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Rhythms: We display biological _____ that are tied to the passage of time. (Sleep)
Rhythms
Circadian Rhythms (Sleep)
24-hour biological cycles influential in the regulation of sleep and other physical responses
Rhythyms: The exposure of light (Zeitgerber: time giver) _______________. (Sleep)
Readjusts people's biological clocks by affecting the activity of the hypothalamus
True or false: The hypothalamus is a circadian clock. (Sleep)
True
Hypothalamus: Suprachiasmatic Nucleus (SCN) (Sleep)
Influenced by light; controls the release of melatonin in the pineal gland, which makes us sleepy; light reaches the SCN directly in mammals (retinohypothalamic pathway)
Brain structures for arousal: Reticular information (Sleep)
(Ascending fibers) influence physiological arousal
Brain structures for arousal: Locus coeruleus (Sleep)
Located in the pons
Brain structures for arousal: Hypothalamus (Sleep)
Histamine; Orexin or hypocretin: Necessary to stay awake, inhibition of orexin can cause rats to fall asleep quickly
Brain structures for arousal: Narcolepsy (Sleep)
Lack hypothalamic cells that produce orexin
EEG and Sleep: Stage 1
Lasts 5 to 10 minutes, EEG theta waves
EEG and Sleep: Stage 2
Brief bursts of higher-frequency brain waves
EEG and Sleep: Stage 2 K-complex
Sharp waves; temporal inhibition of neuronal firing; they occur after a sudden interruption within the sleeper's environment, i.e. noise
EEG and Sleep: Stage 2 Sleep Spindles
Generated in the thalamus; Brief: 500 ms, inhibition, the greater number of sleep spindles in participants who napped, the more they were refreshed to performed on a learning task
EEG and Sleep: Stage 3 and 4
Slow-wave sleep; high-amplitude, low-frequency delta waves become prominent; synchronization of low-waves. Reduction of sensory input
EEG and Sleep: Stage 5 (REM sleep)
Rapid Eye Movement; high-frequency beta waves in some areas; most dreams occur during this stage (they also happen during stages 3 and 4)
Sleep Disorders: Insomnia
Chronic problems in getting adequate sleep
Sleep Disorders: Causes of Insomnia
Anxiety and tension, depression
Sleep Disorders: Narcolepsy
Irresistable onsets of sleep durign normal waking periods
Sleep Disorders: Causes of Narcolepsy
Lack hypothalamic cells that produce orexin; Huntington's disease
Sleep Disorders: Sleep apnea
Frequent, reflexive gasping for air (of a minute) that awakens a person
Sleep Disorders: Causes of Sleep apnea
Obesity, genetics, hormones, old-age deterioration of the brain mechanisms that regulate breathing
Sleep Disorders: Night terrors
Abrupt awakenings form NREM sleep accompanied by intense autonomic arousal and feelings of panic
Sleep Disorders: Nightmares
Anxiety-arousing dreams that lead to awakening
Sleep Disorder: Local phenomenon
You may have substanial inhibition in one brain area and not so much in another
Sleep Disorders: Sleepwalking
Motor cortex is awake
Sleep Disorders: REM behavior disorder
People who move around vigorously during their REM periods, acting out their dreams --> GABA deficiency
Sleep Disorders: Lucid Dreaming
Monitoring areas are awake (frontal)
Sleep Disorders: Sleep Paralysis
Waking up while you still cannot move
Fatal Familial Insomnia (FFI) (What happens if we don't sleep?)
Inherited rare disease, onset occurs when a critical amount of protein PrP is converted to protein PrPres; Greater amounts of PrPres than normal in thalamus --> degeneration of thalamus
Fatal Familial Insomnia (FFI) consequences (What happens if we don't sleep?)
Absense of sleep spindles and k-complexes; deep sleep is reduced, REM sleep can happen during waking state; weight loss, elevated sympathetic activation, hallucinations, epileptic seizures, coma, death
Energy Conservation: Sleep
Sleep conserves energy during inefficient times; automatic nervous system; analogous to hibernation
Sleep and memory
Memories that are more important will be consolidated better during sleep
Sleep and memory: EEG patterns during sleep
Resemble those that occur during learning
Sleep and memory: Sleep spindles
Increase in number after new learning
Sleep and memory: Adjustments
The brain makes adjustments when we learn new things; strengthening new synapses; weakening or removing old synapses that are not used anymore
Sleep and memory: Reactivation process
Associated with consolidation begins when a memory is formed, but it becomes strong during sleep
Working Memory: There may be ____ working memory systems
Two working memory (shorterm) systems, for spatial and object memory
Working Memory: The ____ and ___ visual pathways from the _____ and the ______ project to prefrontal cortical regions and support two kinds of short-term memory
Dorsal, ventral, parietal, temporal; The dorsal stream enables vision for action and the ventral stream, vision for perception
Processes in Short Term Memory and LTM: Encoding (from sensory system into Short Term Memory)
Visual objects: right prefrontal and right parahippocampal cortex; Words: left prefrontal and parahippocampal cortex
Processes in STM and Long Term Memory: Consolidation (into Long Term Memory)
Medial temporal lobe: After further processing that involves the hippocampus, the permanent memory storage may require the outermost layer of the cortex, layer I, which has few neuronal cell bodies but is packed with synapses; Engrams: What pathway (visual cortex for visual objects, auditory cortex for auditory objects)
Processes in STM and Long Term Memory: Retrieval
Requires attention (frontal areas). Retrieval from LTM makes the memories plastic again and they can be updated -- important for PTSD memory
Long-Term Explicit Memory: Episodic Memory
Memory of life experiences centered on the person herself
Long-Term Explicit Memory: Semantic Memory
Knowledge about the world -nonautobiographical knowledge-. I.e. ability to recognize family, friends, information learned in school...
