Cognitive Neuroscience Exam 4

Learning

Change in behavior from experience

Memory

Ability to recall prior experience

Engram

Physical memory trace

• [A mental representation of a previous experience, corresponds to a physical change in the brain, most likely involving synapses]

Neuroplasticity

Brain’s ability to change biologically and functionally based on experience

•  [nervous system’s potential for change, which enhances its ability to adapt. Required for learning and memory]

Classical (Pavlovian) Conditioning

• Neutral stimulus paired with meaningful stimulus → learned response

• Components:

  • CS, UCS, UCR, CR

• Example: Fear conditioning, eyeblink conditioning

 Operant Conditioning

• Behavior shaped by consequences (reward/punishment)

• Not localized; circuits vary by task context

• Not localized to any particular brain circuit; necessary circuits vary by task context and requirements

• Entirely Voluntary. Learning through the consequences. Rewards and punishments that shape voluntary 

• Behavior - consequence - more or less of the behavior. Operate 

Implicit (Unconscious)

• Skills, habits, priming ,[using a stimulus to sensitize the nervous system to a later presentation of the same or a similar stimulus often used to measure implicit memory; unconscious learning]

• Cannot consciously recall but performance shows learning

• Preserved in amnesia

• Tasks: Pursuit rotor, Gollin figures

Explicit (Conscious)

• Semantic: facts

• Episodic: personal events

• Requires active processing

Explicit Memory

• Key structures:

  • Hippocampus

  • Amygdala

  • Entorhinal cortex

  • Parahippocampal + Perirhinal cortices

  • Prefrontal cortex (short-term & temporal ordering)

Implicit Memory

• Basal ganglia

• Substantia nigra

• Ventral thalamus

• Premotor cortex

Emotional Memory

• Amygdala is central

• Adds emotional significance → stronger encoding

H.M.

Lost ability to form new explicit memories; implicit intact. Surgery to remove parts of the hippocampus because he was having seizures.

J.K.

Parkinson’s basal ganglia→ loss of implicit memory; explicit intact

Boswell

Severe global amnesia after infection

Spatial Memory

• Hippocampus required - organizes explicit memory

• Spatial cells: place, grid, head direction cells

  • place [discharge when rats are in a spatial location, regardless of orientation], 

  • Grid [discharge at many locations, forming a virtual grid invariant to changes in the rats direction, movement or speed

  • head direction cells [ cells discharge when a rats head points in a particular direction

Memory Consolidation

• Hippocampus → cortex transfer

• Reconsolidation: recalling a memory makes it modifiable

•  [when a memory is replayed in mind, it is open to further consolidation.]

Synaptic Basis of Learning

• Synaptic plasticity underlies learning: Synaptic plasticity: ability to use the synapses in different ways. Repurpose neurons. We can use different areas of our brain for different things we can localize which areas of the brain have synaptic changes and that 

• LTP long term potentiation: Strengthening; requires NMDA + glutamate (excitatory). Active potential. Neurons primed for activity. [involves persistent strengthening of synapse based on recent activity patterns; produces a long lasting increase in signal transmission between two neurons. In response to stimulation at synapse, changed amplitude of excitatory postsynaptic potential last for hour to days or more]

• LTD long term depression: Weakening; clears outdated material. EPSP depolarization. Low energy. Helps us forget memories. [low-frequency stimulation produced a decrease in EPSP size. ]

• Structural changes occur in dendrites and connections. 

Habituation is linked to calcium channels. As habituation occurs the amount of calcium going in decreases. With repeated use the voltage activated channels become more resistant to the passage of calcium. 

Sensitization is the opposite of habituation: the process in which we become hyper responsive. We are primed to respond to it.

Synaptic plasticity underlies learning:

Synaptic plasticity: ability to use the synapses in different ways. Repurpose neurons. We can use different areas of our brain for different things we can localize which areas of the brain have synaptic changes and that

LTP long term potentiation

Strengthening; requires NMDA + glutamate (excitatory). Active potential. Neurons primed for activity.

 [involves persistent strengthening of synapse based on recent activity patterns; produces a long lasting increase in signal transmission between two neurons. In response to stimulation at synapse, changed amplitude of excitatory postsynaptic potential last for hour to days or more]

LTD long term depression

Weakening; clears outdated material. EPSP depolarization. Low energy. Helps us forget memories

•  [low-frequency stimulation produced a decrease in EPSP size. 

Cognition

Knowing, planning, attending, recognizing.

Psychological constructs

We store our memories through schemas.Inferred mental abilities (e.g., intelligence). Schema is a framework. We store our memories through schemas. Subjective to who we are and what we are. 

