Cellular Basis of Behavior
Selfish and altruistic patters of gene dispersal are seen in step-parenting. If If the toad has the “prey” stimuli disappear. It still attacks the spot it would have been in and then licks its lips. It does this the 1st time it sees the stimuli (if raised in a laboratory), therefore, it’s instinctive. Crickets have an either/or mechanism. When one side audio fires, (thestimulant gets past the high and low pand pass filter) it suppresses ipsa lateral and fires contralateral legs. Thus it approaches in a zig zag. Small squares cause toad orientation, rectangles too (of many differing dimensions. The bat, uses a higher frequency to which it hears best to avoid the emmiting interferring with reception. The FM component of bat waves are short and good for distance the CF are long and find locatation. The ratio of these vary with terrain demands. Superior colliculus nuerons fire especially when moth wing frequencies stimulate the CF frequencies, via the doppler effect. The FM reacts to minute discontinuites in distance (via placing speakers apart) thus may be like for texture.
Bats primary passion is eating prey. An ordered sequence of behaviors, one probabalistically likely to lead to the next is called a markov chain.
Measure cycles = internal (peak) of hindwing to peak of forewing)
cycle period (of hindwing)
Collect data on hundreds to see if they’re statistically significant. Sensory-motory periferal nervous system nerves are largely one (undifferentiated) in most invertibrates. In vertibrates and invertibrates investigated have central neuronal oscillators. This , thus, arrived early in evolution. But it seems to be a coupled (ie many, one for each set of nerves) oscillator, not just one master one. If you cut leeches into smaller and smaller pieces, they all swim. It appears via studies on leeches’ hearts, that intraneurons, (not motor neurons) do endogenous oscillating. Ganglion Neuromimes are computer simulation neurons. Oscillators can be derived in evolution from one function to to another. Thus a fast wing oscillators may have evolved from a fast walking oscillator. And the differenct oscillators interact with eachother to produce complex behaviors. Headless cockroaches and cats severed at the brainstem below the cerebellum walk fine, gallop fine. Increased pressure on the bottom of the foot causes the foot to go higher. This doesn’t require higher level input. deafferated locusts still fly, but at 1/2 the rate of speed. But artificial stimulation of sensory receptors increased the speed to normal. Thus afferant nerves modify the central oscillator (this is in interneurons in locusts too. But mechanical manipulation of one locust wing affects the others also. So the combination of the two feedback systems create the central oscillating systems. Locusts have 2 sets of eyes and hairs that lead to deviation detecting neurons (DDNs). These are interneurons that only sespond to changes in one direction each. The thoracic interneurons (TIN) are phase cycled. They only go in phases when ‘n’ sync with wing flapping, therefore, 50% when deafferated (?). This LGI command firing is followed by inhibition to ensure the entire sequence happens. This also keeps an unintended firing by water currents on abdomen hairs during escape behavior.
When restrained the crayfish doesn’t do the tailflip as often. It goes from reflexive to more “volitional” in action. The response is also inhibited when eating. The threshhold of disturbance needed for activation was raised. Repeated abdomen type lessen the likelyhood for hours (learning) afferent interneurons do this. Evolutionarily it might have been to stop there being too many energy costly flips.
