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712 Biological Basis of Behavior > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

DIENCEPHALON SLIDES:

Diencephalon is located where and made up of what?

A 
Located rostral to brainstem
Two main structures are
Thalamus 
Hypothalamus 
Also includes the pineal gland

-thalamus and the hypothalamus and the pituitary gland are a part

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2
Q

DIENCEPHALON SLIDES:

what does the thalamus do?

A

The “CPU of the brain” – Processes many signals
Transmits signals from all senses to cortex.
ACTS AS A FILTERING FUNCTION

Olfaction mainly bypasses thalamus.
Types of information processed
Sensory
Motor
Integrative
Regulatory (from diffuse projecting nuclei)

(He says all senses, and its technically correct, aside from olfactory, which goes to limbic brain and olfactory first. Other than that, everything else goes to the thalamus. Even olfactory though has one path that does go to the thalamus. )

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3
Q

DIENCEPHALON SLIDES:

Describe the filtering function of the thalamus

A

“Filtering” function - Helps to select which sensory & motor information will be allowed to pass to and from cortex and in what sequence.
May fail in schizophrenia, causing poor signal-to-noise ratio

(It has a filtering function. They used to call it a switchboard of the brain. And it doesn’t serve a passive function. Relay station and filtering regarding when and what information will go to cortex. It even filters out some information if overworked. Coordinates what goes in and when it goes in.
-meaning that its not filtering out information when you say poor sign-to-noise ratio.)

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4
Q

DIENCEPHALON SLIDES:

What is the thalamus critical for? what critical role does it play?

A

Critical for optimal cortical arousal and attention

Critical for cognitive functioning & coordinating activation including timing & coordination of complex problem solving

(So thalamus is important for optimal arousal (bc too much arousal may cause too much anxiety where its like when you are so anxious that you cant remember it.
-thalamus is also important for attention.

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5
Q

DIENCEPHALON SLIDES:

Lesions to Thalamus do what?

A

Lesions may cause:
Memory, cognitive, executive dysfunction
Dorsomedial nucleus and mammillothalamic tract are damaged in Korsakoff syndrome
Dysfunction of context encoding and time sense
Severe anterograde amnesia
Retrograde amnesia w/ temporal gradient
Pts may not realize deficits.

Difficulties w/ forming concepts, cognitive flexibility, executive functions, language
Apathy, flat affect, confusion, disorientation (sometimes disinhibition, mania)
Difficulty w/ face or pattern recognition, mazes, design reconstruction, unilateral inattention (particularly w/ right-sided lesions

Specific sensory losses (e.g., tactile object agnosia)
“Thalamic pain” – very severe pain
Motor sxs since thalamus receives input from basal ganglia & cerebellum and projects to premotor areas

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6
Q

DIENCEPHALON SLIDES:

What is the primary function of the HYPOTHALAMUS?

A

Primary function is homeostasis/regulation of:
Water/electrolyte balance (ADH, thirst)
Food intake (hunger, satiety)
Temperature (sweating, shivering)
Autonomic activity (blood pressure, rate/force of heart beat, respiratory rate/depth, digestive tract motility, etc.)
Sleep-wake cycle/circadian rhythmicity
General body metabolism

Generates behaviors that are:
Related to survival of animal or species (e.g., drinking, eating, sleeping, coitus, physical protection- fear/rage, drive/responsivity)
Are usually pleasant for the animal

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7
Q

DIENCEPHALON SLIDES:
What three systems does the hypothalamus serve?

BURKE SAYS KNOW THIS FOR THE HYPOTHALAMUS

A

Subserves 3 systems

  1. Autonomic (through effects on brainstem, spinal cord centers)
  2. Endocrine (hormones, releasing factors affecting anterior pituitary)
  3. Limbic (primary output of limbic brain)

(This is REALLY what he wants us to remember for the hypothalamus. That it controls all three of these systems.
All hormones are actually controlled by the hypothalamus. So even though the pituitary says to release the hormones, the hypothalamus is what is the boss of the pituitary.
-limbic system is the emotional part/emotional information (like the amygdala, etc), etc. So like the limbic brain says “this is scary” and what will you do about this? And the hypothalamus then says something like “ok, I’m releasing cortisol, and amygdala, and etc…. To trigger a response)

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8
Q

DIENCEPHALON SLIDES:

What do structural differences in HYPOTHALAMUS related to?

