ZeePedia

Higher Order Brain Functions:Principle of Mass Action, Long-term memory

<< Higher Order Brain functions:Aphasia and Dyslexia, Aphasias related to speech
Higher Order Brain Functions:Brain correlates, Handedness, Frontal lobe >>
img
Neurological Basis of Behavior (PSY - 610)
VU
Lesson44
Higher Order Brain Functions
Objectives:
The students would be familiarized with the role of higher order brain functioning in learning, memory
and amnesias.
Brain correlates:
·  Brain correlates of Learning and Memory, Amnesia, Verbal, Non verbal memory,
·  Famous case of Amnesia, H.M.
Memory is one of the puzzles where biologist, physiologists, neurologists started working early on
Krech (1973) spent a lifetime investigating memory believes that memory is one of the most intriguing
phenomenon. There are many hypotheses and there are many frustrations for those working in this field.
Lashley was pioneer in the area of locating engrams- basically he was a zoologist trying to locate where
memories are " I sometimes feel, in reviewing the evidence on the localization of the memory trace, that
the necessary conclusion is that learning is just not possible. (Lashley 1950)
Memory is defined as information stored in the brain because of sensory and other experience
(Bridgeman 1992, p324) and learning is the acquisition of new memories. However, where exactly is
happening and how? Is there a specific location or diffuse connection and locations?
Lashley formulated two principles: the Principle of Equipotentiality and Principle of Mass Action
Principle of Equipotentiality:
Lashley trained rats to run the maze. The animals learned to discriminate between the light and dark
alleys. They were rewarded for light alleys and punished forgoing into the dark alleys. Lesioning
various parts of the brain, he found that disruption of learning took place after lesions of the visual
cortex. He reported that for retention of visual tasks Visual cortex important. Various parts of cortex
contribute to memory at least for complex behaviors. No one part is more or less specialized than other"
Neurons within a given sensory area is capable of participating in memory formation- all are
equipotential in contributing to the retention of a task. Memories are also discretely located within each
sensory cortex (though diffusely spread in that area) There are also memories for the specialized sensory
function.
Principle of Mass Action:
Lashley's rats were trained on complex tasks utilizing information from various sensory modalities,
requiring visual cues, somato-sensory cues, kinesthetic and even auditory cues. This involves mass
action. Thus, information from all cortical areas is integrated to form complete memories. After the
learning had taken place Lashley lesioned parts of the cortex and found that the greater the extent of the
lesion, the greater the deficits in memory. Retention is related to the size of the cortical areas removed.
Thus, it appeared that cortical area is not important only the extent of damage. Therefore, cortex works
as a whole, the more cortex involved in learning the better it is. The same principle holds for man and
for rats. As an example, soldiers with head bullet wounds exhibited lower IQ on tests performance, and
the lowering of I.Q depended upon the overall amount of brain damage. The amount of remaining
cortex is more important than the region states Grafman and his colleagues 1986)
There are many more questions to memory. It is intriguing to how we learn, forget, how we remember
friends, their faces, spellings of names or generally, telephone numbers etc. The question is also why
older people remember events long past better than immediate past, where are our memories located?
172
img
Neurological Basis of Behavior (PSY - 610)
VU
There are many such questions.
·
Why do different areas store different part of the memory picture, how does it get integrated. One
piece missing how the defect is covered, or compensated.
In the 1950's two different memory storage systems, the Short Term Memory (STM) and the Long
Term Memory (LTM) were hypothesized. Memories are retained in the STM(stored temporarily) when
the physiological changes to store in the long term memory are taking place, the STM memories are
transferred to LTM.
Short-term memory
repeated thinking and reviewing
Long-term memory
Hebb one of the pioneers of neurosciences and of memory research stated that memories remain in STM
temporarily. The reverberating neural activity (neural activity, which goes, round and produces
structural changes in synapses) leads to LTM storage. Thus, the changes in neuronal biochemical
structure are the basis of LTM storage. He proposed a Two-stage memory theory is supported by
everyday evidence that unless you keep repeating telephone number it becomes difficult to recall it!
