Today I read this article about the usage of bound morphemes and their role in helping children who are learning language to correctly identify parts of speech and the relationship between words. The goal of the study was to show that language learners may learn just as much from the affixes of words than their stems when learning a language and trying to figure out how words work together to compose sentences.
Experiment 1 consisted of database analysis of previously collected child utterances and analysed how these utterances displayed the understanding of a word, or its usage in a sentence only by identifying its affixes. This was paired with a control to show how the differences between correctly identified words based on affixes would matched if such groupings were randomly assigned.
Even though the statistics of experiment 1 showed that the part of speech which was correctly identified by its affix most often were nouns, the first grouping of affixes which are considered to be most important by the researcher were related to nouns.
"the following morphological affixes (in parentheses is the class that they
most often predicted, N = Noun; V = Verb ; O = Other). The cues are in decreasing order of importance: -ing (V), -ed (V), -y (O), -er (N), -or (N), -(o)ry (N), -ite (N), -id (V), -ant (N), e- (N), -ite (O), -ate (N), un- (N), -ble (O), -ive (O), an- (N), pre- (N), out- (N), -s (unvoiced; N), bi- (N), -ine (N)." ( 193)
The first five, also the most important to identifying the part of speech, are verb related: -ing (V), -ed (V), -y (O), -er (N), -or (N). Even the affixes which are not directly used to identify verbs are used to distinguish verbs from other parts of speech and thus they do refer to them. -y is common to adjectives even if they cannot be made from verbs so there seems to be multiple factors which contribute to -y being associated with this specific part of speech. In any case there are verbs which fit into each of these affixes as different parts of speech (dust (V): dusting(V), dusted(V), dusty (adj), duster(n). One question I have about this is how some of these adjective forms which include -y but do not appear in verb form, noun form, or appear in neither form got to be? Do their etymologies reveal this? I can be "lazing on a sunday afternoon", but was there ever a time when this would have made me a "lazer"? Likewise why can't we describe an actor, who acts, as "acty"?
The second part of the study looked at the idea that experiment 1 assumed that children at this stage are able to separate words into Stem + Affix and thus are able to identify the Affix. The identification of the affix is key to understanding the results of the experiment 1. A different study in 2001 with 18-21 MO children demonstrated that children were able to identify the correct usage of affixes in speakers even if they could not use these affixes themselves, which demonstrates a degree of understanding of the affixes. The study goes on to suggest that this may come from a language learning mechanism in the brain which is biased toward the beginnings and endings of words.
This phenomena of affixes is common in almost every language world wide. This is something I can tie in with the behavioral/economic psychology that Kahneman talked about in "Thinking". The cognitive process that he identified as "System 1" reads, or presents certain parts of or experienced more biased than others. One story that he told in a TED talk involves someone who's experience listening to a symphony was effectively ruined by the very ending of the recording which was damaged. Kahneman goes on to explain that it was not the experience, but the memory of the experience which was ruined by the "end-bias". Is it possible that a similar cognitive process is happening here, where the memory of the language experience is biased toward the end and beginning of the word. The only difference is that the frame has shifted from a long attention draining symphony to an incredibly short moment. The only difference is the size of the diet of experience.
Experiment 2 looked at how the same tool may function on the phoneme level instead of the morpheme level. This is another device used the researcher to remove any assumptions about the language learner's understanding of the Stem + Affix structure of the given language. The researchers essentially wanted to look at whether the same cognitive device can describe a phonological process instead of a morphological one. The result was that 66% of nouns were identified correctly verses a baseline of 34% (80% were identified correctly in the morpheme-centric experiment 1), 56% of verbs were identified against a baseline of 32% (54% were identified in experiment 1), and 47% of other words were identified verses baseline of 33% (about 30% were identified in experiment 1). The difference between this word-edge phoneme study and the morpheme study was negligible. How much of this comes from the fact that many of the affix morphemes also stand alone as phonemes? (-ing, -s, -ed (-/d/), -ch or -tch). It is important to identify that it can be difficult to find the causation here. Are morpheme-affixes tools for language learners because they also often break down along the same lines as phonemes? Or were speakers of the language more likely to add the phonemes as morphemes because of the ease that this shared trait brings? (I'm not sure these are the right questions which reflect this idea, but surely it is not clear why one influences the other and which one influences which.)