A

Structural differences may be related to sexual behavior, sexual preferences, sexual orientation

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9
Q

DIENCEPHALON SLIDES:

what would lesions to the hypothalamus cause?

A

Lesions or dysregulation may cause:

Obesity, vasomotor sxs of menopause, fatigue, diminished drive, memory deficit (mammillary bodies), diabetes insipidus

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10
Q

DIENCEPHALON SLIDES:

Pineal gland

A

Is indirectly sensitive to light in humans by photic stimulation via neural circuits

Synthesizes melatonin from serotonin via enzymes that are sensitive to diurnal fluctuations in light
In absence of light, synthesis of melatonin is enhanced.
Rhythm is calibrated to 24-hour cycle of photic input to retina (a circadian rhythm).

Deals with Melatonin

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11
Q

DIENCEPHALON SLIDES:
What does melatonin do? where is it from? What system is it a part of?

BURKE SAYS KNOW THIS SLIDE

A

melatonin is released by the pineal glad, is a part of hte diancephalon system..and it modulates sleep-wake switch in hypothalamus and lowers body temperature.

(Burkey Says: Melatonin is actually a derivative of serotonin- so it turns serotonin into melotonin. AND TO REMEMBER that melatonin modulates the sleep wake switch in the hypothalamus and lowers body temperature. )

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12
Q

BASAL GANGLIA SLIDES:

define the basal ganglia and what does it do?

A

Complex set of subcortical nuclei that modulate movement, perception, cognition, emotion

Basal ganglia (BG) get information from cortex, modulate that information, and then modulate frontal cortex via thalamus.

Such modulation results in either increased or decreased excitation of frontal cortex.

In short, BG get information from cortex, modulate that information, and then modulate frontal cortex via thalamus.
Such modulation results in either increased or decreased excitation of frontal cortex

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13
Q

BASAL GANGLIA SLIDES:

What is the striatum comprised of?

A

Striatum - Comprised of the caudate nucleus, putamen, nucleus accumbens

is a part of the basal ganglia

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14
Q

BASAL GANGLIA SLIDES:

What does the striatum do??

A

Receives input primarily from cerebral cortex
Also input from substantia nigra (termination of nigrostriatal pathway)
Projects to other BG
These in turn project primarily to thalamus.
Projects to frontal lobe

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15
Q

BASAL GANGLIA SLIDES:

What happens when there is a disease or problem with Basal ganglia?

A

Diseases of BG disrupt neurochemical interactions among BG.

Resulting in disruption of movements and sometimes disruption of cognition, perception, emotion

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16
Q

BASAL GANGLIA SLIDES:

How are the Basal ganglia separated/how does it work?

A

BG are segregated into parallel circuits (“loops”) that process different types of information.
Called “loops” because they connect cortex with BG, thalamus and back to cortex
In some cases, to very same neuron in the frontal cortex

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17
Q

BASAL GANGLIA SLIDES:

what are the four paralles circuits or loops that make up the basal ganglia loops?

A

Four parallel circuits (“loops”):

Skeletomotor Loop
          Sensory-motor control
Oculomotor Loop
          Control of orientation and gaze
Prefrontal Cortex (Executive) Loop
           Cognitive processes
Limbic Loop
           Emotional and visceral responses
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18
Q

BASAL GANGLIA SLIDES:

Describe the Skeletomotor loop that is a part of the Basal Ganglia, and what happens when damaged?

A

Involved in modulating force/rate/amount of movements, including initiation & control of movement
Not involved in conscious desire to move, in planning details, or in activating muscles
Also helps to smooth movements
Automatic motor subroutines require basal ganglia & cerebellum.
Subconscious habits, motor skills

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19
Q

BASAL GANGLIA:

What happens with Basal ganglia are damaged?