Cross modal transfer:
It is possible to learn with one sensory mode and use what is learnt and retained, in another mode. For
example, the visual scanning of mazes takes place, then one can go through it using the kinesthetic
mode. Humans and higher primates can do that easily but lower animals cannot transfer information
from one modality to another. If memories were diffusely stored then lower animals should also be able
to do the same
Problems and Issues in testing memories:
a) There is no adequate method to identify where memories are stored, where memories stored not
known effectively even after so many years of research,
b) Performance not memory may be affected (if you remember there was a famous joke that if you cut
frog legs the frogs forget to hop across lines--- performance not memory was affected by cutting the
legs)
c) How do we know that connections of other areas are not damaged by lesions to one area? Lesion in
one area may alter connection in other,
d) Lastly, is what we assess if the loss of memory or the loss of retrieval of memory?
173
img
Neurological Basis of Behavior (PSY - 610)
VU
Biological Systems and Memory:
Researches using single cell recordings have shown that learning changes single cells. There are
measured increases in calcium in neurons, decreases in potassium flow, increases in number of certain
synaptic receptors, changes in RNA and proteins. Impaired learning may be due to the deficits in
biochemistry.
RNA:
These are the memory code molecules. There are qualitative and quantitative changes in measures of
RNA and protein synthesis in animals, which have learnt a task. Heredity is memory passed on from
one to another generation. The DNA is the template for RNA-, which determine the structure of
proteins. Hyden and Colleagues (1962) trained rats to walk on a tight rope as compared to normals.
There was increase in increase in RNA in brain cell nuclei. Glassman and colleagues (1974) showed
that changes in RNA and proteins were found after learning a shock avoidance task. Shock avoidance
where the rats had to jump onto a platform at the sound of a buzzer, whereas the controls had a buzzer
but no shock/ and or no platform to jump. These rats were injected with labeled Uri dine (precursor for
RNA), or labeled lysine (precursor for protein), 30 minutes before the experiment. The amount of Uri
dines incorporation decreased with time i.e. RNA synthesis decreased after training and lysine increased
after training. RNA coding for new protein. Labeled Lysine injected carried into cortex and
hippocampus with acquisition. Interesting experiments have also been carried out where rats, chicks and
other species were trained and learnt a task, these animals were decapitated and their brains
homogenized and injected into the normal rats. It was found that the injected animals learnt faster than
untrained or un-injected rats.
Protein synthesis:
Researches on single cell basis of learning have indicated evidence that Proteins synthesis is a necessary
step in long-term memory. Proteins synthesis modifies characteristics and properties of neurons. Drugs
that inhibit protein synthesis impair LTM storage but not STM. The increased inhibition leads to
increased deficits in learning (Bennet et al, 1977). Anisomycin blocks protein synthesis blocked rats
memory of location of the shock but not the memory of location of food!
Other important bio-chemicals are Cyclic Amp, ACTH, Vasopressin, Acetylcholine and NE
Other Influences on Learning and memory:
Stress interferes with learning and retrieval of information. We all are familiar with Blockade before
important paper! Electroconvulsive therapy blocks protein synthesis
Hebb's consolidation theory time required for STM to LTM any interference with consolidation would
result in disruption of long-term recall. If there is a head injury then memory of events prior to injury
lost (retrograde amnesia), destroyed as evidence indicates that a small reminder brings back memories
.In head trauma memory returns after delay or under tranquilizers.
ECT affects both long term and short-term memories: Kalat (1980) "ECT interferes with memories that
are active at the time of ECS regardless of the fact whether formed recently or long ago"
Plasticity and the nervous system
Experiments by Hubel and weasel have shown that anatomical changes take place in the visual cortex
with experiences. Horizontal goggles worn by kittens during early period of development lead to firing
of neurons when horizontal stripes are seen as adults.
174
img
Neurological Basis of Behavior (PSY - 610)
VU
Similarly, if one eye receives more stimulation, the brain area for that eye is enlarged (more neurons
respond)
Shock to the foreleg of young kittens led to a greatly enlarged somato-sensory cortical area (Increased
stimulation led to increased areas for responding).