Human Thought

• Language gives major advantage. Language is one of the ways that we think. It underlies how we give meaning to things. How we categorize. Set rules. Language syntax allows us to communicate with eachother. 

• Time organization

• Motor sequencing supports language evolution

Cell Assemblies

• Hebb: groups of neurons representing perceptions, memories. Interconnection between cells in information A allow it to become information B. new information overlays and when the neurons fire together they wire together.

• Thought emerges from their dynamic interaction: thoughts are firing and wiring.

• How we can create thought and neural networks that integrate with each other and produce conscious thought

Association Cortex (sensory cortexes all have association cortices)

• Temporal → object/auditory recognition. (where we name objects) (knowledge about objects/where we name objects). Recognize objects and process auditions.

• Parietal → movement, somatosensation, spatial relationships (knowing the location. Ability to imagine things) process visual information.

• Frontal → integrates information; planning and decision-making

Temporal

object/auditory recognition. (where we name objects)(knowledge about objects/where we name objects). Recognize objects and process auditions.

Parietal

movement, somatosensation, spatial relationships (knowing the location. Ability to imagine things) process visual information

Frontal

integrates information; planning and decision-making

Temporal Cortex

• Stores knowledge of objects

• Damage → agnosia

Spatial Cognition (Parietal)

• Knowing location and navigation

• Mental imagery and manipulation

• Deficits:

  • Topographic disorientation

    • [inability to find one's way in relationship to salient environmental cues even in familiar environments]

  • Egocentric disorientation

    • [difficulty perceiving relative locations of objects with respect to the self]

  • Bálint syndrome

    •  [disturbance of spatial processing that includes deficits in directing eye gaze peripherally and in comprehending the spatial features of a familiar object] [deficits in spatial behavior are also seen after damage to the posterior cingulate cortex and medial temporal regions] [three primary impairments, 

      • inability to perceive whole visual field, 

      • difficulty focusing, inability to move hand to a specific object. 

      • Optic ataxia - inability to grasp an object because of an inability to grasp or focus]

Attention

• Selective narrowing of awareness

• Single neurons can track attended locations

• Attention can be focused inward or outward.

• Deficits:

• Contralateral neglect

  • [ignoring a part of the body or world on the side opposite that of the brain injury. Particularly severe in right hemisphere damage]

• Extinction

  •  [neglect of information on one side of the body when presented with simultaneously with similar information on the other side of the body

Frontal association cortex: people with frontal lobe injuries tend to be overly focused on environmental stimuli

Parietal association cortex damage can produce contralateral neglect. Ignoring part of the world even if the eye is fine. People will drag their feet because they can't see that they aren't lifting it up. Ignoring a part of the body or world on the side opposite to that of the brain injury

Extinction: when information on one side of the body. Patients with contralateral neglect exhibit this symptom as they begin to recover. People who have it fail to pay attention

Executive Function (Frontal)

• Planning

• Organizing behavior in time + space

• Wisconsin Card Sorting Task → measures shifting/flexibility

• Damage → perseveration: continue to place the same card even after being told no. 

The planning we use our frontal lobe but we also identify the objects with temporal lobe and appropriate movements (parietal lobe)

Mirror Neuron System

• Fires during action + observation

• Supports imitation, social understanding

Cognitive Neuroscience Expansion

• Imaging → links brain networks to cognition  [can help cognitive neuroscientists map the human brain, allow social psychologists (social neuroscience) to explore how the brain mediates social interactions and aid economists in discovering how the brain makes decisions]

• Default network → active at rest/self-reflection

• Default network [default mode, how all brain function series of brain regions that are most active during certain activities] → active at rest/self-reflection [this is where social cognition  self projection] [brain network incoving regions o the frontal and parietal lobes. Higher resolution imaging demonstrated default network is not a single network but composed of at least two parallel networks, including adjacent dorsal and ventral components.] system of brain region that is most active at rest or not focused on what is going on around them. Activation in

• Connectomics → mapping brain connections

  • Human connectome project, combined diffusion tensor imaging DTI and functional magnetic resonance imaging fcMRI

  • Four proposed social-brain networks. The red areas represent the amygdala network light blue is the mentalizing network, dark blue is the empathy network, and green is the mirror/simulation/ action

  • Empathy network does not connect to the amygdala network

Imaging

 links brain networks to cognition  [can help cognitive neuroscientists map the human brain, allow social psychologists (social neuroscience) to explore how the brain mediates social interactions and aid economists in discovering how the brain makes decisions]

Default network

active at rest/self-reflection

[default mode, how all brain function series of brain regions that are most active during certain activities] → active at rest/self-reflection [this is where social cognition  self projection] [brain network incoving regions o the frontal and parietal lobes. Higher resolution imaging demonstrated default network is not a single network but composed of at least two parallel networks, including adjacent dorsal and ventral components.] system of brain region that is most active at rest or not focused on what is going on around them. Activation in

