PSYC 340 1st Edition Lecture 9 Plasticity within the Vertebrate Spinal Cord What you missed last class… I. Learning from an invertebrate A. However, must assume that the axons/action potential in a giant squid also applyto our brains 1. Need to assume/hope that the way an invertebrate learns/remembers is the same way we do a. Research suggests that this is true. 2. Aplysia– seasluga. Why aplysia? Advantages: simple nervous system, large neurons(can see some with the naked eye), invariant neuralanatomy(not a lot of genetic/physical variation.) b. KandelB. Nonassociative learning 1. Habituation a. Touching the siphon = gill withdrawal reflex i. Becomes habituated b. Touching the mantle = gill withdrawal reflex i. Becomes habituated c. However, these two S-R cycles are independent i. Habituating one does not affect the other 1. Sensitization c. General affect: apply shock to tail sensitizes reflexes in the entire aplysiaB. Neural circuit 1. Sensory neuron, motor neuron, facillitory interneuron 2. Changes in amount of transmitter released from SN a. With habituation observe a decrease b. With sensitization observe an increase II. Review: basic neural function A. Resting potential (Na+, K+) 1. Works to keep sodium out of the cell. a. Excess of sodium outside the cell2. Outside of cell = positive, inside = negative a. Sodium (positive) wants to get inside, but keeps getting pumped out. 3. Excess K+ inside the cell; wants to rush out to its concentration gradient but repelled by outside membrane 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.B. Action potential 1. Initiated by depolarizing the cell 2. Rising phase: Na flowing into the cell – depolarization 3. Reestablishing the resting potential:a. K+ flows out 4. Synaptic transmission a. When action potential rises, Ca channel opens up, allowing Ca to flow in (presynaptic neuron) b. Amount of neurotransmitter released depends on the amount of calcium released in the cell i. More Ca = more transmitter ii. vesicles, neurotransmitter c. The time the calcium channels stay open is proportional to the length of the action potential C. Biochemical mechanisms 1. Habituation a. Due to a short-term inactivation of calcium channels b. Long-term is due to reduction in number of synaptic contacts; a structural change. 2. Short-term sensitization a. Biochemical cascade – dominos i. (serotonin, serotonin receptor, G-protein, adenylate cyclase, ATPcAMP, protein kinase, K channel (turns themoff), Ca channel (more Ca into the cell, more neurotransmitter) ii. Increases the duration of the action potential iii. Protein kinase = memory i. Keeps working for four-ish hours 3. Long-term sensitizationa. Depends on making new proteins – engage genes in the cell body b. MAP+PKA engage gene expression i. Engage a cellular switch in the nucleus (CREB) and turns ongenes, which leads to manufacture of new proteins i. Change how protein kinase works – supercharged ii. Genes that also make structural modifications – more synaptic connections Nociceptive (pain fibers) PlasticityI. Nociceptive sensitizationA. Nociceptors detect tissue damageB. Nociceptive pathways relay this signal to the brain1. We care about nociception because it tells us about pain, but pain does not exist in sensory fibers… pain is created in the brain2. We use these big terms because they allow us to discuss tissue damage without invoking the concept of conscious painC. In Aplysia and vertebrates1. If we shock the Aplysia, we see an enhanced response – a kind of Nociceptive sensitization2. The shock allows the Aplysia to detect something that triggers the same fibers associated with paina. It is not designed to detect electric shocks per sayb. Shock activates the nociceptive fibers and the brain processes this as painD. Turns out, we do not need a brain to show these effects1. No brain is necessary to show nociceptive sensitization2. Nociceptive sensitization occurs in the spinal corda. Results: enhanced response, a spinal reflex – because nociceptive sensitization occurs in the spinal cord, not the brain3. Allodynia – pain to stimuli that do not normally elicit pain a. Ex: touch – touching a really bad sunburn; cutting up really hot peppers with no protection on hands and then going and taking out your contacts i. Touching/capsaicin sensitizes spinal neurons in these instances – C-fibersb. Again, the sensitization occurs in the spinal cordII. Studying central sensitization within the vertebrate spinal cordA. Electrophysiological observations1. Studies done by Woolf and his colleagues a. Discovered: C-fibers transmit information very slowly i. Hit thumb a hammer – have time to contemplate/process what just happened2. Used electrophysiological observations to study sensitizationa. Stimulate a fiber and record it in the spinal cordb. Thickness of bar (on visual) shows the strength of response that occursi. Strong input = strong responseii. Moderate input = moderate responseiii. What was of interest: after the strong input, a strong de-polarization (taking neurons -70 up towards zero) occurred– by applying a strong input, Woolf sensitized the nociceptive system- Here, moderate input = strong responseB. Similarity to long-term potentiation (LTP)1. Discovered by Bliss and Lomo (?) – studied the hippocampus2. Phenomena of long-term potentiation (studied later) is very similar to nociceptive sensitizationa. Both have to do with chronic painb. In spinal cord it is easier to relate a neurochemical mechanism to abehavioral mechanismi. Spinal cord is considered a better model system than the hippocampus because of thisc. Same biological mechanisms to create more connections occur here as wellIII. Neurochemical mechanisms ← underlie sensitizations in the spinal cordA. AMPA and NMDA receptors (the key)1. AMPA receptor– acts as a common channela. If you turn it on with glutamate (most common transmitters in thebrain), the cell depolarizesb. Glutamate activates the AMPA channelB. NMDA receptor acts like a gated channel1. Two events: activate glutamate receptor; dislodge the magnesium (Mg) present in the channela. A strong depolarization (of post-synaptic cell) dislodges the magnesium (Mg)b. Glutamate comes from the pre-synaptic cellc. Only if both things happen does calcium get to enter the cell