BPK 306 Lecture Notes - Lecture 32: Resting Potential, Dorsolateral Prefrontal Cortex, Retrograde Amnesia
5 Dec 2017
School
Department
Course
Professor
Document Summary
Hm developed seizures following injury -> to stop the seizures, there was bilateral removal of medial temporal lobes: removal of both hippocampi. This left hm with anterograde amnesia: = inability to form new memories, does not know anything after surgery. Hippocampus = most critical structure for long-term memory, particularly consolidation. Entorhinal cortex = critical for interface between hippocampus and cerebral cortex. Nmda and ampa are both glutamate receptors: ampa = na+ channel, nmda = ca2+ channel. At resting membrane potential -> nmda receptor is blocked by mg2+ which is removed during depolarization. Ca2+ influx through nmda activates intracellular camkii pathway. Causes insertion of ampa receptors on postsynaptic membrane from vesicles. Immediate early genes (iegs) like cfos show when genes are activated such as in ltp: cfos = generic markers that indicate the turning on of proteins. Inter-regional correlations in cfos can show how networks change over time -> such as in fear conditioning = associations.
