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Neurophysiology II.docx

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Western University
Physiology 3120
Tom Stavraky

Neurophysiology II Consciousness, Evoked Potential, EEG & Sleep • Consciousness: awareness of environment & oneself • Two components o Content of consciousness  Cerebral cortex: memory, perceptions of sensory experience (auditory, visual, somatosensory & vestibular) & attention o Level of consciousness  Brainstem reticular formation: awake, alert & sleep Reticular Formation • Ascending reticular activating system – also descending connection o Ascending through the thalamus o Projects to widespread areas of cortex o If you put an electrode into region of a sleeping cat – electrically stimulate at low voltages (small current) – wakes up sleeping cat o Pull electrode out & apply to adjacent region – cat would not wake up but HR increases o Make bilateral legion of ARAS – will become unconscious/coma  Causes bilateral lesion of brainstem  Bilateral lesion of cerebral cortex (ex. decreased oxygen (anoxia), hematoma (blood clot), produces pressure on cortex) o Decerebration  Equivalent to coma  Person who has a lesion in this area – can become decerebrate  No longer an activating system coming from brainstem  Some activating system left – go into persistent vegetative state • • Chronic state • Show partial arousal • Eyelids can move • May swallow • Make random saccades • Participate in sleep-wake cycle • Are they conscious? (~20% of patients have some resemblance to consciousness) o o Concept of ARAS is still in use but is not emphasized (old/simplistic not specific)  Because reticular formation is known to have specific nuclei & pathways with specific neurotransmitters (NE, E, serotonin, dopamine, Ach) that have specific functions  Simple view: • Ascending projections operate by causing depolarization of outer cortical dendrites • Descending projection (reticulospinal) send post synaptic inhibition to α motorneurons of proximal (postural) muscles during REM sleep Primary Evoked Potential • Change in voltage (recorded on an oscilloscope) • Results from summation of extracellular currents associated with postsynaptic potentials • Not due to local currents associated with action potentials • Primary evoked potential evoked by stimulation of sciatic nerve of left o Incoming afferent will release transmitter that goes to postsynaptic neuron o Causes opening channels – in rushes Na  produces depolarization in lower region of cortex o +++ in lower region o Current actually flowing in opposite direction to what you would normally think (up & out and around in a circle) o Depolarization and rest of dendrite is at RMP (negative compared to region where +++) o Electrically stimulate sciatic nerve (thousands of axons – all rushing up to cortex) o Happens in multiple neurons  get massive flows of current in direction in image o Current flows are so big that some current can escape through skill and detected by electrode o o Amplified & an evoked potential is recorded o Short latency: 20 ms (visual 80 ms because takes 60 ms to escape retina) – lasts for 10-15 ms o After 20 ms - primary is associated with massive current flows – produced by depolarization of neurons in somatosensory cortex o Evoked potential DOES NOT HAVE TO DO WITH ACTION POTENTIAL • Put electrodes onto the skull of a person – especially in occipital visual cortex • Record differences in EEG patterns • If subject closes eyes and goes into meditative state – record o Have alpha rhythm – going at 8-10 Hz – synchronized – low frequency – high amplitude o Open eyes – alert state o Have beta rhythm – going at 13-Hz – desynchronized – high frequency – low amplitude o Extreme synchronization occurs during non-REM slow wave sleep – delta waves – frequency of 1-2 Hz EEG • Summation of cortical post synaptic potentials occurring in neurons of the neocortex, particularly pyramidal cells • Cause of EEG is the same as cause of evoked potential o Constant depolarization to outer cortical dendrites o Drive is coming from ARAS  through thalamus to cortex  produce post synaptic potentials at cortex • Not due to currents associated with action potentials • Uses: location of an epileptic focus, location of cortical tumors, diagnosis of sleep disorders Sleep • Neural theory o Sleep is due to changes in discharge of neuronal networks o Might be thought that sleep involve a decrease in neural activity – but this is not the case o Rather neurons in some regions decrease and in other regions increase their activity o Other brainstem neuronal networks control REM sleep • Chemical theory o Sleep is due to a release of chemical ex. adenosine, nitric oxide o Substances work in a biochemical cascade • Characteristics of Non-REM slow wave sleep o 70-80% of sleep o 4 stages seen in EEG o Last stage is deep sleep with large slow waves (Δ 1-2 Hz) i.e. strong synchronization o Sleep walking o Nightmares & night terrors o Decrease in blood pressure, heart rate & respiratory rate • Characteristics of REM (paradoxical) sleep o 20-25% of sleep (4-6 periods/night) o Desynchronized EEG (similar to awake activation) – paradox o Inhibited muscle tone due to spinal inhibition from pons – paradox o Deep sleep o Vivid dreams o Rapid eye movements (saccades), finger twitches, middle ear muscles, whiskers in animals o Genital erection o Fluctuations in heart rate, blood pressure and respiratory rate • REM behaviour disorder o When entering REM sleep, some thrash violently, leap out of bed & can attack partners o Not paralyzed during REM sleep as most people are o Appear to be “acting out their dreams” o To little descending postsynaptic inhibition in alpha motorneurons • Cataplexy o Sudden loss of muscle tone in daily activities often elicited by strong