Long-Term Explicit Memory: Neural Substrates
Temporal-frontal-lobes, ventral stream, temporal lobe: hippocampus and rhinal cortex mainly, acetylcholine, serotonin, and noradrenaline
Long-Term Memory and Hippocampus
Explicit memory, specifically episodic
Long-Term Memory and Hippocampus: Spatial Memory
Morris water maze; hippocampus as a spatial map -- place cells, grid cells found in nearby entorhinal cortex; London taxi drivers: hippocampus activates more when they answer to spatial questions
Long-Term Memory and Hippocampus: Contextual memory
The hippocampus brings together representations from various locations and reconstructs the context
Long-Term Implicit Memory: Fear conditioning, amygdala
Damage to the amygdala abolishes emotional memory but has little effect on other types of implicit or explicit memory
Long-Term Implicit Memory: Procedural learning, basal ganglia
People with Parkinson's disease may have problems with this type of memory
Procedural Memory and Basal Ganglia: Basal Ganglia
Stratium, Globus Pallidus, Substantia Nigra; gradual learning of habits; reinforcement-based teaching (trial and error); related to procedural memory; this type of learning is less flexible; you may need to use frontal cortex at the beginning, otherwise it takes a long time to learn
Procedural Memory and Basal Ganglia: Prefrontal Cortex
It is more flexible, switching respones
Long-Term Potentiation: Glutamate Receptors (AMPA and NDMA)
NDMA receptors are blocked by magnesium (positive ions); they open after depolarization
Long-Term Potentiation: Calcium
When calcium (together with sodium) enters through the NDMA channels, it will lead to the release of the protein CREB, that goes to the nucelus and alters genes (gene expression) that can last for months or years
Long-Term Potentiation: Brain-derived neurotrophic factor (BDNF)
These effects are modulated by the BDNF; repeated activation will lead to action protentials that back-propagate into dendrites and release BDNF; BDNF can increase NMDA activity
Amensia: Anterograde amensia
Disruption of memory for experiences after the onset of amnesia
Amensia: Retrograde amensia
Disrupt memory for things learned prior to the event that initiated the amnesia
Amensia: Time-dependent retrograde amnesia
Injury severity determines how far back in time the amnesia extends. People usually start remembering with the passage of time and they only end up with amnesia for a few seconds to minutes for events preceeding the injury
Amnesia: Henry Molaison (HM)
Removed his hippocampus to end his epilespy; he suffered from anterograde amnesia and retrograde amnesia; severe impairement of episodic memory (he could not describe any event that happened after the surgery); people with amensia are as impaired at imagining the future as they are describing the past; better implicit than explicit memory; intact working memory but as soon as he was distracted, the memory was gone within seconds (impaired long term memory); intact procedural memory
Attention definition
Narrowing or focusing awareness selectivity to a part of the sensory environment or to a class of stimuli
Consciousness definition
Synonymous at a primary level with awareness and at a secondary level with awareness of awareness (first person experience of the events that you are aware of)
Attention is primarily a _______ process that ___________.
Top-down process that selects information from a specific part of the sensory world, such as a point in space or an object
Consciousness is not so ____________.