Connectomics

mapping brain connections

• Human connectome project, combined diffusion tensor imaging DTI and functional magnetic resonance imaging fcMRI

• Four proposed social-brain networks. The red areas represent the amygdala network light blue is the mentalizing network, dark blue is the empathy network, and green is the mirror/simulation/ action

• Empathy network does not connect to the amygdala network

Theory of mind

Understanding others’ mental states

Empathy

medial prefrontal involvement

Reflective system

deliberate  (slow, rule following, neutral: lateral prefrontal cortex, medial temporal, posterior parietal cortex)

Reflexive system

fast, emotional  (ventromedial prefrontal cortex, ventral striatum [nucleus accumbens])

Left hemisphere

language, analytic tasks

Right hemisphere

spatial, holistic tasks

Split-brain studies

confirm specialization

Females

language + verbal fluency

Males

spatial + mental rotation

Females

greater interhemispheric connectivity

Males

greater intrahemispheric connectivity

Brain disorders arise through interactions among:

• Genetic/epigenetic factors

• Developmental abnormalities

• Cell death

• Loss of connections

• Stress/environment

Diagnosis & Classification

• ICD [International Classification of Diseases][World Health Organization International Classification of Diseases] [medical one]

• DSM [Aids in diagnosis and treatment begins from the premise that labeling a condition will lead to understanding of the condition and ways of treating it] [Labeling leads to understanding]

• RDoC [Research Domain Criteria: to understand the nature of mental health and illness in terms of varying degrees of dysfunction in general psychological/biological systems. Understanding the basic biological function will lead to understanding the malfunction and treatment] [understanding biology leads to understanding]

• Symptoms ≠ mechanisms

Treatment Approaches

• Behavioral modification [therapist apply the principles developed from laboratory studies of learning by reinforcement, including operant and classical conditioning]

• Cognitive-behavioral therapy (change the thought, change behavior. Cognitive therapy is just events and thoughts.)

• Neuropsychological rehabilitation (retraining the brain to complete tasks) [Therapy aims to retrain people in the fundamental cognitive processes they lost and exploit those that remain. Neurocognitive programs are being developed to improve functional outcomes within the limitation of a brain injury (following TB and stroke)]

• Psychotherapy: mental health treatment 

• Physical activity (activates many parts of the brain)

• Music therapy (Activation of motor and premotor cortices 

• VR therapy - The patient interacts with a virtual world like a character in a computer game

• Real-time fMRI + biofeedback [Real-time fMRI individuals learn to change their behavior by controlling their pattern of brain activation; behavior-modification techniques using biofeedback

• Form of neural plasticity in which in the individual learns new strategies guided by brain activation 

Schizophrenia Symptoms

• Delusions (beliefs that distort reality). 

• Hallucinations (perceptions that don’t align with reality) Distorted perceptions

• Disorganized speech/behavior: incoherent statements. Word salad. 

• Disorganized behavior or Excessive agitation

• Catatonia (slowed movement)

• Negative symptoms: blunted emotions or loss of interest and drive: the absence of some normal response

Biological Correlates of Schizophrenia

• The genetic concordance 80% of twins.

• 300 mutations of ten different genes

• Enlarged ventricles (thinner cortex) 

• Thinner cortex (impacted frontal lobe and medial temporal lobe)

• Excessive pruning

• Dopamine, GABA, glutamate dysfunction

• Decreased

Major Depression

• Worthlessness

• Guilt

• Sleep change

• Slowed behavior

• Suicidal ideation

Bipolar Disorder

Alternation of depression + mania

• Mania -unhelpful anxiety 

• Anxiety disorders - physiological response

Stress Reactivity / HPA Axis

Excess cortisol damages feedback systems

• HPA hypothalamic-pituitary-adrenal circuit; controls the production and release of hormones related to stress

• Constant inflammation from stress has negative impact

Treatment

• SSRIs

• Ketamine

• CBT

Neurogenesis thought to be involved

Anxiety Disorders

• Phobias

• Panic disorder

• OCD

• PTSD

• Generalized anxiety disorder

Treatment

• SSRIs benzodiazepines - xanax highly addictive, high threshold for tolerance

• CBT exposure

Traumatic Brain Injury (TBI)

• Most common in people <40 yrs and men

• Coup + contrecoup injury (specific type of injury: coup is where it starts, contrecoup coup. Frontal lobe has more damage) (hit the back of your head not processing vision well) shearing happens when axons and neurons have friction rubbed across them. (hematoma bruise, edema swelling).

