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73 Cards in this Set
- Front
- Back
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central pattern generators
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groups of neurons that cause rhythmic behaviors by alternately activating groups of muscles
-even in the absence of direct feedback from muscles themselves the generators can have these patterns of rhythmic excitation |
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reciprocal inhibition
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in this, each neuron makes an inhibitory synapse onto the other and they need to display postinhibitory rebound to get a rhythm (w/out excitation)
EXAMPLES: -swimming in clione -feeding in helisoma -stomata gastric ganglion in crustaceans -swimming and leech and lamprey |
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postinhibitory rebound
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-after the membrane potential of the cell has been hyperpolarized for a short period of time, the cell becomes more excitable than usual.
-gives the alternation of AP in each neuron rhythmically which ultimately causes alternation of muscle activity -cells with this property have a lot of Na channels open at rest (some inactivated, which is removed by hyperpolarization) --threshold is lowered by the increased number of Na channels that can be activated. (simplest model: two neurons in swimming clione) |
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Clione Swimming
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-swim by moving a pair of wing like structures that are alternately flexed in a dorsal and ventral direction
-have one upswing and one downswing neuron on each side of nervous system -an AP in an upswing neuron generates and inhibitory postsyn potential (IPSP) in downswing neuron -movement is conveyed to motor neurons that innervate muscles, producing the rhythmic swimming |
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Helisoma feeding
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-radula for protracting, retracting, hyper-retracting in eating
-3 different sets of muscles activated to allow three phases to occur -have more than one network consisting of 3 interneurons and 3 motor neurons -excitation by interneurons via 5-HT and dopamine -S1 and S1 interneurons more excitation based while S3 is stimulated by postinhibitory rebound -communication through bursts of AP instead of single AP seen in clione -get a phase 1<-->2 rhythm when receiving something helisoma dislikes (regurgitation) -dopamine gives rhythmic pattern almost always while 5-HT sometimes does but also can give a 2<--> behavior. |
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Movement of food through crustacean stomach
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chews in mouth-->esophagus-->stomach w/ cardiac sac for food movement-->gastric mill-->pylorus used as sieve (will push back food particles if too large)
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Muscles/neurons in Crustacean stomach
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-stomatogastric ganglion controls processes in the stomach
-contain 30 neurons that control stomach muscle movements--has 3 central pattern generators (pyloric CPG is focus) - |
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Pyloric CPG
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-consists of 14 neurons
-AB neuron is the only interneuron while the rest are motor neuron that directly innervate the pyloric muscle -all chemical synapses are inhibitory (reciprocal inhibition) but there are also electrical synapses -external inputs excite AB and no neurons are active without this input -rhythmic bursting |
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AB as a conditional burster (pyloric CPG)
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-NTs can put AB into conditions where it can burst on its own
--Dopamine turns off some of the cells neuronal functions -5-HT does this to other neurons -the other neurons are not endogenously bursting but they can generate a single long burst of AP in response to a brief depolarization when inputs from other ganglia are also activated -depending on which inputs and what NT are present, activity will differ-->modulatable system |
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command neurons
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-tasks are regulated (turned on and off) by a command system of neurons
-a command neuron is a neuron whose activity is both necessary and sufficient to trigger an entire coordinated behavior EXAMPLE: the swimming leech -consist of touch sensory, gating and trigger neurons |
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leech swimming
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-body is divided into segments and undulates when swimming as a result from the alternate contraction and relaxation of muscles in the body wall if animal
-rhythmic bursts of AP in motor neurons in each ganglion are timed so one wave travels from the front to the rear of the animal |
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network that controls leech swimming
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-result of a rhythmic output by a CPGs found in each segmental ganglion
-touch sensory neurons feedback to trigger neurons at head end of animal (sufficient to stimulate swimming) -gating neurons in each segment stimulated by trigger neurons (one stimulus can allow a long sustained firing) -CPG is sustained only as long as gating neurons are active but gating neurons to not provide the rhythm |
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how lampreys swim
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-lateral, side to side contraction and relaxation sequence
-frequency of contractions can change -2 CPG inhibit one another -have excitatory and inhibitory stretch receptors at skin to provide feedback onto CPGs to ensure coordination |
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learning
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a change in behavior as a result of experience
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nonassociative learning
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represented by a change in intensity of a behavior in response to some sort of stimulus; simple change of response to stimuli
-Types: 1. habituation 2. sensitization |
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associative learning
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-requires two inputs: initially neutral stimulus causing enhanced response only after pairing with a meaningful one
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Habituation
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-type of nonassociative learning
-a reduction in response to a repeated stimulus (e.g. not feeling clothes after wearing them for a little) |
