The Central Nervous System: Part C

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Chapter 12 - The Central Nervous System
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The Central Nervous System: Part C
The Central Nervous System: Part C
Presentation transcript:

The Central Nervous System: Part C 12 The Central Nervous System: Part C

Functional Brain Systems Networks of neurons that work together and span wide areas of the brain Limbic system Reticular formation

Limbic System Structures on the medial aspects of cerebral hemispheres and diencephalon Includes parts of the diencephalon and some cerebral structures that encircle the brain stem

Diencephalic structures of the limbic system Corpus callosum •Fornix Fiber tracts connecting limbic system structures Septum pellucidum Diencephalic structures of the limbic system Corpus callosum •Fornix •Anterior thalamic nuclei (flanking 3rd ventricle) •Anterior commissure Cerebral struc- tures of the limbic system •Hypothalamus •Mammillary body •Cingulate gyrus •Septal nuclei •Amygdala •Hippocampus •Dentate gyrus •Parahippocampal gyrus Olfactory bulb Figure 12.18

Emotional or affective brain Limbic System Emotional or affective brain Amygdala—recognizes angry or fearful facial expressions, assesses danger, and elicits the fear response Cingulate gyrus—plays a role in expressing emotions via gestures, and resolves mental conflict Puts emotional responses to odors Example: skunks smell bad

Limbic System: Emotion and Cognition The limbic system interacts with the prefrontal lobes, therefore: We can react emotionally to things we consciously understand to be happening We are consciously aware of emotional richness in our lives Hippocampus and amygdala—play a role in memory

Three broad columns along the length of the brain stem Reticular Formation Three broad columns along the length of the brain stem Raphe nuclei Medial (large cell) group of nuclei Lateral (small cell) group of nuclei Has far-flung axonal connections with hypothalamus, thalamus, cerebral cortex, cerebellum, and spinal cord

Reticular Formation: RAS and Motor Function RAS (reticular activating system) Sends impulses to the cerebral cortex to keep it conscious and alert Filters out repetitive and weak stimuli (~99% of all stimuli!) Severe injury results in permanent unconsciousness (coma)

Reticular Formation: RAS and Motor Function Helps control coarse limb movements Reticular autonomic centers regulate visceral motor functions Vasomotor Cardiac Respiratory centers

(touch, pain, temperature) Radiations to cerebral cortex Visual impulses Auditory impulses Reticular formation Descending motor projections to spinal cord Ascending general sensory tracts (touch, pain, temperature) Figure 12.19

Electroencephalogram (EEG) Records electrical activity that accompanies brain function Measures electrical potential differences between various cortical areas

(a) Scalp electrodes are used to record brain wave activity (EEG). Figure 12.20a

Brain Waves Patterns of neuronal electrical activity Generated by synaptic activity in the cortex Each person’s brain waves are unique Can be grouped into four classes based on frequency measured as Hertz (Hz)

Types of Brain Waves Alpha waves (8–13 Hz)—regular and rhythmic, low-amplitude, synchronous waves indicating an “idling” brain Beta waves (14–30 Hz)—rhythmic, less regular waves occurring when mentally alert Theta waves (4–7 Hz)—more irregular; common in children and uncommon in adults Delta waves (4 Hz or less)—high-amplitude waves seen in deep sleep and when reticular activating system is damped, or during anesthesia; may indicate brain damage

Alpha waves—awake but relaxed 1-second interval Alpha waves—awake but relaxed Beta waves—awake, alert Theta waves—common in children Delta waves—deep sleep (b) Brain waves shown in EEGs fall into four general classes. Figure 12.20b

Brain Waves: State of the Brain Change with age, sensory stimuli, brain disease, and the chemical state of the body EEGs used to diagnose and localize brain lesions, tumors, infarcts, infections, abscesses, and epileptic lesions A flat EEG (no electrical activity) is clinical evidence of death