• Cognitive slowing, personality change

• Concussion → risk of CTE [Neurofibrillary tangles, plaques, , Alzeimers D, Parkinson’s D (mild TBI)

• Recovery: most gains first 6–9 months; memory recovers slowest. [talking about concussion to moderate and severe. Post concussive syndrome, carrying symptoms with them. Residual problems with memory.]

Stroke

• Ischemic vs hemorrhagic [blockage (more common), bleeding. Strokes create] 

• Glutamate + Ca²⁺ toxicity [Release massive amounts of glutamate, causing hyperpolarization and toxic levels of calcium. Brain tissue become swollen and inflamed

Diaschisis (remote shutdown areas distinct from the damage are functionally depressed) [when corpus callosum and part of the brain is pushed aside and against the skull

Stroke Treatment

• t-PA (within hours) [Tissue plasminogen activator, must be administered within 3-5 hours to be effective. If t-PA not available they will be given a neuroprotectant to block the cascade of events, breaks down ischemic stroke]

• Rehabilitation [music and singing. Speech therapy. Transmagnetic stimulation.

• Constraint-induced therapy: intact limb is held in a sling for several hours per day, forcing the patient to use the impaired limb. An important component of these treatments is a posttreatment contract in which the patients continue to practice after the formal therapy is completed.

• TMS (Transcranial magnetic stimulation, Magnetic coil placed over the scalp induces an electrical current) 

• Music-based therapies

Epilepsy

• Recurrent, spontaneous seizures

• Focal vs generalized [focal: very specific. Can have motor or sensory systems associated with it. Generalized starts focally and spreads] [

• Generalized: tonic–clonic sequence [Tense up, and then convulse]

• Status epilepticus → emergency [administer a GABA agonist or glutamate antagonist. (intractable epilepsy: antiseizure drugs fail to control the condition completely)

• Treatment: GABA agonist, glutamate antagonist, DBS, surgery.

Multiple Sclerosis

• Autoimmune demyelination

• Women > men

• Remissions and relapses [brian can remyelinate. Over time causes black hole in the brain]

• Causes may include infection, immune mechanisms, Vitamin D deficiency 

• [impact cortical grey matter more than white matter]

Alzheimer Disease

• Progressive cognitive decline

• Amyloid plaques [clumps of abnormal protein, chiefly in the cortical areas]

• Neurofibrillary tangles [accumulation of microtubules from dead cells found in both neocortex and allocortex]

• Cortical atrophy

• Loss of neurotransmitters

Parkinson Disease

• Loss of dopamine in substantia nigra

• Symptoms:

  • Tremor at rest

  • Rigidity

  • Bradykinesia

  • Postural issues

• On-off episodes

• Emotional/cognitive changes possible

Hippocampus in Explicit Memory

• [memory processing center] [Consolidates new memories. In Consolidation or stabilizing a memory trace after learning, memories move from hippocampus to diffuse regions in the neocortex]

Amygdala in EM

•  [emotional processing][key structure in emotional memory] [amygdala has close connections with medial temporal cortical structures and the rest of the cortex]

Entorhinal cortex in EM

• [first area to show death in alzheimers, main interface between hippocampus and neocortex] [Receives projections from parahippocampal and perirhinal cortices] 

Parahippocampal + Perirhinal cortices in EM

• context and object recognition [gyri that helps hippocampus and entorhinal. Perirenal is what pulls in the visual information ventral. Parahippocampus pulls in from dorsal stream] [Parahippocampal cortex receives connections from the parietal cortex. Believed to take part in visuospatial processing. Parirhinal cortex received connections from the visual region of the ventral stream. Believed to take part in visual object memory]

Prefrontal cortex in EM

(short-term & temporal ordering) [the prefrontal cortex is central to maintaining temporary (short term) explicit memories and memory for the recency (chronological order) of explicit events

Basal ganglia in IM

[Receive input from the entire neocortex and send projections first to the ventral thalamus and then to the premotor cortex. Also receive widely and densely distributed projections from dopamine-producing cells in the substantia nigra] {procedural and habit learning} behavior

Substantia nigra in IM

[basal ganglia receive widely and densely distributed projections from dopamine-producing in the substantia nigra] [dopamine appears necessary for basal ganglia circuits to function and may indirectly participate in implicit memory formation] {modulating motor movement and reward function as part of the basal ganglia circuitry}

Ventral thalamus in IM

[receives projections from the basal ganglia 1st] {coordinating information between the hippocampus and medial prefrontal cortex for system consolidation (strategy shifting)}relays motor information

Premotor cortex in IM

•  [receives projections from the basal ganglia 2nd] {Preparing and selecting movements based on sensory and cognitive information}