BIO 400: Exam 3 Study Guide
BIO 400: Exam 3 Study Guide BIO 400
Popular in Biology of Adaptive Behaviors
Popular in Biology
This 8 page Study Guide was uploaded by Emily.nicole on Sunday November 1, 2015. The Study Guide belongs to BIO 400 at Syracuse University taught by Dr. Paul Gold in Spring 2015. Since its upload, it has received 27 views. For similar materials see Biology of Adaptive Behaviors in Biology at Syracuse University.
Reviews for BIO 400: Exam 3 Study Guide
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 11/01/15
Review for Quiz 3 Lecture 16Protein Synthesis 1 ● Memory Formation: ○ protein synthesis independent (shortterm memory) ○ protein synthesis ependent (longterm memory) ○ phases of memory consolidation. ● a CNS manipulation that attenuates amnesia may be unrelated to the primary effects of the amnestic agent. For example, Flood et al., (1977) found that amnesia induced by the protein synthesis inhibitor anisomycin was attenuated by either amphetamine, strychnine or picrotoxin ● An examination of the literature about the attenuation of protein synthesis inhibitor induced amnesia led to some surprising conclusions. First, puromycin amnesia is attenuated by treatment with saline in a manner that is time dependent to the puromycin treatment. It seems that puromycin somehow blocks the expression of memory. However, if this is true, then the massive inhibition of protein synthesis produced by puromycin is not a necessary or sufficient condition to prevent the formation of new memories. ● Therefore, other inhibitors of protein synthesis that are known to produce amnesia must necessarily have additional actions. It was proposed that protein synthesis inhibitors produce amnesia through their cumulative widespread effects on many neural and endocrine systems. Second, the amnesia produced by protein synthesis inhibitors is not very robust and is readily reversed by a wide variety of attenuating treatments. Third, the conclusion that the amnestic effects of protein synthesis inhibitors may not be related to inhibition of protein synthesis is best supported by several studies showing that agents that either attenuate or potentiate protein synthesisinduced amnesia do nothing to significantly alter the rate of protein synthesis in the CNS. Protein Synthesis: ● Transcriptiongenetic code (DNA) transcribed ( copied) on mRNA in cell nucleus ● Translation mRNA leaves molecules and travels to ribosomes in the cytoplasm where to coded info is translated into specific amino acid (polypeptide )sequences in a protein→ folded Memories after EXPERIENCES: ● Short Term Mem: vulnerable to disruption, active state has rapid decay ○ LTM is less vulnerable, inactive state and slow decay Challenges to prevailing models: ● 90+% PSI is required for memory impairments. ● PSIs do not impair memory for training with high footshock, for extinction training, olfactory memory. ● Can block amnesia / rescue memory with: ■ amphetamine clonidine ■ isoproterenol caffeine ■ nicotine naloxone ■ corticosterone AChE inhibitors ■ clenbuterol (βadrenergic agonist) ■ propranolol (βadrenergic antagonist) ● Can also block amnesia with: ○ peripheral adrenergic antagonists (block stress to PSI?) Conclusion from HC + Amygdala studies: ● Protein synthesis inhibition can impair both short and longterm memory ● A function of brain system more than treatment → Particularly when viewed in the context of the rapidity (within minutes) with which brain structure can change, the need for the three Ts transcription and translation and transport – to cause these changes seems unlikely. Lecture 17Protein Synthesis 2 Lecture 18 Krebs Cycle ● The cAMP responsive element binding protein (CREB) is a nuclear protein that modulates the transcription of genes with cAMP responsive elements in their promoters. Increases in the concentration of either calcium or cAMP can trigger the phosphorylation and activation of CREB. This transcription factor isa component of intracellular signaling events that regulate a wide range of biological functions, from spermatogenesis to circadian rhythms and memory . Here we review the key features of CREBdependent transcription, as well as the involvement of CREB in memory formation. Evidence from Aplysia,Drosophila, mice, and rats shows that CREBdependent transcription is required for the cellular events underlying longterm but not shortterm memory. While the work inAplysia and Drosophila only involved CREB function in very simple forms of conditioning, genetic and pharmacological studies in mice and rats demonstrate that CREB is