PSYC 340 1st Edition Lecture 15 Current LectureWhat you missed last class… (03.12.15)I. Pavlovian Conditioning in Aplysia A. Pairing specific enhanced sensitization B. 2 stimuli – touching the siphon and touching the mantle 1. Mantle = CS+; Siphon = CS-; Shock = US2. Gives stronger response with paired cue (CS+, mantle) than the unpaired (CS-, siphon) a. Shows that pairing matters C. CS allows Ca++ to enter, which fosters the conversion of ATP to cAMP by adenylate cyclase 1. Shocking the animal activates facilitatory interneuron; long story short, allows more calcium to enter the systema. Leads to greater sensitization 2. This is basically all due to adenylate cyclase – works better in the presenceof calcium a. If there is more Ca++ in the cell, more cAMP is madeb. More cAMP means more protein kinase activated, which means more potassium channels closed, which means more sensitization c. Touching the mantle allows an action potential and allows more calcium in the cell d. adenylate acts as a coincidence detector – senses that both the facilitatory neuron is engaged and that there is more calcium to bepresent 3. Order of this matters – need calcium to be present first II. Cerebellum and Conditioned Eyeblink (Thompson) A. Engram – underlying mechanism of learning and memory 1. Pairing specific enhanced sensitization for Pavlovian conditioning B. Advantages of the eyeblink paradigm 1. Really well defined variables 2. Best characterized form of learning 3. Animals are rather reliable at showing this effect 4. Easy to map the behavior A. This diagram is the circuitry that underlies the eyeblink paradigmB. Methods: 1. Lesion: electrolytic and neurochemical (spares fibers of passage)a. Inference of function through dysfunction These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.i. Shows necessity of the region – if there is learning withoutthe region, then it is not necessary to learning 2. Activation a. Shows that activating these systems are sufficient to learning b. Substitution and mimicry 2. Recording Activity a. If this region is critical, we will see it light up during learning a. Are these neurons activated when I say they are activated? C. Look back at the diagram – neural pathways 1. Information regarding the US comes in through the trigeminal nucleusa. Lesioning this area = there is no US = there is no learning 2. UR comes down through the reflex pathway, to the reticular formation, the cranial motor nerve, then to show eyeblinking 3. CS comes through the auditory nuclei a. Lesioning this would affect the CS/CR, but would not affect the UR. 4. US and CS get married at the interpositus nucleus 5. Train them up, then lesion the inferior olive, there will still be a CR, but then they are heading towards extinction 6. The line then bar means there is an inhibitory effect a. Example: after you learn, the relationship between the interpositus nucleus turns off the inferior olive b. Leads to blocking! i. Once you expect the US, it turns off the US pathway; makes the US less effective c. Depends on the inhibitory transmitter GABA i. We can reduce this by using a drug that blocks GABA – bicucullin (GABA-A antagonist) ii. Give bicucullin – you will learn the US! Cerebellum and Conditioned Eyeblink ParadigmAmygdala and Emotion I. Anatomy A. Man (Phineas Gage) lesioned his amygdala in an accident 1. Very rare; usually safe 2. He showed normal memory, thinking, etc. a. But he didn’t show fear B. Components of the limbic system C. Organization II. Role in FearA. Sensory information comes in through the thalamus 1. Signal is sent to the basolateral amygdala (BLA) a. Information about pain; more coarse information about the stimulus (loud auditory stimulus rather than saying location, frequency, volume, etc.) 2. Other information is relayed through various cortical areas; becomes elaborated; reaches the hippocampus a. Also sent to the BLA; gets coarse info about CS and also the more elaborate info about the CS B. The CS and the US are glued together in the BLA – where associative learning takes place C. NMDA is important in the amygdala 1. The joining of the CS and the US in the BLA is depending on the NMDA receptors a. If you block it using a druge such as MK-801 (a NMDA antagonist,) you will block fear conditioning D. PAG – Periaqueductal Gray 1. Produces freezing behavior 2. Analgesia 3. If you lesion this section, you will lose this freezingE. Startle, blood pressure, heart rate, respiratory rate, etc… come from different system 1. All come from the central nucleus of the amygdala a. Will show no signs of fear is lesions (like Phineas Gage) b. However, will still learn about fear, or possibly feel fear; just no physiological symptoms III. Negative feedback and the Rescorla-Wagner model (McNally) A. Teaching signal to lateral amygdala is modulated by vlPAG B. ^ - Vt, where lambda is the US and Vt is what you expect C. As you develop an expectation of the US, the US will become less effective D. In the amygdala, you get two signals: one is the shock (US) and what you expect1. Turns off the US pathway through analgesia 2. US signal sent the amygdala gets weaker, and learning stops E. PAG is doing the ^ - Vt computation F. Described in a neurobox Encoding Complex Stimulus Relations I. Basic properties A. Distinction between explicit (mediated/declarative) and implicit (unmediated) learning 1. Unmediated/implicit – no cognition is involved a. What we have been talking about 2. Now, where are moving on to mediated/explicit/declarative learning – cognitive processing is involved B. Role of the hippocampus 1. Required by explicit learning 2. Man with seizures got his hippocampus taken out a. Stopped the seizures, but he also lost the ability to explicitly learn new information b. Extreme kind of version of Alzheimer’s c. He was okay with things that happened before the removal of his hippocampus, but couldn’t tell you anything that happened after II. Phenomena A. Trace eyeblink conditioning 1. You don’t need hippocampus or forebrain with delayed conditioning (CS right up until the US) a. However, if you have a gap between CS going off and onset of US, the hippocampus is necessary (trace conditioning) 2. Eliminated by hippocampal lesions 3. Disrupted in patients with hippocampal damage (Clark & Squire) a. Patients without the