LECTURE 11 \u2013 PHS 3341.docx - LECTURE 11 \u2013 PHS 3341 SPECIAL CORTICAL FUNCTION 7.0 Explain the and describe the brain waves 7.1 Describe the stages of

LECTURE 11 u2013 PHS 3341.docx - LECTURE 11 u2013 PHS...

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Unformatted text preview: LECTURE 11 – PHS 3341 SPECIAL CORTICAL FUNCTION 7.0 Explain the electroencephalogram and describe the brain waves 7.1 Describe the stages of sleep and discuss their functions 7.2 Explain the function of the reticular activating system 7.3 Briefly define hemispheric lateralization 7.4 Describe the stages of memory, categories of memory, and discuss the processes involved in transfer of information Sleep: An Active Process (124-126) • Consciousness refers to subjective awareness of the external world and self • States of consciousness in decreasing order of arousal level: 1. maximum alertness 2. wakefulness 3. sleep (stages 1–4 and paradoxical) 4. coma • Sleep is not just decreased mental alertness but is an actively initiated and maintained process with its own neural circuits and neurotransmitters that runs counter to those for active consciousness • Sleep is initiated by the brain and performs functions beneficial to the brain • Not accompanied by a reduction in neural activity • Leading theories of why we need sleep are restoration, recovery and memory consolidation EEG Patterns during Sleep • Alternating between slow-wave sleep and paradoxical (REM) sleep • Slow-wave sleep is characterized by slow waves on the EEG • • • REM sleep is characterized by an EEG pattern similar to that of an alert, awake individual Also exhibits rapid eye movements, paralysis of non ocular muscles, dreaming, and abrupt changes in behavior Eyes are active during sleep but the rest of the muscles in the body are inactive by descending pathways Electroencephalograms • Electroencephalogram = EEG • Represents EPSPs and IPSPs in the cell bodies and dendrites located in the cortical layers • Used as a clinical tool in the diagnosis of cerebral dysfunction • Height of EEG doesn’t reflex the strength of the signal Extracellular voltage changes within the cerebral cortex are just strong enough to be carried through the cerebrospinal fluid, dura mater, skull and scalp to be detected as very small voltages by scalp electrodes (1/1000 th the size of an action potential) The scalp electrodes don’t detect individual neuron depolarizations but instead detect groups of neurons depolarizing at the same time. The larger the group the greater the amplitude measured by the scalp electrode. It does not measure action potentials. The size of EEG voltage fluctuations depends on the number of cortical neurons undergoing graded potentials at the same time – synchrony. Neurons with simultaneous dendritic depolarization, seen most dramatically in epilepsy Figure 3-23 EEG patterns during wake and different types of slow-wave and paradoxical sleep. Note that the EEG pattern during paradoxical (REM) sleep is similar to that of an alert, awake person, whereas the pattern during slow-wave sleep displays distinctly different waves. Wakefulness and Sleep Role of the Reticular Activating System (RAS) • Sleep and wakefulness are integrative functions that are controlled by the reticular activating system – Arousal (in the thalamus), or awakening from a sleep, involves increased activity of the RAS. – When the RAS is activated, the cerebral cortex is also activated and arousal occurs. – The result is a state of wakefulness called consciousness. – The RAS becomes active in REM sleep and correlates with dreaming. - RAS has connections to cortex & spinal cord. Many types of inputs can activate the RAS---pain, light, noise, muscle activity, touch but not smell (smelling salts) Coma is sleep-like state A person in a deep coma (upper RAS damage) has no reflexes. A person with lower RAS impairment (fentanyl overdose) looses brainstem functions like respiratory and cardiovascular control. Figure 3-22 The reticular activating system. The reticular formation, a widespread network of neurons within the brain stem (in red), receives and integrates all synaptic input. The reticular activating system, which promotes cortical alertness and helps direct attention toward specific events, consists of ascending fibres (in blue) that originate in the reticular formation and carry signals upward to arouse and activate the cerebral cortex. These projections are at the basis of cholinergic disruption of memory and ordered thought scopolamine treats motion sickness but can cause amnesia Damage to this nucleus does not result in a coma like it would in the reticular activating system, but it results in dementia Hippocampus – main site for memory formation Awake state • Depends on acetylcholine - cholinergic cell groups, located in the midbrain promote cortical activation during waking • Depends on adenosine – caffeine is an antagonist of brain