The third experiments tested the use of word-edges to identify unknown words which lacked a syntactic context. The idea here is that the only tool is the word endings where as the other experiments assumed or at least left unclear the role of the stem. This experiment specifically tries to avoid stems which may be easily identified on their own, looking only at the role that the affixes play in the identification process. The study looked at three groups. All groups were trained on 500 word types and tested on 4,230 words. This method worked best to identify verbs overall.
Showing posts with label cognitive science. Show all posts
Showing posts with label cognitive science. Show all posts
Sunday, February 12, 2012
Saturday, February 11, 2012
Principles of Neuroscience
Lecture 2:
Primarily focused on what happens on the cellular level (this lesson is a summary of the cellular mechanisms which lie underneath)
CogSci focuses more on the higher level of the “systems” level (language, thought etc) , this lesson is a background of the systems level
The Neuron-Soma (the cell body, maintains the metabolic functions of the cell, the bulbous end of a neuron cell, can be considered the cell body )The Nucleus is contained within the Soma.
Neurons have processes (bodies which extend from the soma): the sending process or axon (how information flows from the soma to other neuron cells, the dendrites (the receptors or receive branch of the neuron cell), the dendrites then have spines or knobs which contain receptors, the synapse is the gap between any pair of neurons, neurons are linked by these physical extensions from the soma called processes, they link in such a way that they are not connected but leave a small gap called a synapse.
Information is transferred between neurons when a nucleus changes its electrical properties in some way. This electrical change causes some kind of chemical release into the synapse space between the dendrites of two neurons this process is then repeated in the dendrites of the receiving neuron, thus transferring information to the second neuron cell.
The physiological changes that allow for communication in neurons: a cell has a membrane, this prevents the flow of some ions (either from inside to outside of the cell membrane or across the membrane, the main point is that it is regulated), in the resting potential or electrical difference between the outside with respect to the inside of the cell is -70 milivolts (a very small amount of electrical energy, or change across the membrane) it is negative because of the trapped or captured positively charged ions (Na in the example Ivry gives) against the membrane of the cell.
During Neural transmission there are gradual changes in the membrane physiology, as different receptor events take place (it could get “excited” meaning that the negative charge across the ion is increased, or inhibitory processes or hyperpolarized) As these changes accumulate something called an action potential happens, this is where the changes in the membrane are so great that the charge is reversed to +50 millivolts and channels in the membrane are opened up which allow for Na to enter . This triggers the release of neurotransmitters. The Action Potential is generated right along the top of the axon non the dendrite.
De-Polarization, reaches threshold, channels open, physiological processes push the sodium back out, release electrical pulse towards the dendrites and the process is resolved and the cell membrane repolarizes.
Synaptic Transmission is the result of an Action Potential. When there is an action potential there are terminal points of the axon controlled by calcium (which is another ion, ions like to bond to other ions which makes these “bonding events” which change the chemistry of the neuron cell more likely) , these calcium channels open up at the Axon terminal. This causes transmitters to bind to the membrane of the axon either pre synaptic or post synaptic they are able to release transmitters into the synapse.
A presynaptic event takes place as part of the axon process or the process of the sending neuron cell
A post synaptic event takes place as part of the dendrite process or the process of the receiving cell
Little vesicles at the end of the axon, which contain neuron transmitters, allow these transmitters to be sent across the synapse to receptors on the dendrite by way of calcium channels formed by ions bound to the membrane.
This is actually two processes. The axon passively empties its neurotransmitters into the synapse because of the calcium bond pathway. In a separate event the Dendrite will have receptors for that specific neurotransmitter which allow the
neurotransmitter to bond with the dendrite as it is transferred out of the synapse.
This will then change a cause in the permeability of the membrane post synoptically (on the dendrite of the receiving neuron) This can be either a depolarization (excitatory, increase in membrane potential) or hyper polarization (inhibitory, decrease in membrane potential), this is very local process which happens only the dendrites but it can accumulate to the membrane of the entire receiving cell and the process starts over.
