Essay (Rusty) Flashcards
1) With regard to consciousness, describe the specific role of the dorsal and ventral pathways. Next, describe what your world would be like if each pathway was selectively destroyed.
The dorsal pathway functions as the “where” (how) control of behavior. If your dorsal pathway was destroyed, you would have great difficulty guiding actions, looking towards things, or grabbing/pointing at objects. You would have simultanagnosia, or “tunnel vision” – you could recognize individual objects, but could only focus on one object at a time. (i.e. Balint’s syndrome). The ventral pathway functions as the “what” for conscious perception. If your ventral pathway was destroyed, you would have difficulty distinguishing objects. Objects would look like unrecognizable abstract sculptures that don’t evoke emotions or have associations. You also might be at risk for eating some nasty or dangerous things (i.e. Kluver & Bucy syndrome)
We saw a groundbreaking study on monkeys and movement. Briefly describe what the researchers did, what they found, and the implications of this study.
First, researchers trained a monkey to play a “video game” using a joystick, in exchange for delicious treats. After the monkey became proficient, they observed the monkey’s neuronal activation patterns while playing the game and using the joystick. Next, they implanted electrodes into the specific neurons, which were hooked up to the video game computer. They were able to calibrate the computer to play control the game according to the neuron firing. Next, they disconnected the joystick (but left it in place), and found that the monkey could control the game just by firing those specific movement neurons. Eventually, they took away the joystick entirely, and the monkey learned to play the game just by imagining the joystick movement. Finally, they hooked up a giant bionic arm to the computer, and it followed the motor movement patterns that the monkey was imagining. In essence, the researchers found that by attaching electrodes to specific motor neurons, the output from those electrodes could emulate movement on electronic and mechanical devices. This has big implications for people who have lost limb. It can be used to develop artificial limbs which can use fine motor movement, by means of replicating the natural output of motor neuron firing.
We talked about 3 different animal models of human neuropsychological diseases in class: the kindling model, the transgenic mouse model, and the MPTP model. Briefly discuss the experiments that led to the development of each of these models, and what disorder each model tells us more about.
The kindling experiment induced seizures on rats via periodic stimulations to the amygdala. It eventually caused permanent neural changes, and convulsions occurred spontaneously, but only if kindled by stimulations done over a long period of time. This model tells us more about epilepsy, as the kindling phenomenon is comparable to the development of human epilepsy following a head trauma. The transgenic mouse experiment introduced human genes (which accelerated amyloid synthesis) into mice. They found the mice had plaque distribution comparable to Alzheimer’s, with high plaque density in the hippocampus. However, there were no neurofibrillary tangles. The model leaves the question of whether plaques are a cause or a consequence of Alzheimer’s, but it shows that accelerated amyloid synthesis plays an important role in the disease. The MPTP experiment found that synthetic heroine produced the symptoms of Parkinson’s in monkeys. It contained a neurotoxin called MPTP. MPTP causes cell loss in the substantia nigra, and a decrease in dopamine, like that seen in Parkinson’s. This model shows that substantia nigra cell loss may play an important role in PD, and it gives insight into possible treatment for Parkinson’s: MPTP animal studies found deprenyl (which blocks MPTP’s effects) can slow the progression of Parkinson’s.
What type of amnesia did H.M. have? State specific tasks that he could and could not complete. Finally, briefly discuss the scientific contributions of H.M.’s case to the field of memory & the brain.
HM had mild retrograde amnesia and severe anterograde amnesia – he had a problem with. HM could repeated digits as long as the time between learning and recall was within the duration of STM. On a mirror drawing task, he showed improvement with practice: he showed skill memory as a result of classical conditioning. However he could not complete a block-tapping memory span test (showing the amnesia was not limited to one sensory modality). In terms of scientific contributions, his case demonstrated that the medial temporal lobes are involved in memory. It also shows that STM and LTM are distinctly separate. It also shows that memory consolidation is the primary issue with anterograde amnesia: he could not move memories from STM to LTM. It also shows that some memory could be stored somewhere, but it couldn’t get recalled (see mirror drawing task).