Merzenich carried out an experiment where he joined the third and index finger by sewing them
together, the area for this "one" finger becomes large. If the thumb is removed the areas for thumb in the
cortex becomes smaller. MRI's studies of violinist's brains showed that their cortical auditory areas
were enlarged as compared to normals.
Super Plasticity in growing Brain?
There have been studies which have shown that an early start e.g. for musicians, for language
proficiency, for players, for gymnasts, there is need to start early. As the information, being sent to the
sensory cortices when learning is taking place. In language learning, the left hemisphere growth spurt is
recorded on EEG between 2-4 years of age, and another 12-15 years again only in the left hemisphere.
There is increasing research in the early development and the neuronal stimulation, nerve growth factor,
and stem cell research.
Brain correlates of Learning and Memory, Amnesia, Verbal, Non-verbal memory, tests
Amnesia is a memory disorder, and patients suffering from Amnesia have been studied to find out more
about how memory works. One of the most famous cases of amnesia is
H.M: pure amnesic: H.M. had severe epileptic seizures and for treatment of epilepsy, surgery was
carried out when he was 27 years old. In addition, after the surgery he has been in the time freeze of
being stuck at 27 (even 40 years later) HM has amnesia for events prior to surgery, and has no LTM. He
actually lives in the present, in STM. He ahs no IQ loss as assessed by IQ tests. He has been tested for
memory using the mirror drawing task, the digit span test, Block tapping memory span test, Incomplete
pictures test, and even eye blink Pavlovian type conditioning response. He has damage in the temporal
region and this has provided evidence of the importance of temporal lobe (and hippocampus) in
memory.
AMNESIA
·
Anterograde:loss of ability to learn new information. The amnesic can remember events before
surgery or injury. The complex perceptual motor learning abilities however are intact in these
patients. Karsakoff's syndrome is the severest form of Anterograde Amnesia, where damage is
to the mammilliary bodies and temporal lobe
·
Retrograde. This form of amnesia is inability to remember event, which had occurred before
brain damage. Confabulation is creation of pseudo memories to fill gaps.
·
Alzheimer's disease is one of the major diseases, which leads to severe memory loss. This is the
most common cause of dementia ( memory and intellectual impairment) research has provided
evidence of Neurofibrils, amygdloid plaques, neural degeneration, also reduction in ACH as the
underlying pathology in Alzheimer's Studies on amnesiacs have shown:
1. Hippocampus is not the location of Long term memory nor is it important for retrieval of long
term memories
2. It is also not the location for immediate memories
175
img
Neurological Basis of Behavior (PSY - 610)
VU
3. Hippocampus is involved in transforming STM to LTM
Studies have also shown the importance of mammilliary bodies, and the Dorsomedial Thalamus in
memory.
References:
