, many drugs can induce a hyper-sensitive state of the senses.
Q14) Also, is the reason night vision is green because of the rod spectrum around 500 nm?
A14) Yes, plus using narrow frequency light will induce dark adaptation.
Q13) I understand when an on center bipolar is, and an off center bi polar... but in the slide right before you show a hypothetical horizontal cell affecting the soma of the bipolars directly, you name these bipolars as on center OFF SURROUND and off center ON surround... what do these off surround on surround mean?
A13) The cells are named after the condition to which they respond. If the only connection to the bipolars are the receptor cells, then they are refered to as On or Off centre. However, if the horizontal cells are bringing information to them from the receptors in the surrounds, then we can expand the names to include the contrasting surround state.
Q12) Do we need to know the material about drugs from feb. 13th for this exam?
A12) Nah. Those slides are not even posted. We will be dealing with drugs in the third Unit. We have enough to worry about with Unit 2.
Q11) Hi I was wondering if you could fix the links for the videos on the visual system cells on the wiki and if you could also post the videos that showed the patients with damage to Broca's and Wernicke's areas...Thanks
A11) The cell recording links on the website (not the wiki) are fixed. Movies You will need Windows Media Player (available on the Bevoware download site). The Wernike's and Brocas movies are quite large. I will have to reduce them.
Q10) I've read a few places that the receptive field of a photoreceptor is the area of the retina which that photoreceptor occupies, but also that a receptive field is the space on which if a stimulus is provided, it will alter the membrane potential of a sensory neuron...and these two things seem to conflict if I assume that there exist horizontal cells modulating the response of neighboring photoreceptors. Seems to me like the receptive field for a cone in the fovea could be just the teeny area it occupies, but that the receptive field for a rod further out may also include the surround. Doesn't the receptive field of a photoreceptor depend on connections or am I just confused?
A10) We have actually not talked about what the receptive field for an individual receptor would be. Only in terms of a ganglion cell. So... I would not worry about it (but in my opinion, the receptive field is the sum of the effects of all the cells interacting with the receptor).
Q9) I had a quick question about the Fornix. We discussed in class that it takes primary sensory info from the thalamus. On wikipedia it says that the fornix carries signals from the hippocampus to the mammillary bodies and septal nuclei.
A9) We will deal with the fornix on the final. You can skip it for now.
Q8) Does ipecac work on the vestibular system?
A8) Ipecac is an emetic. It is believed to work in two ways: one, it irritates the mucosal lining, and two it activates a center in the medulla that directs the gag reflex.
Q7) There is some symmetry in the horizontal plane. I have a problem with this because if localization of sound horizontally depends when the signal reaches the ear, how can you tell whether it came from in front of you or behind you?
A7) This is the role of the pinna. Sounds coming from in front of you sound differently from those behind you.
Q6) Does the auditory canal selectively amplify certain frequencies due to resonance?
A6) Actually, yes. But we did not discuss this.
Q5) In the taste bud activation pathway, do they release glutamate or serotonin as the neurotransmitter because I'm getting mixed signals from the book and the review session.
A5) That is because we don't really know. At least serotonin. Maybe ATP. Glutamate is activating the Umami receptors, but it has also been seen to be released from these same taste buds. Go figger.
Q4) As far as retinal circuits go, I don't understand what the positive and negative signs refer to. The synapse for the photoreceptor to the on center bipolar cell is negative and the synapse from this cell to the oncenter ganglion cell is positive. I would have thought these signs would be switched if the (+/-) referred to glutamate release versus no glutamate released at the synapse.
A4) No. The sign is not stating whether glutamate is being released. It denotes whether the synapse is excitatory or inhibitory.
For help understanding the grid illusion with the flashing grey dots, follow this link: Hermann.
Q3) For the blue-center, yellow-surround retinal circuit, what photoreceptors are the center and surround bipolar cells wired to? "Blue" cones I get in the center, but yellow comes from.....being wired to rods that respond to yellow wavelengths?
A3) This is true-ish outside the fovea. But inside the fovea it is a combination of red and green photoreceptors acting in opposition to blue.
Q2) I was wondering if you could help me understand something. In lecture, you discussed the difference between Ipsilateral and contralateral as:
ipsilateral- visual info coming from an eye that crosses contralateral-visual info coming from an eye that does not cross
A2) This is backwards: ipsi means "same"; contra means "opposite".
Ispilateral connections from the retina to the LGN are the eye on the same side.
Q1) My question is, where does the crossing of visual info occur? At the optic chiasm?
A1) Yes.