Selective; it summarizes all information pertinent to the individual and its environment
Attention Networks: Alerting Network
Reticular Activating System --> Locus coeruleus (Noradrenaline) acts to prepare regions (alertness) especially in prefrontal and posterior parietal cortex for detecting stimuli rapidly
Attention Networks: Orienting Network
Acetylcholine; Prioritizes sensory input by selecting a sensory modality or a location in space
Attention Networks: Dorsal Attention System
Top-down visuospatial; right-lateralized (neglect syndrome)
Attention Networks Functions: Default mode network (Brain Networks)
Thinking about one's past thinking about the future, or mind wandering (i.e. mPFC, PCC, medial temporal areas)
Attention Networks Functions: Salience network (Brain Networks)
Most active when a behavioral change is needed. If the salience network is not functioning properly, the default network shows excessive activity, leading to lapses in attention (i.e. ACC, insula)
Attention Networks Functions: Dorsal attention system
Top-down visuospatial; right-lateralized (i.e. right IPS, FEF)
Synchrony: How does our brain choose important events from among all of the ongoing sensory information? (Attention)
The attentional system induces synchrony across a population of neurons that assess some sensory signal; importance of temporal positions of action potentials (i.e. several inputs to a given neuron arrive together)
Synchrony: Increasing activity
Increasing activity in the attention network increases brain synchrony globally; increasing activity in the default network may have the opposite effect -- loss of global syndrome
Attention: Meditation
Meditation reduces activity in the default mode network and increases in salience and central executive network connectivity; increased activity of anterior cingulate during meditation
Anatomical Areas: Broca's area (Language)
Inferior frontal gyrus (44 and 45 of Broadmann's map)
Anatomical Areas: Wernicke's area (Language)
Superior temporal gyrus (22 of Broadmann's map)
Anatomical Areas: Hesch'l's gyrus (other important areas for language)
Primary auditory cortex (41, 42)
Anatomical Areas: Premotor area 6 (other important areas for language)
Facial movements (mirror neurons), the dorsal part of the area 6 (SMA) is important for rhythmic mouth movments that articulate sounds
Anatomical Areas: Visual areas (other important areas for language)
Left fusiform cortex (important for reading)
Fluent Aphasias: Wernicke (Language Disorders)
Poor comprehension, paraphasias (the production of unintended syllables, words, or phrases during speech, i.e. "pike" instead of "pipe") and anomias; fluent speech and poor repetition
Fluent Aphasias: Transcortical (Language Disorders)
Extrasylvian regions (POT junction); poor comprehension, paraphasias and anomias; fluent speech and good repetition
Fluent Aphasias: Conduction aphasia (Language Disorders)
Disconnection of fibers that connect language comprehension and speech areas; they can understand language and they may speak fluently (speech sounds and movements are retained), but usually speech is impaired because it cannot be conducted from one region to the other; they may have problems with repetition
Fluent Aphasias: Anomic aphasia (Language Disorders)
May involve damage of pathways in frontal, temporal, and/or parietal lobes; amonia and occasional paraphasias ("spot" instead of "pot"); fluent speech
Nonfluent Aphasias: Broca (Language Disorders)
Speech is impaired, naming is impaired; repetition is limited (i.e. only single words); problems with complex syntax or grammar
Pure Aphasias: Agraphia (Language Disorders)
Writing (normal speech); several types of damage can lead to this problem (i.e. damage in the superior or middle frontal gyri, parietal lobe, sometimes occurs together with alexia)
Pure Aphasias: Alexia (Language Disorders)
Reading (normal speech)
Pure Aphasias: Anarthria (Language Disorders)
Incoordination of the musculature of the mouth
Review: Action Potential
Stimulation that reaches the treshold leads to a massive depolarization of the neuron (sodium channels open and allow sodium inside the membrane)
Review: Peak of Action Potential
Sodium channels close and beacuse potassium channels are still open (potassium ions exit the cell), polarization occurs and the membrane returns to its resting potential
Review: The refractory period
Right after the AP, the membrane is in a refractory period during which it resists the production of other APs; sodium channels are close, potassium exit the cell
Review: Propagation of the action potential
Positive charges (in the inside) depolarize the next area of the membrane, that reaches its treshold and opens its sodium channels; the action potential is regenerated at that point and so on
Review: Hemianopia or hemianopsia
Blindness of half visual field (right or left) because of damage in left or right V1
Review: Blindsight or cortical blindness
Sometimes people with anopsia or hemianopsia respond to the stimuli that they don't consciously see (specific characteristics of the stimulus such as a movement can help)
Review: Cortical color blindness
Damage of a V4 area; imagery and memory are affected too
Review: Visual agnosia
Inability to recognize visual information; geniculostriate and what (ventral) pathways
Review: Apperceptive (Object agnosias)
Inability to develop a percept (i.e. they cannot copy an object)
Review: Associative agnosia (Object agnosias)
Inability to recognize an object despite its apparent perception (i.e. they can copy an object, but cannot recognize it)
Review: Prosopagnosia (Visual agnosia)
Difficulty recognizing familiar faces; bilateral damage of fusiform area (right hemisphere is more important)
Review: Alexia or word blindess (Visual agnosia)
Inability to read; damage of left fusiform area affects word recognition (they can read letter-by-letter). They can use motion (tracing the letters) to read
Review: Simultagnosia (Ataxia)
Patients have problems to perceive more than one object at a time. This rare symptom can occur because of damage in different areas i.e. doral stream (it can occur in patients with Balint's syndrome -- spatial attention problem)
Review: Amusia, Heschl's gyrus (Auditory Disorders)
Impairement to make pitch discriminations; much larger Heschl's gyrus in musicians
Review: Auditory hallucinations (Auditory Disorders)
Spontaneous activity in the auditory regions
Review: Wernicke's aphasia (Auditory Disorders)
Disturbed word recognition, the extreme form being "word deafness", an inability to recognize words despite hearing of pure tones