receptors for adenosine: Decaf 12 mg, Espresso 75 mg, Brewed 200 mg, Red Bull 80 mg • Adenosine makes you tired, amount increases throughout the day • Caffeine inhibits adenosine • Depends on histamine – antihistamines have a powerful hypnotic effect and for this reason are often used as nonprescription sleep aids • Depends on the neuropeptide orexin in the hypothalamus – orexin neurons strongly excite various brain nuclei with important roles in wakefulness including the histamine and acetylcholine systems and play an important role in stabilizing wakefulness and sleep. Lobes in the Cerebral Cortex • Each hemisphere divided into four lobes: – Occipital lobes: houses visual cortex – Temporal lobes: houses auditory cortex • Hippocampus – only 3 layers instead of 6 – Parietal lobes: receiving and processing of somatosensory input – Frontal lobes: voluntary motor activity, speaking, and elaboration of thought The Frontal Lobes • Primary motor cortex: plan and execute movements • Motor homunculus: depicts the location and relative amount of motor cortex devoted to output to the muscles of each body part The Parietal Lobes • Somaesthetic sensations • Somatosensory cortex • Proprioception • Sensory homunculus – The size of each body part indicates the relative proportion of the somatosensory cortex devoted to that area The Association Areas • Motor, sensory, and language areas account for only about half of the total cerebral cortex • Remaining areas are called association areas – Prefrontal association cortex – Parietal–temporal–occipital association cortex – Limbic association cortex Language • Broca’s area: speaking ability • Wernicke’s area: language comprehension • Language disorders – Aphasias – Speech impediments – Dyslexia Figure 3-12 Cortical pathway for speaking a written word or naming a visual object. The grey arrows and square numbers with accompanying explanation indicate the pathway used to speak about something seen. Similarly, appropriate muscles of the hand can be commanded to write the desired words. Hemispheric Lateralization - In terms of anatomical appearance and definitive function, the brain is equally distributed into right and left hemispheres. - However, language is found on only one side and this is usually the left-hand side even in left-handed individuals. - The left hand side is also dominant for fine motor control in right handed people. - Each hemisphere is somewhat specialized relative to more subtle types of mental activities. The left cerebral hemisphere excels at logical, analytic, sequential and verbal tasks such as math, and philosophy. The right cerebral hemisphere excels at non-language skills especially spatial, perception, artistic and musical talent. - The left processes fine detailed (calculating), fragmentary information where as the right hemisphere views the world in big picture, holistic way. Of course the two hemispheres are heavily interconnected by the corpus callosum but on the whole there's a tendency for left hemisphere dominance to be associated with thinkers whereas right hemisphere dominance characterizes creativity. Plasticity and Neurogenesis of Brain Tissue • Ability to change or be functionally remodelled in response to the demands placed on it – More pronounced in early developmental years (children – 700 synapses per second) • When an area of the brain is destroyed, other areas of the brain may gradually assume some or all of the functions of the damaged region • Plasticity – process for memory formation Memory • Memory is the storage and retrieval of information. Storage and retrieval are separate processes, they use different brain structures and can be damaged separately by different brain disorders • The three principles of memory are: – Storage – occurs in stages and is continually changing – Processing – accomplished by the hippocampus and surrounding structures – Memory traces – chemical or structural changes that encode memory • The hippocampus lies within ventricular floor in the temporal lobe but is considered to be part of the limbic lobe. Bilateral damage produces permanent anterograde amnesia. – HM o 2 kinds of amnesia formation of memories (anterograde) & recall of memories (retrograde amnesia)) Stages of Memory • The two stages of memory are short-term memory and long-term memory • Short-term memory (STM, or working memory) – a fleeting memory of the events that continually happen • STM lasts seconds to hours and is limited to 7 or 8 pieces of information • Long-term memory (LTM) has limitless capacity Memory • Storage of acquired knowledge for later recall – Short-term: seconds to hours – Long-term: days to years – Working memory: temporarily holds and interrelates various pieces of information relevant to a current mental task protein synthesis inhibitors impair LTM for a variety of behavioral tasks when infused into the brain around the time of training or following memory