Epilepsy A victim of epilepsy may lose consciousness, fall stiffly, and have uncontrollable jerking Epilepsy is not associated with intellectual impairments Epilepsy occurs in 1% of the population

Absence seizures, or petit mal Epileptic Seizures Absence seizures, or petit mal Mild seizures seen in young children where the expression goes blank Tonic-clonic (grand mal) seizures Victim loses consciousness, bones are often broken due to intense contractions, may experience loss of bowel and bladder control, and severe biting of the tongue

Control of Epilepsy Anticonvulsive drugs Vagus nerve stimulators implanted under the skin of the chest can keep electrical activity of the brain from becoming chaotic

Consciousness Conscious perception of sensation Voluntary initiation and control of movement Capabilities associated with higher mental processing (memory, logic, judgment, etc.) Loss of consciousness (e.g., fainting or syncopy) is a signal that brain function is impaired

Consciousness Clinically defined on a continuum that grades behavior in response to stimuli Alertness Drowsiness (lethargy) Stupor Coma

Two major types of sleep (defined by EEG patterns) State of partial unconsciousness from which a person can be aroused by stimulation Two major types of sleep (defined by EEG patterns) Nonrapid eye movement (NREM) Rapid eye movement (REM)

Sleep First two stages of NREM occur during the first 30–45 minutes of sleep Fourth stage is achieved in about 90 minutes, and then REM sleep begins abruptly

Awake REM: Skeletal muscles (except ocular muscles and diaphragm) are actively inhibited; most dreaming occurs. NREM stage 1: Relaxation begins; EEG shows alpha waves, arousal is easy. NREM stage 2: Irregular EEG with sleep spindles (short high- amplitude bursts); arousal is more difficult. NREM stage 3: Sleep deepens; theta and delta waves appear; vital signs decline. NREM stage 4: EEG is dominated by delta waves; arousal is difficult; bed-wetting, night terrors, and sleepwalking may occur. (a) Typical EEG patterns Figure 12.21a

Sleep Patterns Alternating cycles of sleep and wakefulness reflect a natural circadian (24-hour) rhythm RAS activity is inhibited during, but RAS also mediates, dreaming sleep The suprachiasmatic and preoptic nuclei of the hypothalamus time the sleep cycle A typical sleep pattern alternates between REM and NREM sleep

(b) Typical progression of an adult through one night’s sleep stages Awake REM Stage 1 Stage 2 Non REM Stage 3 Stage 4 Time (hrs) (b) Typical progression of an adult through one night’s sleep stages Figure 12.21b

Importance of Sleep Slow-wave sleep (NREM stages 3 and 4) is presumed to be the restorative stage People deprived of REM sleep become moody and depressed REM sleep may be a reverse learning process where superfluous information is purged from the brain Daily sleep requirements decline with age Stage 4 sleep declines steadily and may disappear after age 60

Sleep Disorders Narcolepsy Insomnia Sleep apnea Lapsing abruptly into sleep from the awake state Insomnia Chronic inability to obtain the amount or quality of sleep needed Sleep apnea Temporary cessation of breathing during sleep

Language Language implementation system Basal nuclei Broca’s area and Wernicke’s area (in the association cortex on the left side) Analyzes incoming word sounds Produces outgoing word sounds and grammatical structures Corresponding areas on the right side are involved with nonverbal language components

Storage and retrieval of information Two stages of storage Memory Storage and retrieval of information Two stages of storage Short-term memory (STM, or working memory)—temporary holding of information; limited to seven or eight pieces of information Long-term memory (LTM) has limitless capacity

Outside stimuli General and special sensory receptors Afferent inputs Temporary storage (buffer) in cerebral cortex Data permanently lost Data selected for transfer Automatic memory Forget Short-term memory (STM) Forget Data transfer influenced by: Retrieval Excitement Rehearsal Association of old and new data Long-term memory (LTM) Data unretrievable Figure 12.22