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sensitization
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-type of nonassociative learning
-an enhanced response to a noxious stimulus |
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memory
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storage and recall of learned events
-types: 1. short-term 2.long-term i) nondeclarative ii) declarative |
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Short term memory
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lasts seconds to minutes in time frame
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long term memory
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-retention and recall for minutes to years
-types: 1. nondeclarative 2. declarative |
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nondeclarative long term memory
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memory for skills (e.g. riding a bike)
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declarative long term memory
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memory for events (e.g. preparing for an exam)
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Aplysia gills
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-gill withdrawl paired with abdominal ganglia
-breath with gills in order to extract O2 from water -withdraw gills underneath mantle for protection (siphon helps take sea water in and with protection) -spraying the siphon/mantle causes gill withdrawal in experiments but these animals live in environments with moving water/waves so they need to habituate |
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Aplysia habituation
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-gill contraction/protection habituated to wave motion but noxious stimuli can cause dishabituation (sensitization)
-habituation is short term, goes away after a few hours -habituation is not about responsiveness of MN but rather the reduction in Glutamate release |
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Aplysia sensitization
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-facilitator neurons are in the abdominal ganglion as well and are involved in sensitization--they synapse with the presyn. sensory neuron
-in sensitization, Glut release increases -5-HT is release by facilitator neuron and receptor for 5-HT is Gs (activates adenylyl cyclase, cAMP, PKA, phosphorylation of proteins) -PKA phosphorylates S Current K Channel, which closes it, allowing depolarization in cell to last longer -time course of mechanism determined by channel phosphorylation (short time frame unless there is continuous stimulation of the facilitator neuron) |
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Associative Learning in Aplysia
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-classically conditioning
-can apply a conditioned stimulus of water jet with unconditioned tail shock-->will see enhanced response that can last for hours -Uses CREB (cAMP response enhancement binding protein) -also involves a change in amount of excitatory NT release from sensory neuron -cAMP kinase phosphorylates CREB, increase new protein synthesis, increase NT release over a longer time scale HAVE to have simultaneous activity in sensory neuron and facilitator neuron to have affect on CREB |
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Associative Learning in Aplysia
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-classically conditioning
-can apply a conditioned stimulus of water jet with unconditioned tail shock-->will see enhanced response that can last for hours -Uses CREB (cAMP response enhancement binding protein) -also involves a change in amount of excitatory NT release from sensory neuron -cAMP kinase phosphorylates CREB, increase new protein synthesis, increase NT release over a longer time scale HAVE to have simultaneous activity in sensory neuron and facilitator neuron to have affect on CREB |
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Drosophila Paired Training (and Dunce Fly)
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-odorant+shock
-mutated flies cannot remember pairing (what is the protein associated with the dunce?) --has mutation in cAMP phosphodiesterase (PDE) which dissociates cAMP to AMP -indicates that you can have too much or too little (since you do need cAMP in learning) |
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Rutabaga Fly
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-Another memory mutant
-cant produce cAMP in high enough levels: defect in calcium/calmodulin-dependent adenylyl cyclase (responsible for synthesis of cAMP) |
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Drosophila model showing importance of CREB
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flies lacking CREB exhibit impaired long-term retention
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Long-Term Potentiation
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(LTP)
-cellular model of learning and memory -long term changes in synaptic efficacy, evoked by experience. -most fully investigated in the hippocampus -There is associative and nonassociative types of LTP -no direct behavioral outcome from causing an LTP -due to changes in BOTH pre and postsynaptic cell |
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Associative LTP
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any type of LTP that requires an NMDAR
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Hippocampal LTP
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-long term enhancement in synaptic strength due to experience
-hippocampus required for learning new declarative things, not for bringing back old memories. |
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Hippocampus
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-around, under ear, around base of temporal cortex (one on both sides)
-main circuitry runs cross section of hippocampus, not length CIRCUITRY -perforant pathway: entorhinol cortex to dentate gyrus -Mossy Fiber Path: Dentate gyrus which stimulates pyramidal cells CA3 (not as involved in associative LTP) -Shaffer collaterol commisural path: CA3 to CA1 |
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Stimulations involved in LTP
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-need both presynaptic stimulation with postsynaptic depolarizations (when tested separately, no LTP induced)
(all synapses are glutamenergic) -weak stimuli (even tetanic stimulating ones) do not produce an LTP nor strong ones at low stimulation -Depol of postsyn most likely for removal of Mg from NMDAR (using KA/AMPA receptors) |
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Role of Ca in LTP and other influences causing synaptic strength
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PRESYN
-increases in Ca release POSTSYN -Increased Ca concentrations in LTP activates Ca dependent calmodulin kinase (protein kinase-can autophosphorylate) (--PIP2-->PLC-->DAG-->IP3-->PKC activated by Ca release-->phosphorylation of GAP-43 which potentially makes new spines/synapses, providing changes in synaptic strength.) -Silent synapse concept. |