A

Damage can result in either:
Hypokinetic symptoms
(Loss/decrease of motor/cognitive ability)

Hyperkinetic symptoms
(Involuntary movements
Depending on where exact lesion is located
within BG and on what neurochemical
interactions are affected)

Determines whether thalamus (and, therefore, cortex) is understimulated or overstimulated

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20
Q

BASAL GANGLIA:

define Hypokinetic Dysfunction, and describe what diseases are associated.

A

DAMAGE to BG, and getting Hypokinetic symptoms:
Loss/decrease of motor/cognitive ability

DISEASE:
Parkinson’s disease (PD)
Akinesia (dyskinesia)
Bradykinesia – Slowed movements

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21
Q

BASAL GANGLIA:

Describe what happens with Parkinsons disease?

A

AKA ideopathic Parkinsonism, primary Parkinson’s
Motor sxs due to loss of dopaminergic neurons of substantia nigra that project to striatum of BG
Results in decreased excitation from BG to thalamus with resulting hypokinetic sxs

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22
Q

BASAL GANGLIA:

Describe what happens with Akinesia (dyskinesia)

A

– Difficulty initiating activity
Loss of postural reflexes (tends to fall backward)
Shuffling gait, as if feet were stuck in place, w/ decreased arm swing and appearing stiff w/ little neck movement
Sometimes followed by nearly normal gait but difficulty stopping or falling

23
Q

BASAL GANGLIA:

Describe what happens with Bradykinesia

A

Slowed movements .

* Brady = slow. think like bradycardic.

24
Q

BASAL GANGLIA:

Describe symptoms of Dyskinesia, which is commonly associated in Parkinsons disease

A

Masked face, blank stare (decreased blink)
Hypokinetic dysarthria – Decreased intonation, low volume, variable speed of speech
Writing may be small (micrographia), cramped, jerky.

25
Q

BASAL GANGLIA:
Describe parkinson’s disease?

(this is a lot, he is unlikely to ask specific questions about this, but good to review for when seeing it)

A

EPS (extrapyramidal symptoms) due to improper balance of neurotransmitters in BG
Akathisia (restlessness)
Muscular rigidity (bent over, “cogwheel rigidity”)
Resting (pill-rolling) tremor
EPS are caused by excessive acetylcholine (ACh) activity (disinhibition) in some neurons because ordinarily DA blocks ACh release in basal ganglia

Clinical picture of patient
Sitting or standing with pill-rolling tremor
Blank stare (decreased blink)
Masked face
Flexed (stooped) posture
Paucity of movements

Depression is common.

Some experience apathy or psychotic sxs.

Mood & cognitive sxs due to loss of neurons in locus coeruleus (NE), dorsal raphe nucleus (5-HT), nucleus basalis of Meynert (ACh), in addition to substantia nigra
Depression in 40%-60%, but low suicide rate
May have sensory sxs (e.g., pain).

Mental deterioration, slowed cognition (bradyphrenia), memory deficit, in 20-50%

About 31% of PD pts develop dementia (7x’s more frequently than normal individuals)
Impairments in:

Procedural memory – Ability to remember how to do procedures/tasks

Working memory – Ability to remember information for 15-30 secs, which impairs pt’s ability to comprehend complex instructions or sentences

30% of PD pts w/ dementia also suffer from Alzheimer’s disease.
Complicates Rx because acetylcholinesterase inhibitors for Alzheimer’s Disease further increase the excessive cholinergic activity present in PD.

26
Q

BASAL GANGLIA:

define Procedural memory –

A

Ability to remember how to do procedures/tasks

27
Q

BASAL GANGLIA:

define Working memory –

A

Ability to remember information for 15-30 secs, which impairs pt’s ability to comprehend complex instructions or sentences.