required for a variety of complex forms of memory, including spatial and social learning, thus indicating that CREB may be a universal modulator of processes required for memory formation. Epinephrine enables memory in KO mice: ● CREB deficiency impairs water maze learning, which is predominantly attributable to a marked increase in wall hugging (thigmotaxis). A, Water maze learning in Creb CamKCre7 was indistinguishable from wildtype littermates. B, Creb NesCre mice displayed a significantly increased swim path length. C, Marked reduction of CREB in the forebrain did not impair spatial memory. D, Apparent deficits of spatial memory in Creb NesCre mice during probe trial 1. E, Pooling of four Creb mutant strains (Creb CamKCre7, Creb NesCre, Creb, and Creb comp) and three wildtype strains, respectively, contrasts the performance deficits of CREBdeficient mutants with their littermate controls. F, In mutant strains, the percentage of thigmotaxis is markedly increased. Twoway ANOVA with repeated measures with days 1–14 and genotype (mutant and wild type) as factors was used for the analysis of the values depicted in Figure 4. The p values represent the genotype effect. ● Intra Amygdala Injections of CREB Antiese impair memory: ○ depressed CREB in antiese CREB CONCLUSIONS ● Suppressed trainingrelated release of NE after CREB antisense treatment may contribute to memory impairments, suggesting mechanisms beyond inhibition of protein synthesis. ● Possible alternative mechanisms are also suggested by EPI reversal of memory loss in CREB KO mice. ● More generally, the findings suggest a possible role of CREB in local circuit dynamics that may modulate memory formation. Action potential: The system is set with potential energy to accomplish its goal. The need for energy is for replenishment of ions after an action potential. Memory : The system is set with potential energy to change connections. A need for protein synthesis is to replenish proteins after memory formation. Lecture 19 LTP 1 Longterm potentiation (LTP): A putative synaptic mechanism for memory. Longterm potentiation is an enduring form of synaptic plasticity. LTP can be studied in intact awake rats and mice, in anesthetized rats and mice, and in brain slice preparations taken from rats and mice. In each case, electrical stimulation is (test stimulus) can be delivered to afferent fibers and the resultant summated / field EPSP can be recorded in the postsynaptic neuron. Delivering a brief 1sec duration train of high frequency (e.g. 100 Hz) stimuli (i.e., the tetanus) to the afferent nerve produces two types of enhancement in the postsynaptic neuron. First, there is a transient facilitation called posttetanic potentiation (PTP) that dies away after several minutes. Second, following the PTP is an enduring enhancement of the EPSP called LTP, which can last for hours to days to months. Lecture 20 LTP 2 EPSP’s:Single Neuron Spike (AP) vs Population Spike Experimental design: Stimulate a bundle of presynaptic axons e.g. hippocampal perforant path Use extracellular recording electrode to measure monosynaptic EPSP e.g. dentate gyrus ● Record population response before and after high frequency stimulation ● Increase in population response indicates potentiation Hippocampal slice preparations have supported and extended the findings of Bliss and Lomo Longterm potentiation (LTP): a candidate cellular mechanism of memory ● Some properties of learned behaviors: ○ Experiencedependent ○ Input specific ○ Rapid induction ○ Longlasting ● Some properties of LTP: ○ LTP is experiencedependent ■ Need stimulation to induce a large change in synaptic strength ○ LTP is input specific ■ Only the conditioned (tetanized) pathway is potentiated ○ LTP is induced rapidly ■ Conditioning stimulation needed for only a few seconds ○ LTP is longlasting ■ Can last hours to days Lecture 22 LTP 3 ● stuff on mice: ○ reaching tasks Lecture 24 Weinberger Review: ● Learning and memory involve the storage of specific sensory experiences. However, until recently the idea that the primary sensory cortices could store specific memory traces had received little attention. Converging evidence obtained using techniques from sensory physiology and the neurobiology of learning and memory supports the idea that the primary auditory cortex acquires and retains specific memory traces about the behavioural significance of selected sounds. The cholinergic system of the nucleus basalis, when properly engaged, is sufficient to induce both specific memory traces and specific behavioural memory. A contemporary view of the primary