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Silent synapse concept
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-in postsyn, only NMDAR until LTP introduced which causes AMPAR to be put in place too (some may exist prior to this to allow depol for NMDARs)
-Ca calmodulin kinase possibly phosphorylates these AMPAR (opposite for LTD) |
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Long Term Depression
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LTD
-lower frequency stimuli: opposite of LTP -still requires pre and post syn to be involved -needs all the same players as LTP (Ca/Cam Kinase, Ca, etc) -low concentrations of Ca lead to activation of phosphoprotein phosphatases, dephosphorylation of synaptic protein (unidentified) |
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What Function of NS depends on
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1. individual properties of neurons and glia
2. modulators that are present that can modify 1 3. patterns of connection of neurons that can be changed by 2 acting on 1 4. activity dependent changes in synaptic function |
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What sets up the NS (steps)
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1. determination
2. proliferation 3. migration 4. axon elongation 5. synapse formation 6. synapse rearrangement |
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developmental stages
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-in blastocis stage a single cell divides to form a sphere of cells called the blastula
-gastrulation occurs when cell invaginates to form more than one layer of cells -cells come close to one another, mesoderm contacting ectodermal layer -folding of neural plate and neural crest invaginate and form notochord and neural tube NEURAL PROGENITORS FORMED neural tube-->CNS, glia, and other support neural crest-->PNS, schwann cells |
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Tests on the animal cap
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-Animal Cap: layer of ectoderm that stretches from dorsal to ventral side of embryo-->when in a dish, always becomes epidermis
-area known as the Spemann organizer causes ectodermal tissue to develop a secondary NS -If animal cap is cultured with spemann organizer, the cells take on properties of neural tissue (so spemann organizer has neural inducers) OVERALL -ectoderm alone makes epidermis -ectoderm with mesoderm makes neural tissue -with neural inducers, makes neural tissue -dissociated ectoderm alone makes neural tissue -ectoderm with BMPs becomes epidermis |
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Neural inducers and BMPs
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-when a BMP contacts an epidermal cell, it binds to a receptor (a protein kinase) that consists of two different subunits (type I and II BMP receptor subunits)
-when bound, the receptor triggers a series of events starting with phosphorylating itself and Smad 1 -Smad 1-P binds to Smad 4 -Smad1-Smad4 complex enters the nucleus and influences transcription -causes epidermal formation activation -neural inducers bind BMPs and block their binding to receptors-->neural genes transcribed |
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Radial Glial Cells
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-form early in development
-become scaffolding for neurons to migrate on -later become bergman glial cells |
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Differentiation of the Cells in the Neural Tube
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in cell cycle:
-cells move (attached to both sides) from ventricular zone up through mantle to marginal zone (towards pial surface) -cells move back down, release from pial surface -split into two cells, then reattach to pial surface POSTMITOTIC -cells migrate away from ventricular zone to form mantle zone with processes in the marginal zone -the three layers of organization is seen in spinal chord |
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How/when are fates of neurons determined?
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-before or after birthday
-before or during migration -lineage (genetically preprogrammed) -some sort of external favors interact with tissue during development --> COULD BE ANY |
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Neural crest cells
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-migrate very early
-become sympathetic (NE) or parasympathetic (ACh), sensory neurons, and schwann cells |
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What makes a cell para vs sympathetic
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-factors that the cells run into will determine this
-in dish, all cells put in with heart organ will become cholinergic; if they dont run into factor, they will be noradrenergic -identified factors: CDF (cholinergic differentiation factor) or LIF (leukemia inhibitory facotr--same), CNTF example of influence of extrinsic factors influence neuronal fate |
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Fruit Fly eye
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-compound eye that can detect UV light
-each unit is ommatidium made up of 8 photoreceptors --7th cell is the one that senses UV light and is last cell to be determined -flies missing 7th photoreceptor: have mutation in sevenless (sev) and bride of sevenless (boss) which prevents differentiation |
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Pathway regulating 7th photoreceptor cell differentiation in fruit fly
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-integral membrane protein boss (product of boss gene) on R8 activates SevRTK (product of sev gene), a receptor tyrosine kinase
-SevRTK activates Ras-->Raf-->MEK-->MAP kinase which has several targets -MAP kinase phosphorylates the protein Yan, degrading it (it normally blocks differentiation) -MAP kinase causes other similar deegradation and activation of transcription factors that promote neuronal differentiation |
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Learning about the primary visual cortex of the cat
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-Carla Shatz used 3H-thymidine to label cells during embryonic development (more differentiation of those cells led to less and less expression of it)
-found that interior cells developed sooner than the outer cells --outer cells need to migrate through other cells (layer one is pushed up first though) -this shows the importance of neuronal birthday |
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Reeler Mouse
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-cells in cortex unable to migrate through the first developed layers (have 1, 6,5,4,3,2)