28
Q

BASAL GANGLIA:

describe “parkinonism”

A 
Parkinsonism - Syndrome of sxs of Parkinson’s due to:
Side effect of antipsychotics (particularly typical antipsychotics)
Metoclopramide (Reglan)
Toxins
TBI
Stroke
Encephalitis
Meningitis
29
Q

BASAL GANGLIA:

Hyperkinetic Dysfunction

A

Disruption of chemical interactions within skeletomotor loop
Results in increased excitation of thalamic neurons, which results in excessive stimulation of the cerebral cortex

Includes Choreiform movements - Generalized irregular dance-like movements of limbs
     Sydenham’s chorea
     Chorea gravidarum
     Huntington’s disease
            Part of tardive dyskinesia
30
Q

BASAL GANGLIA:
Describe Sydenham’s chorea (St. Vitus’ dance)

BURKE SAYS KNOW THIS

A

Most common cause of chorea
Occurs primarily in females, typically after a bout of rheumatic fever

(BURKEY SAYS: Also known as st vitus dance. Know this something about atacking antigen… there are jerky dance like movements)

31
Q

BASAL GANGLIA:

describe Athetoid movements -

A

Continuous writhing of distal portions of extremity
is found in Huntington’s disease, Sometimes in treated Parkinson’s disease, and is Part of tardive dyskinesia

(burke says: This is more like slowing, writhing (kind of like writhing in your hands but slower than the other one). Note parkinson’s – its also hypokinetic. But obviously diseases are complicated. )

32
Q

BASAL GANGLIA:

Describe/define Huntington’s chorea

A

It is HYPERkinetic disturbance. is:
Inherited disease causing abnormality in BG, which leads to over-stimulation of frontal cortex, resulting in choreiform & athetoid movements

Huntington’s chorea
Progressive, untreatable, autosomal dominant defect on short arm of chromosome 4
Defective executive loop and cortical atrophy in temporal & frontal lobes causes cognitive deficits.

33
Q

BASAL GANGLIA:
Describe the cognitive dysfuntion associated with Huntingtons

BURKEY SAYS KNOW THIS

A 
Huntington's Cognitive dysfunction:
Attention
Slowed processing
Defective retrieval primarily due to lack of organization
Decreased verbal fluency and speech
Visuospatial dysfunction
Thinking, reasoning problems
Executive dsysfunction

(Notes say: CVLT can be used to assess verbal fluency, thus can be used to look at executive frontal lobe function. People with huntingtons have diffiiculty with this test. KNOW: that there are cognitive dysfunctions and then give some flavor of that. )

34
Q

BASAL GANGLIA:

Descirbe the psychiatric sxs assoc with huntingtons

A

With Huntingtons, Psychiatric sxs:
Depression is the most common sx; high suicide rate
May experience mania or hypomania, anxiety, emotional lability, irritability, aggressiveness, apathy late in disease

(NOTES SAY:Frequently huntingtons has psychiatric sxs as well as cognitive sxs. Depression is the most common, and suicide is really really high. Burke says its good to know the base rate for pts with huntingtons. And also know the base rate for suicide for huntingtons. The caudate nucleus becomes highly calcified when you have huntingtons (bc you have a lack or dying off of neurons). How to rule out primary versus secondary diagnosis of depression in huntingtons: rule out premorbid functioning or premorbid sx of depression
-also really good
-AT TIMES< THEY MAY EPERIENCE MANIA OR HYPOMANIA, EMOTIONAL LABILITY, etc. ITS DYSFUNCTIONING IN THE PREFRONTAL CORTEX. You cant heal this, there is no cure, but you can still do therapy in order to provide psychoeducation and therapy. You emphasize that it is a neurological disease. Results in dimentia and is fatal.
Its not a depression that is secondary or a reaction to having a disease, but instead is an actual sx of the neurological process. )

35
Q

BASAL GANGLIA:

Describe the prognosis of Hutningtons.