retrieval, suggesting that protein synthesis is a critical step in LTM storage in the brain. Short-Term and Long-Term Memory: Different Molecular Mechanisms • Different molecular mechanisms involved – Short-term memory – brain network circuity activity • Habituation • Sensitization – Long-term memory • Activation of specific genes that control synthesis of proteins needed for lasting structural or functional changes in pre or postsynaptic membranes • Memory increases RNA synthesis Short-Term Memory • Different molecular mechanisms involved in short-term and long-term memory – Short-term memory • Habituation: decreased responsiveness to a repetitive and indifferent stimulus • Sensitization: increased responsiveness to mild stimuli following a noxious stimuli Amnesia • Amnesia refers to the loss of memory • Anterograde amnesia is the loss of memory for events that occur after the trauma; the inability to form new memories. Storage • Retrograde amnesia is the loss of memory for events that occurred before the trauma; the inability to recall past events. Recall Transfer from STM to LTM • Factors that effect transfer of memory from STM to LTM include: – Emotional state – we learn best when we are alert, motivated, and aroused – Rehearsal – repeating or rehearsing material enhances memory - studying – Association – associating new information with old memories in LTM enhances memory – Automatic memory – subconscious information stored in LTM Categories of Memory • The two categories of memory are fact memory and skill memory • Fact (declarative) memory: – Entails learning explicit information – Is related to our conscious thoughts and our language ability – Is stored with the context in which it was learned – This is what Henry M lost from the removal of his hippocampus Skill Memory • Skill memory is less conscious than fact memory and involves motor activity • It is acquired through practice • Skill memories do not retain the context in which they were learned Comparison of Two Distinct Types of Memory • Declarative memories: “What-type memories,” processed in the hippocampus and associated structures, known as fact memory • Procedural memories: “How to memories,” processed in the basal ganglia and cerebellum • The prefrontal cortex serves as a temporary storage area associated with planning, problem solving, organizing, and inhibiting impulses Structures Involved in Fact Memory • Fact memory involves the following brain areas: – Hippocampus and the amygdala, both limbic system structures – Specific areas of the thalamus and hypothalamus of the diencephalon – Ventromedial prefrontal cortex and the basal forebrain Structures Involved in Skill Memory • Skill memory involves: – Basal ganglia – mediates the automatic connections between a stimulus and a motor response – Portion of the brain receiving the stimulus – Premotor and motor cortex Brain regions involved in declarative (a) versus skill memory (b). ACh and memory/cognition. Figure 3-19 Pathways for long-term potentiation Powerful excitation – opens up the NMDA channel - Causing calcium to enter (like a second messenger) acts on the nucleus to produce more AMPA receptors o Increases the RNA production which ultimately results in this AMPA production o Calcium also acts on nitric oxix synthase (gas – no vesicle release, passes thru PM) can go in any direction Acts on presynaptic terminal – modifies it to release more glutamate = incr more vesicles and efficiency to its release The molecular basis of learning is potentiation at synapses within a neuronal circuit. It can occur either pre or postsynaptically. One simple way is by unblocking the Mg++ (which normally silences the NMDA receptor) – a postsynaptic potentiation. The gaseous neurotransmitter nitric oxide can act presynaptically to increase neurotransmitter release to a given stimulus. Long term potentiation is seen in the hippocampus and results from an increase in synaptic strength at a synapse (increased synaptic weight) following a strong stimulus (B). Note the potentiated response (solid line in C) to a single input pulse relative to that seen in A. - Big stimulation Incr in presynaptic vesicles and post synaptic receptors Mechanisms of Memory • Neuronal RNA content is altered • Calcium, cyclic AMP causes nucleus to produce more • Dendritic spines change shape • Extracellular proteins are deposited at synapses involved in LTM • Number and size of presynaptic terminals may increase • More neurotransmitter is released by presynaptic neurons • New hippocampal neurons appear (rare and highly localized) • Long-term potentiation (LTP) is involved and is mediated by NMDA receptors • Synaptic events involve the binding of brain-derived neurotropic factor (BDNF) • BDNF is involved with Na+, Ca2+, and Mg2+ influence at synapses • Disruption of BDNF leads to arrest of intellectual development at 2 years of age ...
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