Hippocampal damage in rats hurt their spacial, but not cued learning. THey can go to a visible platform and know it is safety, but not a hidden platform previously found. Place cells take a while to establish, but are stable once done. They are facilitated by visual cues, but maintain relations when the cues are taken away. In rats, place cells can represent more than one place. Hippocampal damage hurts spacial memory. But lessions that happen long after learning have less effects. Probably because its just an encoding locale. Establish a place cell in the light take the rat out, put it back in the dark to establish a new place cell. THen turn on the lights! The second place cell maintains dominance. Teach rates a maze on space cues. Without cues, it uses the same place cells. But if it doesn’t get the maze right we see the wrong place cells. We can see the rats spacial thinking. Maps are made where a place cell represents one area in one situation and another in another. They don’t interfere with eachother. I’d then think they are pawns in deeper processing. In sleep they replay the place cells learned while awake. This may be consolidation. There are also head direction cells. They don’t care where the rat is just the head’s direction. Postsubcicular cells (PSC) fire when the rat is currently looking at something. Anterodorsal (ADN) cells fire when the rat will be looking at something in the near future. LTP in the CA1 region of the hippocampus requires 1-Cooperativity: several afferent fibers must fire together 2 - associativity: weak inputs arriving at the postsynaptic cell normally couldn’t induce LTP, But if they happen at the same time as stronger ones, they achieve LTP. 3 - Specificity: It can be restricted to specific pathways in the hippocampus or inputs and the hippocampus. The predominant excitory neurotransmitter in the brain is glutamate. One type of glutamate receptor is activated by N- methyl D-Aspertate (NMDA). To depolarize a cell makes it more positively charged inside. The extra charge pushes the Mg ++ ion out of the channel (likes repel). The NMDA receptor only when it binds glutamate. Thus, the NMDA receptor is described as being “doubly gated.” by both voltage and transmitter; it is only open when glutamate binds to the receptor AND the neuron is depolarized. other non-NMDA receptors can also dislodge the Mg++ ion COPY 377-380Glutamate binding to non-NMDA receptors induce depolarization primarily through the influx of Na+ions into the ost synaptic cells. But NMDA allow Na+ and Ca++ is required for the induction of LTP. Also copy pg 400 The import of Ca++ also being necessary is that this only happening on specific parts of dendrites called “dendritic spines” accounts for specificity. Why is Ca++ important? This isn’t fully understood, but it induces secondary messenger systems, especially / Calmodulin kinase (CaMkII) and protein kinase. There is early LEP and late LTP. ELTP doesn’t require CAMP or protein synthesis (1-3 hours). ELTP depends critically on CAMP signalling cascade in pyramidal cells & the synthesis of new proteins. LTP also happens in other regions of the brain. Older rats have diminished LTP ease. When “knockout mice” mice with a specific thing not encoded ((in this case no genes for tyrosine kinase) which is involved in a signalling cascade implicated in the induction and maintenence of LTP)) they needreally strong input for LTP. Some for knowckouts lackingCaMKII and they had less place cells that were less precise and stable. Knockouts without in NMDA had severe deficits in LTP and place cells weren’t correlated. But they did okay on cued tests.
Songs of birds reveal species and individual identity, where one was born and raised, where he is currently, if he owns territory or is just passing through , willingness to breed and potential as a provider. There are accents. Young birds do rambling sounds. This is called “subspeech”. This is followed by the “plastic” stageand the “crystalized stage” in non-open-ended , age limited learners. These phrases are after the listening phase in which they hear, but don’t try. The length of the listening (sensory) phase is flexible. There is much now in a birds song, but this is paired down before crystalization. And some have incredible memories. Birds learn the song of birds they see (over recorded or seen, but not heardfathers). They even do different species songs of seen birds over their own species songs taped (sometimes). But generally one has preference for its own species song. If they’ve never heard a song, they react much more to the playing of conspecific thean non-conspecific song. Birds can onyl accessthe memory of their songs by hearing them sung. Testosterone can make female canaries sing. There is lateralization, but reversed after lesioning sizes of brainpart grow alot during singing season. Sizes of brain parts grow alot during singing seasons. This happens to females who get testosterone too. Repetoire is correlated with size and there is neurogenesis (the birth of new neurons). Tis is nearly all in the vocal area and greater for young, learning males than older males or females. In sparrows this gain is greatest when establishing memories of future songs. Simulation in an production portion of the brain makes the finch skip to the next part of the song. Deaf birds also skip forward. Celss havebeen found that only respond to the finches own singing. THis has a path to production as doesthe learning center. So the bird can hear and compare to a prelearned template.One canary song precedes copulation. It causes the female to stick her chest out raise her tail and lift her wings and shake them. THis only happens to the conspecific song unless lesions happen. Therefore, the area of song in the female that corresponds to the males helps in song discrimination and recognition. THis is an elegant solution to optomize the conservation of neuronal real estate by evolution. Isolated birds sing some of their species song: So its partly innate.