A

Gradually choreiform & athetoid movements increase until pt is bedridden
Later stages characterized by severe dementia
Fatal after 10-20 yrs
No cure
Genetic testing available for first-degree relatives, who have a 50% chance of carrying mutant gene
x

36
Q

BASAL GANGLIA:

describe Tardive dyskinesia -

A

Repetitive choreic or athetoid movements that affect face, trunk, hands, feet
Sxs may be temporary or permanent
Caused by chronic Rx w/ antipsychotics, especially neuroleptics (typical antipsychotics)

(MY NOTES say:
Drugs like halliwell. This is an iatregenic – meaning caused by medical intervention

With tardive dyskinesia: like a really slow facial movement and tweeks. from first generation typical antipsychotics (now they use atypical antipsychotics aka second generation), things like hallidol will cause this, and even if ended immediately with the first sign of symptoms:50% of pts will continue getting symptoms for the rest of their life, even if medication removed right away, 25% sx will go away,and 25% will..??? lost track here.)

37
Q

BASAL GANGLIA:

Tardive Dyskin. and the underlying process..

A

Antipsychotics antagonize D2 receptors throughout brain, including those on striatal neurons (targets of nigrostriatal tract).
Prolonged antagonism of D2 receptors causes hypersensitivity or upregulation of D2 receptors leading to excessive DA activity in skeletomotor loop involving BG, causing hyperkinetic sx’s

38
Q

BASAL GANGLIA:

Describe Dystonia

A
  • Persistent contraction of muscles
    Painful muscle spasms involving neck (spasmodic torticollis), back, eyes (oculogyric crisis), larynx (laryngospasm), hand (“writer’s cramp”), foot
    Most common cause is SE of antipsychotic
    May occur hrs-days after initiating drug
    May occur in PD, Huntington’s, thyroid disease, hypoparathyroidsm.
39
Q

BASAL GANGLIA

Describe Tourette’s syndrome

A

(akaGilles de la Tourette’s):
Involuntary tics & involuntary movements
Multiple motor tics accompanied by at least one vocal tic for a period of at least 1 year

Excessive D2 activity in basal ganglia, especially right caudate

May involve circuit including prefrontal cortex 
Also may experience:
Obsessions, compulsions
Hyperactivity, impulsivity
Learning disabilities
Waxing & waning course
Absence of progressive deterioration
Spontaneous remission occurs for lengthy intervals (yrs)
Complete remission in 10%
Onset before 18 yrs of age
Male to female ratio of 3:1
Prevalence of 0/.05-0.09%
Only 10% manifest coprolalia (cussing) & echolalia (repeating what was said).

(NOTES SAY:Excessive dopamine with D2 receptor, in basal ganglia, especially in the rt caudate.
-this is all likely…. But they still don’t know entirely what causes.It has higher comorbidity with attention deficit disorder. There are some behavioral treatments, such as working behaviorally to inhib a response with increased awareness. )

40
Q

BASAL GANGLIA

Basal Ganglia Dysfunction

A

BG dysfunction (including loops including frontal cortex) may occur in:
Attention-Deficit/Hyperactivity Disorder (ADHD)
Sxs of inattention, executive disinhibition, hyperactivity
Schizophrenia
OCD
Depression
Autistic spectrum disorder.

(NOTES SAY: Basal ganglia, in a loop with the prefrontal cortex is the neuroanatomy of ADHD. The ventral tegmental area projects up to the nucleus accumbens. This is the mes. Lymbic pathway. So that this pathway and has to do with dopamine.basal ganglia dysfunction is also tied to schizophrenia, OCD depression and austism. So you can have multiple disorders all with dysfunction in the same system. )

41
Q

LIMBIC SYSTEM:
made up of what?

BURKE SAYS KNOW THIS!!!

