QandA
From NeuroWiki
Q6) What are the purpose of the mu receptors on the VTA? The medial prefrontal cortex can release opioids onto them to... inhibit the VTA dopaminergic release?
A6) The mu receptors are part of the excitatory pathways that lead to addiction, it is believed. The are other receptors (kappa-opioid receptors) that we did not discuss. These allow for negative action on the VTA from the preFrontal cortex.
Q5) Is the Colliculospinal tract the same thing as the Tectospinal Tract b/c they both originate @ the Superior colliculus.
A5) yes.
Q4) Referring to slide 6 from 04.04’s notes. Ca+2 binds to the ligand-gated RyR receptor in the SR which then opens to allow Calcium to flow in. Calcium, once in the cytoplasm, accumulates and depolarizes the cell to trigger the voltage-gated DHPR receptor (in the T-tubule) to open to let calcium then flow out into the SR?
A4) This is backwards. This is the arrangement of DHPR and RyR in the striated muscle. In part b) of the slide, the DHPR senses the depolarization of the membrane as a result of the opening of the nicotinic receptors. This causes the voltage sensor- the little red + on the green transmembrane segment to be attracted to the relative negative charges outside the cell. This movement tugs on the tether to the RyR to open it and let Ca out of the SR.
Ca and/or Na leak is the reason the the RyR opens in the cardiac pacemaker cells.
Q3) I am a bit confused about the descending pathway that causes paralysis during sleep because during lecture you mentioned that the GABAergic projections from the pontine reticular formation go to the deep cerebellar nucleus. Na mentioned during the review that the projections were to the dorsal nucleus of clarke, but the purves book mentions that the projections are to the dorsal column nuclei.
A3) Close. The GABAergic projections are on the Dorsal Nucleus of Clark (DNC) that Na mentioned. They also go to the Dorsal Column Nuclei (DCN), of which we learned about the gracile and cuneate nuclei. What I mentioned in class was that the abbreviations are confusing: the DCN in this case refers to gracile and cuneate nuclei that bring proprioceptive information to the cortex (Spinocortical tract). The DNC (Clark's Nucleus) brings this information to the cerebellum (Spinocerebellar tract). In both cases, proprioceptive information is being inhibited. However, none of these cause paralysis. The direct role of GABAergic projections in this case is to numb the sleeper. The paralytic effects come from glycinergic projections to the motor neurons in the lower spine. The circuitry prior to these glycinergic neurons is complex (and in reality, not very well defined). While the originating neurons are GABAergic, there are many intervening connections that involve serotonin, acetylcholine, and glutamate.
Q2) You mentioned losing motor control because of damage to the Rubrospinal Tract, but still having reflexive ability (throwing a ball at them and their hand going up quickly). However, then you mentioned damage to some area would render you completely lacking motor control. I'm a little confused because my notes mentioned Rubrospinal Tract both times
A2) This seems to be a confounding of several types of damage. The rapid reflex after a long delay in initiation is due to damage in the substancia nigra of the basal ganglia. The rubrospinal tract is a long set of descending fibers that originate in the red nucleus cross the spinal cord almost immediately and remain contralateral to their source input for the remainder of the spine. It is insufficient to say damage to the tract. There must also be some distinction where along the tract the damage occurs.
Q1) Damage to the area of decussation in the Rubrospinal Tract will cause the loss of motor control?
A1) This is a little vague. If you damage the entire spinal cord (a complete transect, well then, sure). But if you had a small lesion below the red nucleus, but above the pyramidal decussation- on the side of the red nucleus, then you would retain cerebellar control, and lose some of your volitional movement.