Neurotransmitters are specific chemicals contained in the vesicles of the cells which are able to travel over the synapse between two different cells. There are over 100 types of neurotransmitters and more are added every year. Scientists debate what the difference between a hormone and neurotransmitter are in some cases they are able to resemble each other. Ex: dopamine, serotonin, glutamine, epinephrine.
The receptors of dendrites have very specific “affinities” for neurotransmitters. Specific neurons are sensitive to receive specific neurotransmitters and send specific neurotransmitters. Generally cells are only able to transmit a single type of neurotransmitters but their receptors may be able to receive more than one type of neurotransmitter.
Because of this difference in affinities and the physical structure of the neuron cell it is possible that the locality of the production and distribution of certain neurotransmitters/chemicals differ. Dopamine for example is produced in one part of the brain. The central and stem structures contain most of the neurons which produce dopamine, but the axons of the cells may extend and as a result there are many cells throughout the brain which are able to receive dopamine. The same is true of serotonin. The central structures of the brain produce the chemical, but it is distributed throughout the brain.
Other cells in the brain: blood vessels, the glial cells (metabolic functions, repair, maintenance of the neuron cells in many ways, these are the cells the ensure that the “society” of neuron cells overall is functioning, they are charged with “cleaning up” the dead neuron cells) glial cells may improve the conduction of signals, this may be because there are two different types of glial cells which form a myelin, a covering or sheath of fatty tissue around the axon which speeds the transmitter. It does this by essentially being a membrane which conducts electricity better than the axon.
Another set of glial cells are called astrocytes which from the blood-brain barrier. Glial cells prevent the blood system from directly coming in contact with neurons. Astrocytes do this by allowing oxygen to pass from the blood over their cell bodies to the neuron cells.
There is an interesting field of research that studies the specifics in the relationship between the roles of the astrocyte and the neuron. Astrocytes and Neurons reacted similarly to outside stimuli and scientists therefore wonder if the astrocyte plays are role in the transfer of neurotransmitters that is greater than previously thought. Does this come from the fact that increased activity in the neurons as a result of outside stimuli simply means that the neurons then require more oxygen thus activating the astrocytes to play this intermediary role between the neurons and the blood cells? Other studies have selectively shut down the astrocytes because of differences between the chemical properties of the two cells. The paper written about this showed that this increased the neuron activity. Glial cells may modulate the sensitivity of the cells they are associated with. These cells regulate the activity of the neuron cell in some way.
Neurons cannot fire indefinitely, when the release neurotransmitters they must enter a refractory “recovery” period before they fire again.
There are probably 11 billion neurons in the cerebral cortex (twice as much if you include the sub-cerebral cortex and older parts of the brain). How do all of these small processes which happen at a sub-atomic level in the synapse control a complicated process like cognition? There are many types of size and shape of neurons. All neurons are very different. Some axons can be three feet long. Some have large dendritic arbors but few axons. Neurons are not more densely packed in humans than other mammals, we have more neurons only be virtue of the size of the human brain.
Interconnectivity is an important part of the process. There is more than a one to one connection. Massive dendritic arbors have many axons connecting them. Some neurons have 5,000 synapses. Each neuron is therefore only a few synapses away. Because of the intense interconnectivity between dendrites and axons information can travel to any part of the brain very quickly. Each neuron only contributes a tiny part to this process. Large cognitive events only take place because of massive numbers of neurons acting at the same time.
Parallelism- Many to Many communication between neurons. Any single neuron influences many neurons and is influenced by many many neurons. Parallelism at the system level: inputs at any part of the brain travels in a parallel way throughout the brain simultaneously because the neuron architecture, not from one region to another, more like to all regions all the time. Not a serial chain
Plasticity- there is some sort of change in the neuron. Learning is a structural change in the neuron. Development constantly reshapes the structure of the neurons. The receptors/neuron structures/ change the physical shape of the nervous system all the time, this allows for changes in the relationship between different parts of the brain. This can be talked about in terms of hardware (more dendrites, neurons, axons) or software (neurotransmitters, chemicals, receptors) the line between them is not clear at times because the receptors are physical part of the brain which corresponds directly to a specific “software” chemical in the form of a neurotransmitter.