Worker bees are females. Males are ony drones and don’t do anything else. Nectar is carbohydrate and pollen is protein. Bee trips are usually 2 - 2.5 miles The go circituously and return. Foraging bees scout recruits learn the dance and follow the beaten path. THe “waggle dance” is also done when foragers try to find a good hive locale for a new colony. THe swarm watches many wwaggle dances and then “decides”. Bees associate reward with color with color distinction, after 3 trials their memory lasts a long time. THis is after poor memory in the 2nd and 3rd minute after learning. THey learn during approach. They learn many characteristics ofa flower together. If one is altered they must relearn all. Sucrose causes hungry bees to do the probiscus extend reflex (PER). A single pairing with an odor trains the PER. An odor that has been paired with no sucrose is inhibited for pairing purposes later. We can study neural components of PER because bee and other insects are separated into specialized sections. Studies involved cooling brain nodes with cold needles. This is reversible. Bee brain neurons are small. But a single neuron that is necessary for pairing has beenfound. It can be paired with the CS. The cell that indicates reward has been identified (US in PER). If the reward comes after it works, not if the reward comes after. THis is with real sucrose and neuron stimulation. Associative learning is done by OCTAPAMINE. This neurotransmitter is realized to the neuron by several sense pathways.
Aplysia is a type of mullosc. IT has big neurons and does associative learning. Habitation is like extinction. Dishabitation is like relearning a previously sensitized stimulus. They learned a response to a shock for four days, like the bee, they learn quickly (1 pairing) has effect and CS must precede the US for learningAs with humans, distributed learning is more effective than massed training for long term learning. There is a neuron that connects the sensory and motor ganglia in automatic sensitization. Presynaptic release of seratonin from sensory nerves cause greater EPSP. The seratonin apparently stops the release of potassium and therby maintains the action potential. The cAMP and Kinase protein having the regulatory subunit broken off from the catalytic subunit is the same as in humans. There are also other non-sensory neurons invoved and intra neurons involved. Here they lay back huge exactly at conditioned learning. Apparently the action of the sensory nerves stimulates the motor neurons. When paired the firing is stronger (more millivolts). This research also points to a change in presynaptic otential. The paired sensory nerve is weaker with a smaller Calcium Potassium swap. Perhaps this leads to the same level of presynaptic sensory charge dropping more seratonin and therefore creating a bigger reaction in the post synaptic motor neuron. Indeed seratonin can cause the motor reflex and repeated seratonin application creates short term sensitization. Long term sensitization, however, can can be achievedwithout seratonin. The seratonin, therefore, apparently causes protein synesis and in many synapses. Transcription blockers show that though the seratonin is necessary, it isn’t sufficient. The accompanying protein synthesis is required for short and long term behavioral memory facilitation. This protein synthesis creates more axonal process and synaptic endings and sit as of transmitter release. Another found these sites decrease (in both they modified the number). cAMP is implicated in the molecular basis of this. It also reduces the potassium current in the sensory cell discussed before. cAMP activates the catalytic part of the PKA which is in the nuceus of the sensory neuron. Copy 18, pg 520. This part of PKA induces cAMP responsive elements (CREB) to bind to cAMP response element bonding protein (CREB). This causes immediate transcripter genes to turn on.
Fruit flies are drosohila. THey live a weak (but temperature speeds the birth - adult scycle speed). Benzer’s research technique is to breed an inbred uniform strain, then use a chemical that causes DNA mutation. Most die, but often there is a single gene mutation of the drosphilas 5000 genes. Genes have been found that alter courtship, circadian rhythmvisual function, neural development, learning and memory. Drosophila were conditioned via shock and odor. In some locales the odor had no shock. Thus place in learning were separate and extinction was also learned. Some cannot learn and others learn but forget soon. It isn’t just instinct messed up, cause their learning was impaired in many situations. The flies have memories like other species, more training increases learning to a point; Where it gets it or doesn’t. Also they have short term and long term memory. THere are 4 basic mutant types studied in learning defects. All are short on cAMPThe same chemicals used in human memory. This mechanism must have involved early. And like a pea creates a big snowball, its use was built upon. Due to smallness it is so hard to isolate neurons. One mutant has 20 times the normal potassium voltage and stops reflex reaction (acclimation to the stimulus takes place quickly) others do it slowly (and they have reduced cAMP synthesis (as opposed to the first which acclimated). There is a “mushroom body” in the fly brain (as was in the bee). It is a coincidence detector. A technique called detection enhancer allows us to see where genes express themselves. Mutant genes are expressed in the mushroom body. In drosophila it appears there is a different switch for spaced and massed learning. Protein synthesis isn’t required for short term memory. Long term memory is CREB involved. Heightening it can decrease memory time.
Ocular neurons exist in a rudimentary way prenatally in many animals. Afterbirth they grow and the dyes compete for dominance in two stages. This competition was studied by transplanting a 3rd eye into a frog head near where the normal ones go.