-they are deficient in Reelin which is release by first layer -stil make correct connections and survive (numerous differnt factors like this shape development) |
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Nerve Growth Factor (+exp done on it)
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NGF
-made of 3 different subunits in a dimer (so 6 total) -beta is the functional part of the dimer and acts on sympathetic neurons, snesory neurons, BFcholinergic neurons EXPERIMENT -a muscle tumor implanted in wall of embryo, caused a lot of axon/dendrite outgrowth |
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Neurotrophin Receptors
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(-neurotrophins: NGF, BDNF, NT-3, NT-4/5)
-NGF greatest affinity for TrkA-->causes two subunits of the receptor to come together (dimerization) -BDNF and NT-4/5 bind TrkB most often -NT-3 binds TrkC and sometimes TrkB -in high concentrations the neurotrophins will bind any of the receptors -Another receptor, truncated Trk will bind the neurotrophins but elicit no function (no signaling region) -Will also bind P-75 which is a LANR (low affinity neurotrophin receptor) that seems to amplify the affects of other bound receptors in the same cell |
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Signaling Pathway of neurotrophin receptors
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-both parts of the receptor have tyrosine kinases that can phosphorylte other proteins on tyrosine residue
-can phosphorylate each other ("autophosphorylate) -provide binding site for other proteins -PLCgamma has SH2 domain that binds P on kinase and gets activated-->DAG and IP3 (all membrane bound)-->Ca release -PI3 can also bind receptor, causing cascade that leads to cell survival (anti-apoptotic) |
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Signaling Pathway of NTR activating ERK
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NTR (TrkA) binds Shc which phosphorylizes it-->Grb2 binds that-->Sos causes exchange of GDP for GTP on membrane bound Ras
-Ras activates Raf which phosphorylates MEK which phosphorylates two parts of ERK (serine/threonine and tyrosine) which is also a kinase |
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neurotrophin receptor mediated endocytosis
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-binding of neurotrophins to Trk can cause endocytosis of the neurotrophins and receptors
-the endocytosed material can then be transported back to the cell body and cause gene transcription |
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Sources of trophic factors
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-glial cells
-muscle cells -astrocytes -other neurons |
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Ciliary Neurotrophic Factor
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-CNTF
-improve survival of embryonic motor neurons -present in myelinating schwann cells -CNTF receptor is a trimer--actual receptor portion (CNTF-R alpha) does not span membrane while other two (gp130 and LIFR beta) do, they are JAK kinases, tyrosine kinases |
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How do axons grow
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-in more rare cases, some cells leave behind an axon as it migrates
-most data suggests that axons have predetermined extension destinations (somewhat) -formation of the growth cone |
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Growth cone
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-guides the outgrowth of neurites
-microtubules provide structural support and tracks (central core) -vesicles supply proteins (central core) -outer part of the central core is devoid of those things but has a lot of actin for mechanical movement -filopodia (has bundled actin) extend out of lamellipodia (has cross linked actin) -actin needs to attach to a surface as it is made -polymerization mostly responsible for the outgrowth |
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movement of growth cone
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-continual cycle of polymerization and depolymerization of actin
-at the tip of the growth cone, actin is continually assembled and is disassembled at the back end -speed of outgrowth depends on how well the cone adheres to the substrate --physical coupling of F-actin cytoskeleton and substrate--many molecules serve as a physical link |
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Substrate Adhesion Molecules
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-the basement membrane containing fibronectin and laminin which promote cell binding through integrins
-integrins are in the plasma membrane of neurons |
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integrin receptors/laminin
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-integrins are in the plasma membrane of neurons
-bind fibronectin and laminin -exist as dimer -integrin binds actin/cytoskeleton and can signal in backwards or forward direction -laminin is a trimer with a number of binding sites |
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Neural Cell Adhesion Molecule
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NCAMs
-can bind fibronectin -allows physical binding of two cells -bind to other CAMs |
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Attractive and Repulsive Forces in Axon outgrowth
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-guidance molecules affect direction of movement of growth cones
-Types: 1. chemorepulsion/attraction 2. contact-dependent attraction/repulsion |
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Sensory Neurons in Grasshoppers
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-a neuron sends its axon twds the CNS
-G-sema1 on the surface of these cells diverts the outgrowth -axons continues diversion until it contact the processes of another neuron that provides and attractive substrate for the axon to cross |
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Sema 3A
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guides formation of dendrites in opposite direction as axon
-has highest concentration at pial surface -moves according to a gradient |
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Netrins
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-guide axons of neurons to the spinal cord (floor plate)
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Affect on axon growth by NT
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some cell axons grow until in the presence of serotonin while others are unaffected
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Synapse Formation
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-when an axon reaches an appropriate synaptic target a signal must stop that axons from growing further
-target selection: usually independent of firing |
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AMPHIBIAN RETINAL SYSTEM
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LEARN
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