(Optical neurons on infant and adult felines) Infant has more dendrites than the adult, but the adult dendrites are larger. Vision may require the pruning of many dendrites in order to develop more fully certain specific ones.
Primarily focused on what happens on the cellular level (this lesson is a summary of the cellular mechanisms which lie underneath)
CogSci focuses more on the higher level of the “systems” level (language, thought etc) , this lesson is a background of the systems level
The Neuron-Soma (the cell body, maintains the metabolic functions of the cell, the bulbous end of a neuron cell, can be considered the cell body )The Nucleus is contained within the Soma.
Neurons have processes (bodies which extend from the soma): the sending process or axon (how information flows from the soma to other neuron cells, the dendrites (the receptors or receive branch of the neuron cell), the dendrites then have spines or knobs which contain receptors, the synapse is the gap between any pair of neurons, neurons are linked by these physical extensions from the soma called processes, they link in such a way that they are not connected but leave a small gap called a synapse.
Information is transferred between neurons when a nucleus changes its electrical properties in some way. This electrical change causes some kind of chemical release into the synapse space between the dendrites of two neurons this process is then repeated in the dendrites of the receiving neuron, thus transferring information to the second neuron cell.
The physiological changes that allow for communication in neurons: a cell has a membrane, this prevents the flow of some ions (either from inside to outside of the cell membrane or across the membrane, the main point is that it is regulated), in the resting potential or electrical difference between the outside with respect to the inside of the cell is -70 milivolts (a very small amount of electrical energy, or change across the membrane) it is negative because of the trapped or captured positively charged ions (Na in the example Ivry gives) against the membrane of the cell.
During Neural transmission there are gradual changes in the membrane physiology, as different receptor events take place (it could get “excited” meaning that the negative charge across the ion is increased, or inhibitory processes or hyperpolarized) As these changes accumulate something called an action potential happens, this is where the changes in the membrane are so great that the charge is reversed to +50 millivolts and channels in the membrane are opened up which allow for Na to enter . This triggers the release of neurotransmitters. The Action Potential is generated right along the top of the axon non the dendrite.
De-Polarization, reaches threshold, channels open, physiological processes push the sodium back out, release electrical pulse towards the dendrites and the process is resolved and the cell membrane repolarizes.
Synaptic Transmission is the result of an Action Potential. When there is an action potential there are terminal points of the axon controlled by calcium (which is another ion, ions like to bond to other ions which makes these “bonding events” which change the chemistry of the neuron cell more likely) , these calcium channels open up at the Axon terminal. This causes transmitters to bind to the membrane of the axon either pre synaptic or post synaptic they are able to release transmitters into the synapse.
A presynaptic event takes place as part of the axon process or the process of the sending neuron cell
A post synaptic event takes place as part of the dendrite process or the process of the receiving cell
Little vesicles at the end of the axon, which contain neuron transmitters, allow these transmitters to be sent across the synapse to receptors on the dendrite by way of calcium channels formed by ions bound to the membrane.
This is actually two processes. The axon passively empties its neurotransmitters into the synapse because of the calcium bond pathway. In a separate event the Dendrite will have receptors for that specific neurotransmitter which allow the
neurotransmitter to bond with the dendrite as it is transferred out of the synapse.
This will then change a cause in the permeability of the membrane post synoptically (on the dendrite of the receiving neuron) This can be either a depolarization (excitatory, increase in membrane potential) or hyper polarization (inhibitory, decrease in membrane potential), this is very local process which happens only the dendrites but it can accumulate to the membrane of the entire receiving cell and the process starts over.
Neurotransmitters are specific chemicals contained in the vesicles of the cells which are able to travel over the synapse between two different cells. There are over 100 types of neurotransmitters and more are added every year. Scientists debate what the difference between a hormone and neurotransmitter are in some cases they are able to resemble each other. Ex: dopamine, serotonin, glutamine, epinephrine.