emption ex. collapse when about to hit a baseball o Attack is short-lived and does not impair consciousness or memory o Too much descending post synaptic inhibition of alpha motorneurons Hypothalamus & Limbic System Limbic System • Ring of phylogentically primitive & essential (reptilian) cortex around brainstem & interconnecting structures • Limbo means border • Limbic system is the rostral (front) – border of the brain stem • Concerned with emotion, memory, certain motivated behaviors • Structures: hypothalamus, amygdala, hippocampus, cingulate cortex, septum, anterior nuclei of thalamus • Behaviours: feeding, drinking, rage, fear, sexual pleasure, pain & motivation • Fear & Rage o Patients infected with rabies (attacks limbic cortex) show profound changes in emotional state o Experiments bouts of terror & rage o Ex. fights (slap face) – neocortex getting control of & road rage • Pain o People with damage to cingulate cortex (where some pain afferents terminate) feel the sensation of pain but are not bothered by it o I.e. they are missing the emotional component of pain response • Can’t lesion cortex if they feel pain o Delicate o Surrounded by many structures – may damage those structures Hypothalamus • Less than 1% of the volume of brain • Most functions are vital to survival (unlike neocortex where you can take out 1% and it is still functional) • Evolved in animals before mammals • Receives a wide range of sensory information • Compares sensory information with set points • Coordinates a variety of: autonomic, endocrine & behavioral responses o Homeostasis o Coordinating emotional behaviours • Neurons that respond to different properties of the blood o Osmoreceptors o Glucose receptors o Thermoreceptors o Na receptors o Fat/leptin receptors  Leptin (hormone) – produced in fat storage cells and is secreted following feeding (satiety signal)  In some cases, obesity has been associated with mutation in the gene for leptin or the gene for the leptin receptor  No satiety after eating leads to more eating • Interactions with limbic system • Inputs from retina – visual information (circadian rhythms) • Interactions with thalamus (relay control centre) • Outputs of hypothalamus o Posterior pituitary – release of oxytocin, antidiuretic hormone (ADH) o Hypophyseal Portal Veins to Anterior Pituitary – release of LH, FSH, ACTH o Medulla  spinal cord – autonomic nervous system axons • Lesion through midbrain – end up with decerebrate animal – no initiation of spontaneous behaviour • Can make another lesion – leave brainstem intact & leave hypothalamus intact – can remove the entire hemisphere (basal ganglia & thalamus) Parental behaviour Circadian rhythm of every homeostatic mechanism controlled by the hypothalamus Aspects of Hypothalamus • Neural centre o Particular physiological parameter is not controlled by one neural centre o Ex. neurons in limbic system, hypothalamus, medulla & spinal cord contribute to regulation of blood pressure • Problems with stimulations & lesions o Although hypothalamus is small – it’s packed with complex array of cell groups & fibrous pathways o Many ascending & descending pathways to & from cerebral cortex & brainstem pass through hypothalamus o Some results of older stimulation & lesion studies have shown to be caused by involvement of the pathways passing through hypothalamus o Electrically stimulates E and then sleeps/or becomes aroused – stimulates E but also stimulates axon that passes through hypothalamus (going somewhere else) o Stimulate nuclei – control more than one particular variable (eating & rage) o Intermingling of neurons from different specific nuclei • Set point o Hypothalamus regulates basic life processes by comparing sensory information (from sensory input & circulating blood) with biological set points o Ex. if hypothalamus is cold (deviation from set point) it activates a variety of autonomic (cutaneous vasoconstriction), endocrine (increase thyroxine) & behavioral responses (shivering, moving to warmer environment) o Set points for a variety of physiological processes include temperature, blood sugar, sodium, osmolality, hormone levels & body weight o Damage (lesions) to the hypothalamus can change set points o Ex. change in set-point: fever  Pyrogens (ex. interleukins) from bacteria may reset the thermostat in hypothalamus to a higher than normal temperature  Paradoxical situation – high temp., but fever pushes it higher (attempt to conserve or generate heat: shivering)  Treat with aspirin o Ex. change in set-point: experimentally made lesion of ventral medial hypothalamus (eating)  Lesion regarded as satiety centre for eating  overeat • Feedback, feedforward o In examples previously considered hypothalamus has operated by means of feedback control o Also operates by means of feedforward or anticipatory mechanisms o Ex consider a person in shorts & t-shirt who enters a room at 5°C  Temperature receptors in the skin detect the cold & send information to hypothalamus  Hypothalamus activates heat conserving/producing mechanisms before internal temperature begins to fall  Feedforward mechanisms may be activated if a subject thinks about going into cold o Mechanisms improve speed of the body’s homeostatic response & minimizes fluctuations in variable being regulated o In theory if feedforward signals worked perfectly there would be no change in regulated variable o In conclusion, some hormones are controlled by negative feedback mechanisms o However, in healthy mammals under ordinary circumstances, body temperature, blood pressure, feeding & other variables are regulated without resorting to negative feedback (homeostatic) reflexes o It is assumed that these functions are governed by as yet ill-understood feedforward signals origina
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