A

cingulate cortex (aka limbic cortex)
temporal lobe
amygdala
hippocampus

OR MORE SPECIFICALLY...
Amygdala
Hippocampal formation
Mammillary bodies (of hypothalamus)
Anterior thalamus
Cingulate cortex
Fornix (connects hippocampus & mammillary bodies)

ACCRDING TO NOTES KNOW: Know these and this group bc this is a very very famous loop. KNOW THAT THE LIMBIC STRUCTURE IS THAT MEMORY AND EMOTIONS SYSTEMS ARE CONNECTED TOGETHER> AND THAT THAT IS CALLED THE LIMBIC SYSTEM

42
Q

LIMBIC SYSTEM:

Describe the cortical and subcortical regions of the limbic system

A

Comprised of subcortical & cortical structures that encircle brainstem, thalamus, basal ganglia
Subcortical portion involved with subconscious, fast responses to stimuli with positive or negative values
Cortical portion mediates conscious feelings
Important for survival of species, including motivation, emotion, memory

(NOTES SAY:Subcortical portion is basicaly designed to have really fast processing. The corical portion is tied to conscious. Or cortical portion is connected to what an indiviual is feeling
-sometimes the brain will respond before the conscious does. Like they may start sweating, increased heart rate, etc when they experience fear, but before they realize that its happening.)

43
Q

LIMBIC SYSTEM:
What is the amygdala tied to?

BURKE SAYS KNOW THIS SLIDE

A

Learning emotional significance of stimuli, particularly with biological significance
Presence of food, water, salt, mates, rivals
Prosody & facial expressions (particularly fear, anger, sadness)
Responding to innate fears & learning new fears (conditioning)
The most important structure in brain for fear
Anxiety disorders associated w/ hyperactive amygdala

(notes say: Amygdala is tied to fear, sex, food, facial expressions, prosody of speech it tends to be more negative and respond to things like fear, anger, and sadness, but it also shows the positive. Also sometimes pts will have difficulty understanding faces when there are issues with the amygdala.KNOW THIS SLIDE REALLY WELL. The amygdala is the most important structure in the brain for fears. Anxiety, and other anxiety disorders, will often show overactive amygdala. Amygdala coordinates/starts the “fear response” or basically the freeze response. Amygdala is pretty permanent, and may only take one trial learning at times. Like with PTSD pts, sometimes you can get them to lay down other tracks over the earlier ones, but they will still be there.
)

44
Q

LIMBIC SYSTEM:

What does the amygdala coordinate?

A

Coordinates emotional responses:
Autonomic & endocrine responses via output to hypothalamus, brainstem
Defensive behavior via output to brainstem
Conscious awareness via output to prefrontal cortex, cingulate cortex

(NOTES:Autonomic (sympathetic espeically, but also parasympathetic) and endocrine (hormonal system), this sends hormons to hypothalamus and brainstrem. It ouputs to the hypothalamus and brainstem. When brainstem, it is defensive behavior. )

45
Q

LIMBIC SYSTEM:

Hippocampus is known for what?

A

Critical for declarative long-term memory.
Receives input from cortex
Associates various inputs
Sends processed information back to these cortical areas where their synapses are modified (stored in memory)
Damage occurs in Alzheimer’s disease.

(NOTES SAY:Receives input from cortex (from the various sensory modalities/parts of cortex, such as smells, things heard, etc. after receiving info, it sends it back
Not all long term memories are storied in the hippocampus (a lot of info it stored throughout the brain). The actual storing of the information itself involves the hippocampus. Sx of alzheimers occurs in the hippocampus.)

46
Q

LIMBIC SYSTEM:

nucleus accumbens

A

Major role in craving, pleasure, addiction
Brain response to natural reinforcers & recreational drugs associated with elevated levels of extracellular dopamine in NA

(NOTES:This is the reward center. It is tied to reinforcers and recreational drugs associated with more DOPAMINE. So the nucleus accumbens sucks up dopamine and likes it. Unfortunately, when too much dopamine is sucked up, it is a problem bc you have too much dopamine)

47
Q

LIMBIC SYSTEM:
QUESTIONS.