1. Carlson N.R. (2005) Foundations of Physiological Psychology Allyn and Bacon, Boston
2. Pinel, John P.J. (2003) Biopsychology (5th edition) Allyn and Bacon Singapore
3. Bloom F, Nelson and Lazerson (2001), Behavioral Neuroscience: Brain, Mind and Behaviors (3rd
edition) Worth Publishers New York
4. Bridgeman, B (1988) The Biology of Behaviour and Mind. John Wiley and Sons New York
5. Brown,T.S. and Wallace.(1980) P.M Physiological Psychology. Academic Press New York.
6. Bradshaw J.L. and Mattingley, J.B. (1995) Clinical Neuropsychology:  Behavioral and Brain
Sciences. ACADEMIC PRESS
7. Bridgeman, (1992) p324, graham 354, Carlson, Brown and Wallace 474, Pinel 268
176
Table of Contents:
  1. INTRODUCTION:Descriptive, Experimental and/ or Natural Studies
  2. BRIEF HISTORICAL REVIEW:Roots of Behavioural Neurosciences
  3. SUB-SPECIALIZATIONS WITHIN THE BEHAVIORAL NEUROSCIENCES
  4. RESEARCH IN BEHAVIOURAL NEUROSCIENCES:Animal Subjects, Experimental Method
  5. EVOLUTIONARY AND GENETIC BASIS OF BEHAVIOUR:Species specific
  6. EVOLUTIONARY AND GENETIC BASIS OF BEHAVIOUR:Decent With Modification
  7. EVOLUTIONARY AND GENETIC BASIS OF BEHAVIOUR:Stereoscopic vision
  8. GENES AND EXPERIENCE:Fixed Pattern, Proteins, Genotype, Phenotypic
  9. GENES AND EXPERIENCE:Mendelian Genetics, DNA, Sex Influenced Traits
  10. GENES AND EXPERIENCE:Genetic Basis of behavior, In breeding
  11. GENES AND EXPERIENCE:Hybrid vigor, Chromosomal Abnormalities
  12. GENES AND EXPERIENCE:Behavioral Characteristics, Alcoholism
  13. RESEARCH METHODS AND TECHNIQUES OF ASSESSMENT OF BRAIN FUNCTION
  14. RESEARCH METHODS AND TECHNIQUES OF ASSESSMENT OF BRAIN FUNCTION:Activating brain
  15. RESEARCH METHODS AND TECHNIQUES OF ASSESSMENT OF BRAIN FUNCTION:Macro electrodes
  16. RESEARCH METHODS AND TECHNIQUES OF ASSESSMENT OF BRAIN FUNCTION:Water Mazes.
  17. DEVELOPMENT OF THE NERVOUS SYSTEM:Operation Head Start
  18. DEVELOPMENT OF THE NERVOUS SYSTEM:Teratology studies, Aristotle
  19. DEVELOPMENT OF THE NERVOUS SYSTEM:Stages of development, Neurulation
  20. DEVELOPMENT OF THE NERVOUS SYSTEM:Cell competition, Synaptic Rearrangement
  21. DEVELOPMENT OF THE NERVOUS SYSTEM:The issues still remain
  22. DEVELOPMENT OF THE NERVOUS SYSTEM:Post natal
  23. DEVELOPMENT OF THE NERVOUS SYSTEM:Oxygen level
  24. Basic Neuroanatomy:Brain and spinal cord, Glial cells, Oligodendrocytes
  25. Basic Neuroanatomy:Neuron Structure, Cell Soma, Cytoplasm, Nucleolus
  26. Basic Neuroanatomy:Control of molecules, Electrical charges, Proximal-distal
  27. Basic Neuroanatomy:Telencephalon, Mesencephalon. Myelencephalon
  28. Basic Neuroanatomy:Tegmentum, Substantia Nigra, MID BRAIN areas
  29. Basic Neuroanatomy:Diencephalon, Hypothalmus, Telencephalon, Frontal Lobe
  30. Basic Neurochemistry:Neurochemicals, Neuromodulator, Synaptic cleft
  31. Basic Neurochemistry:Changes in ionic gates, The direct method, Methods of Locating NT
  32. Basic Neurochemistry:Major Neurotransmitters, Mesolimbic, Metabolic degradation
  33. Basic Neurochemistry:Norepinephrine/ Noradrenaline, NA synthesis, Noadrenergic Pathways
  34. Basic Neurochemistry:NA and Feeding, NE and self stimulation: ICS
  35. Basic Neurochemistry:5HT and Behaviors, Serotonin and sleep, Other behaviours
  36. Basic Neurochemistry:ACH and Behaviors, Arousal, Drinking, Sham rage and attack
  37. Brain and Motivational States:Homeostasis, Temperature Regulation, Ectotherms
  38. Brain and Motivational States:Biological Rhythms, Circadian rhythms, Hunger/Feeding
  39. Brain and Motivational States:Gastric factors, Lipostatic theory, Neural Control of feeding
  40. Brain and Motivational States:Resting metabolic state, Individual differences
  41. Brain and Motivational States:Sleep and Dreams, Characteristics of sleep
  42. Higher Order Brain functions:Brain correlates, Language, Speech Comprehension
  43. Higher Order Brain functions:Aphasia and Dyslexia, Aphasias related to speech
  44. Higher Order Brain Functions:Principle of Mass Action, Long-term memory
  45. Higher Order Brain Functions:Brain correlates, Handedness, Frontal lobe