Transfer from STM to LTM Factors that affect transfer from STM to LTM Emotional state—best if alert, motivated, surprised, and aroused Rehearsal—repetition and practice Association—tying new information with old memories Automatic memory—subconscious information stored in LTM

Declarative memory (factual knowledge) Categories of Memory Declarative memory (factual knowledge) Explicit information Related to our conscious thoughts and our language ability Stored in LTM with context in which it was learned

Nondeclarative memory Categories of Memory Nondeclarative memory Less conscious or unconscious Acquired through experience and repetition Best remembered by doing; hard to unlearn Includes procedural (skills) memory, motor memory, and emotional memory

Brain Structures Involved in Declarative Memory Hippocampus and surrounding temporal lobes function in consolidation and access to memory ACh from basal forebrain is necessary for memory formation and retrieval

(a) Declarative memory circuits Thalamus Basal forebrain Touch Prefrontal cortex Hearing Smell Vision Taste Hippocampus Sensory input Thalamus (a) Declarative memory circuits Association cortex Medial temporal lobe (hippocampus, etc.) Prefrontal cortex ACh ACh Basal forebrain Figure 12.23a

Brain Structures Involved in Nondeclarative Memory Procedural memory Basal nuclei relay sensory and motor inputs to the thalamus and premotor cortex Dopamine from substantia nigra is necessary Motor memory—cerebellum Emotional memory—amygdala

(b) Procedural (skills) memory circuits Sensory and motor inputs Association cortex Basal nuclei Premotor cortex Thalamus Dopamine Premotor cortex Substantia nigra Basal nuclei Thalamus Substantia nigra (b) Procedural (skills) memory circuits Figure 12.23b

Molecular Basis of Memory During learning: Altered mRNA is synthesized and moved to axons and dendrites 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

Molecular Basis of Memory Increase in synaptic strength (long-term potentiation, or LTP) is crucial Neurotransmitter (glutamate) binds to NMDA receptors, opening calcium channels in postsynaptic terminal

Molecular Basis of Memory Calcium influx triggers enzymes that modify proteins of the postsynaptic terminal and presynaptic terminal (via release of retrograde messengers) Enzymes trigger postsynaptic gene activation for synthesis of synaptic proteins, in presence of CREB (cAMP response-element binding protein) and BDNF (brain-derived neurotrophic factor)

Protection of the Brain Bone (skull) Membranes (meninges) Watery cushion (cerebrospinal fluid) Blood-brain barrier

Meninges Cover and protect the CNS Protect blood vessels and enclose venous sinuses Contain cerebrospinal fluid (CSF) Form partitions in the skull

Meninges Three layers Dura mater Arachnoid mater Pia mater

Skin of scalp Periosteum Bone of skull Dura Periosteal mater Meningeal Superior sagittal sinus Arachnoid mater Pia mater Subdural space Arachnoid villus Blood vessel Subarachnoid space Falx cerebri (in longitudinal fissure only) Figure 12.24

Dura Mater Strongest meninx Two layers of fibrous connective tissue (around the brain) separate to form dural sinuses

Dural septa limit excessive movement of the brain Dura Mater Dural septa limit excessive movement of the brain Falx cerebri—in the longitudinal fissure; attached to crista galli Falx cerebelli—along the vermis of the cerebellum Tentorium cerebelli—horizontal dural fold over cerebellum and in the transverse fissure

Superior sagittal sinus Falx cerebri Straight sinus Crista galli of the ethmoid bone Tentorium cerebelli Falx cerebelli Pituitary gland (a) Dural septa Figure 12.25a

Arachnoid Mater Middle layer with weblike extensions Separated from the dura mater by the subdural space Subarachnoid space contains CSF and blood vessels Arachnoid villi protrude into the superior sagittal sinus and permit CSF reabsorption