The receptors of dendrites have very specific “affinities” for neurotransmitters. Specific neurons are sensitive to receive specific neurotransmitters and send specific neurotransmitters. Generally cells are only able to transmit a single type of neurotransmitters but their receptors may be able to receive more than one type of neurotransmitter.
Because of this difference in affinities and the physical structure of the neuron cell it is possible that the locality of the production and distribution of certain neurotransmitters/chemicals differ. Dopamine for example is produced in one part of the brain. The central and stem structures contain most of the neurons which produce dopamine, but the axons of the cells may extend and as a result there are many cells throughout the brain which are able to receive dopamine. The same is true of serotonin. The central structures of the brain produce the chemical, but it is distributed throughout the brain.
Other cells in the brain: blood vessels, the glial cells (metabolic functions, repair, maintenance of the neuron cells in many ways, these are the cells the ensure that the “society” of neuron cells overall is functioning, they are charged with “cleaning up” the dead neuron cells) glial cells may improve the conduction of signals, this may be because there are two different types of glial cells which form a myelin, a covering or sheath of fatty tissue around the axon which speeds the transmitter. It does this by essentially being a membrane which conducts electricity better than the axon.
Another set of glial cells are called astrocytes which from the blood-brain barrier. Glial cells prevent the blood system from directly coming in contact with neurons. Astrocytes do this by allowing oxygen to pass from the blood over their cell bodies to the neuron cells.
There is an interesting field of research that studies the specifics in the relationship between the roles of the astrocyte and the neuron. Astrocytes and Neurons reacted similarly to outside stimuli and scientists therefore wonder if the astrocyte plays are role in the transfer of neurotransmitters that is greater than previously thought. Does this come from the fact that increased activity in the neurons as a result of outside stimuli simply means that the neurons then require more oxygen thus activating the astrocytes to play this intermediary role between the neurons and the blood cells? Other studies have selectively shut down the astrocytes because of differences between the chemical properties of the two cells. The paper written about this showed that this increased the neuron activity. Glial cells may modulate the sensitivity of the cells they are associated with. These cells regulate the activity of the neuron cell in some way.
Neurons cannot fire indefinitely, when the release neurotransmitters they must enter a refractory “recovery” period before they fire again.
There are probably 11 billion neurons in the cerebral cortex (twice as much if you include the sub-cerebral cortex and older parts of the brain). How do all of these small processes which happen at a sub-atomic level in the synapse control a complicated process like cognition? There are many types of size and shape of neurons. All neurons are very different. Some axons can be three feet long. Some have large dendritic arbors but few axons. Neurons are not more densely packed in humans than other mammals, we have more neurons only be virtue of the size of the human brain.
Interconnectivity is an important part of the process. There is more than a one to one connection. Massive dendritic arbors have many axons connecting them. Some neurons have 5,000 synapses. Each neuron is therefore only a few synapses away. Because of the intense interconnectivity between dendrites and axons information can travel to any part of the brain very quickly. Each neuron only contributes a tiny part to this process. Large cognitive events only take place because of massive numbers of neurons acting at the same time.
Parallelism- Many to Many communication between neurons. Any single neuron influences many neurons and is influenced by many many neurons. Parallelism at the system level: inputs at any part of the brain travels in a parallel way throughout the brain simultaneously because the neuron architecture, not from one region to another, more like to all regions all the time. Not a serial chain
Plasticity- there is some sort of change in the neuron. Learning is a structural change in the neuron. Development constantly reshapes the structure of the neurons. The receptors/neuron structures/ change the physical shape of the nervous system all the time, this allows for changes in the relationship between different parts of the brain. This can be talked about in terms of hardware (more dendrites, neurons, axons) or software (neurotransmitters, chemicals, receptors) the line between them is not clear at times because the receptors are physical part of the brain which corresponds directly to a specific “software” chemical in the form of a neurotransmitter.
(Optical neurons on infant and adult felines) Infant has more dendrites than the adult, but the adult dendrites are larger. Vision may require the pruning of many dendrites in order to develop more fully certain specific ones.
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