auditory cortex should incorporate its mnemonic and other cognitive functions. Lecture 26 All assigned Readings Brandon & Cross: ● studied honeybees using rapid Golgi method to show that dendrite spines on calycal interneurons had shorter stems due to head enlargement in bees with greater cumulative flight a one trial place learning event ● newly emerged bees were reared in a small broodless hive with a virgin queen and allowed to take their first orientation flight at 6 and 8 days of age ● spine profiles of 5 flyers and 5 nonflyers were traced in large scale using light microscopy and a modified camera lucida ● overall spine length and stem length were measured on these tracings using a digitizing tablet. ● additional measurements of maximum spine head width, profile areas, and perimeters were made using computer image analysis. ● Examining group differences in spine stem length as a function of overall spine length, our results revealed a clear association between rapid spine stem shortening and the first orientation flight lasting several minutes ● this effect was restricted to only the long spines ● flightinduced stem shortening was accompanied by elongated swelling of the spine head without an appreciable expansion of the spine perimeter Dysgenesis ● Golgi studies reveal abnormally long, thin spines and the absence of short, thick spines on dendrites of cortical neurons in retarded children with normal karyotypes. The degree of dendritic spine loss and abnormality appears to be related to age and the severity of developmental retardation. Dendritic spine "dysgenesis" is a common feature of the microstructural pathology that occurs in profound mental retardation of unknown etiology. Barack, ismail, Robinson→ Stimulating Muscarinic Receptors ● Honey bees begin life working in the hive. At 3 weeks of age, they shift to visiting flowers to forage for pollen and nectar. Foraging is a complex task associated with enlargement of the mushroom bodies, a brain region important in insects for certain forms of learning and memory. We report here that foraging bees had a larger volume of mushroom body neuropil than did age matched bees confined to the hive. This result indicates that direct experience of the world outside the hive causes mushroom body neuropil growth in bees. We also show that oral treatment of caged bees with pilocarpine, a muscarinic agonist, induced an increase in the volume of the neuropil similar to that seen after a week of foraging experience. Effects of pilocarpine were blocked by scopolamine, a muscarinic antagonist. Our results suggest that signaling in cholinergic pathways couples experience to structural brain plasticity. I think the one above is saying that the muscarinic receptors are shown to have more volume due to increased synapses from the experience of being outside. Meaning, the strentgh of the synapses is strengthened. But why would the volume be higher? ohh duh bigger brain area with experience, means more sensitive to stimulus, therefore less stimulus =LTP Simon Levay: ● The anterior hypothalamus of the brain participates in the regulation of maletypical sexual behavior. The volumes of four cell groups in this region [interstitial nuclei of the anterior hypothalamus (INAH) 1, 2, 3, and 4] were measured in postmortem tissue from three subject groups: women, men who were presumed to be heterosexual, and homosexual men. No differences were found between the groups in the volumes of INAH 1, 2, or 4. As has been reported previously, INAH 3 was more than twice as large in the heterosexual men as in the women. It was also, however, more than twice as large in the heterosexual men as in the homosexual men. This finding indicates that INAH is dimorphic with sexual orientation, at least in men, and suggests that sexual orientation has a biological substrate Long Term Potentiation as a Model for Studying Mechanisms of Learning and Memory: ● LTP is a stable and enduring increase in the magnitude of the response of neurons after afferent cells to the region have been stimulated with bursts of electrical stimuli of moderately high frequency ● In the hippocampus, there are 2 kinds of LTP and they interlock to make Cshaped regions : the hippocampus and the dentate gyrus, with adjacent subiculum (subicular complex or hippocampal gyrus) ● LTP is a kind of synaptic plasticity that underlies certain forms of learning and memory→ therefore, it can be used to investigate the mechanisms ● Although definite LTP & LTD ( depression decreased magnitude)
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'