Skin of scalp Periosteum Bone of skull Dura Periosteal mater Meningeal Superior sagittal sinus Arachnoid mater Pia mater Subdural space Arachnoid villus Blood vessel Subarachnoid space Falx cerebri (in longitudinal fissure only) Figure 12.24

Pia Mater Layer of delicate vascularized connective tissue that clings tightly to the brain

Cerebrospinal Fluid (CSF) Composition Watery solution Less protein and different ion concentrations than plasma Constant volume

Cerebrospinal Fluid (CSF) Functions Gives buoyancy to the CNS organs Protects the CNS from blows and other trauma Nourishes the brain and carries chemical signals

Right lateral ventricle (deep to cut) Superior sagittal sinus 4 Choroid plexus Arachnoid villus Interventricular foramen Subarachnoid space Arachnoid mater Meningeal dura mater Periosteal dura mater 1 Right lateral ventricle (deep to cut) Choroid plexus of fourth ventricle 3 Third ventricle CSF is produced by the choroid plexus of each ventricle. 1 Cerebral aqueduct Lateral aperture Fourth ventricle CSF flows through the ventricles and into the subarachnoid space via the median and lateral apertures. Some CSF flows through the central canal of the spinal cord. 2 Median aperture 2 Central canal of spinal cord CSF flows through the subarachnoid space. 3 (a) CSF circulation CSF is absorbed into the dural venous sinuses via the arachnoid villi. 4 Figure 12.26a

Choroid Plexuses Produce CSF at a constant rate Hang from the roof of each ventricle Clusters of capillaries enclosed by pia mater and a layer of ependymal cells Ependymal cells use ion pumps to control the composition of the CSF and help cleanse CSF by removing wastes

containing glucose, oxygen, vitamins, and ions (Na+, Cl–, Mg2+, etc.) Ependymal cells Capillary Section of choroid plexus Connective tissue of pia mater Wastes and unnecessary solutes absorbed CSF forms as a filtrate containing glucose, oxygen, vitamins, and ions (Na+, Cl–, Mg2+, etc.) Cavity of ventricle (b) CSF formation by choroid plexuses Figure 12.26b

Blood-Brain Barrier Helps maintain a stable environment for the brain Separates neurons from some bloodborne substances

Blood-Brain Barrier Composition Continuous endothelium of capillary walls Basal lamina Feet of astrocytes Provide signal to endothelium for the formation of tight junctions

(a) Astrocytes are the most abundant CNS neuroglia. Capillary Neuron Astrocyte (a) Astrocytes are the most abundant CNS neuroglia. Figure 11.3a

Blood-Brain Barrier: Functions Selective barrier Allows nutrients to move by facilitated diffusion Allows any fat-soluble substances to pass, including alcohol, nicotine, and anesthetics Absent in some areas, e.g., vomiting center and the hypothalamus, where it is necessary to monitor the chemical composition of the blood

Homeostatic Imbalances of the Brain Traumatic brain injuries Concussion—temporary alteration in function Contusion—permanent damage Subdural or subarachnoid hemorrhage—may force brain stem through the foramen magnum, resulting in death Cerebral edema—swelling of the brain associated with traumatic head injury

Homeostatic Imbalances of the Brain Cerebrovascular accidents (CVAs)(strokes) Blood circulation is blocked and brain tissue dies, e.g., blockage of a cerebral artery by a blood clot Typically leads to hemiplegia, or sensory and speed deficits Transient ischemic attacks (TIAs)—temporary episodes of reversible cerebral ischemia Tissue plasminogen activator (TPA) is the only approved treatment for stroke

Homeostatic Imbalances of the Brain Degenerative brain disorders Alzheimer’s disease (AD): a progressive degenerative disease of the brain that results in dementia Parkinson’s disease: degeneration of the dopamine-releasing neurons of the substantia nigra Huntington’s disease: a fatal hereditary disorder caused by accumulation of the protein huntingtin that leads to degeneration of the basal nuclei and cerebral cortex