BURKE SAYS KNOW THIS SLIDE

A

Considered the reinforcement pathway and involved in addictions:
Mesolimbic pathway from the ventral
tegmental area (VTA) to the nucleus
accumbens

The most important structure involved in fear conditioning:
Amygdala

Has a critical role in associating stimuli and forming long-term, explicit memories:
Hippocampus

48
Q

THE CEREBRAL CORTEX SOMATOSENSATION:

Describe the Neocortex aka the cerebral cortex

A

Unique to mammals
Higher levels of functioning involving perception, motor output, thinking, planning, language; and aspects of attention, memory, emotion
Connected to all other parts of brain; so it s the ultimate creator of our reality.

49
Q

THE CEREBRAL CORTEX SOMATOSENSATION:

describe brodmann’s areas

A

Broadmann was a neuropscientist who studied the architecture of the brain and then labeled those areas with numbers, each number designating certain function.

No need to know numbers, just that broadman history

50
Q

THE CEREBRAL CORTEX SOMATOSENSATION:
Describe the different areas or ways to break down the posterior lobes
(ex temporal/occipital lobe functions, sensory and association areas)

A

Parietal, Temporal, Occipital Lobes
Receive, encode, store information
Primary sensory areas – Processing of “raw”
somatosensory, visual, auditory stimuli
Secondary association areas – Integrating
information within a modality
Multimodal areas (tertiary association) – Integrating
across functions or modalities

(NOTES:When thinking of posterior lobes/areas, think of SENSATION. Or sensory information. So they receive, encode, and store sensory information. The pimary sensory are is there with somatosensory (senses) , vision (like that there is a light- but no processing here, just the recognition that there is a light), and auditory. Note primary is just the recognition or reception.)

51
Q

THE CEREBRAL CORTEX SOMATOSENSATION:

Describe the Somatosensory area (S-I)

A

Also called “sensorimotor cortex” includes sensory strip posterior to central sulcus (Rolandic Fissure)
S-I allows for conscious perception of touch, proprioception (joint/muscle position), temperature, pain, itch
Arise from specialized receptors that project along specific pathways to specific cortical neurons, which ultimately must integrate information into a single percept
Allows for such skills as stereognosis (the recognition of an object by touch)
Various parts of body are topographically represented by specific neurons within S-I such that areas of greater sensitivity & two-point discrimination (greater resolution) are processed by more neurons, a principle common to all sensory modalities

(Notes say:S1: allows for the conscious perception of touch. (but cerebellum is working on SUBconscious perception).
Things like temperature, pain, and itch on things for somatosensory areas. There are specialized neurons for each of these, so there are different modalities. So there are specialized receptors whose job it is to process that information. And then there are specialized neurons along certain pathways that send on, etc. Stereognosis is the recognition of objects by touch- like if something is in your hand, you can tell what it is by touch or aka holding it. Areas of greater sensitivity and two-point discrimination (like putting two fingers on an area of the body and the person can tell there are two areas/fingers. So more neurons in an area will give you better resolution- in areas with more neurons, you are more able to differentiate between two points of pressure/ incoming data as opposed to one point of interest bc there is less resolution/fewer neurons.

)

52
Q

THE CEREBRAL CORTEX SOMATOSENSATION:

describe the somatosensory in the parietal lobe in regards to learning piano.

A

Its details vary according to experience.
Examples: Compared to each other, a soccer player has relatively more sensory neurons devoted to feet, and a pianist has relatively more neurons devoted to fingers

Posterior parietal cortex
Immediately posterior to S-I
Visuospatial functions
Several integrative functions

(NOTES SAY Think mostly vision and integration)

53
Q

THE CEREBRAL CORTEX SOMATOSENSATION:

describe function of posterior parietal cortex

A

More anterior portion integrates
Tactile sensation from skin with proprioception from underlying muscles & joints
Sensation from two hands (via corpus callosum)
More posterior neurons integrate visual, tactile, proprioception.

(NOTES SAY:It integrates proprioception and tactile sensation. So in the anterior portion of the posterior parietal cortex, it processes basically touch from skin and sensation from the underlying muscles. Even more posterior behind that area are neurons that integrate vision tactile and touch)

712 Biological Basis of Behavior (3 decks)

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