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85 Cards in this Set

  • Front
  • Back
Functions of Nervous Tissues
1. sensing changes with sensory receptors (sensation)
2. interpreting & remembering changes (integration center)
3. reacting to those changes with effectors
In short: communication system, regulator/control system, and command system)
What is a ligand?
ion molecule that bind with protein
2 types of Ion Channels
1. Leakage (non-gated) channel)
2. Gated channels:
- voltage gated
- ligand gated
- mechanically gated
Leakage (non-gated) Channel
* passive (facilitated diffusion)
* always open
* nerve cells have more K+ than Na+ leakage channel
* resulting membrane permeability to K+ is higher
* resting membrane potential is -70mV in nerve tissue
Gated Channels
1. active open/close in response to a stimulus resulting in neuron excitability
2. Types of Gated Channels:
a. Voltage channel:
* open/close in response to change in voltage
* in membranes of sarcolemma/axolemma (skeletal muscle cells), not in motor-end plates
b. Ligand Gated:
* open/close in response to particular chemical stimuli (hormone, neurotransmitter) bind on receptors
* only on motor-end plates
c. Mechanically-gated channel:
* open/close with mechanical stimulations (stretching, pressure, vibrations)
* on smooth muscle cells
Electrical Signals in Neurons
* Neurons are highly excitable due to Voltage Difference Across the Membrane
* Communicate with 2 types of electrical signals:
1. Action-Potential: all/nothing, travel long distances
2. Graded Potential: local membrane changes only
* In living cells, flow of ions occurs via ion channels in the cell membranes
Resting Membrane Potential
* Is the negative ions along inside of cell membrane and positive ions along the outside
--potential energy difference at rest is -70mV
--cell is then "polarized"
Resting Membrane Potential Exist Because:
1. concentration of ions is different inside and outside
--ECF si rich in Na+ and Cl-
--Cytosol is full of K+, Phosphate and amino acids

2. Membrane permeability is different between Na+ and K+
-- greater permeability for K+ (50-100)
-- inflow of Na+ can't keep up with outflow of K+
-- Na/K pump removes Na+ as it leaks into cell
-- Na/K pump ejects 3Na+ for each 2K+ ions into the cell (ratio is 3:2 for Na+ entry to K+loss via passive channels)
--Resting membrane potential is -90mV (equilibrium potential for K+)
--Typical neuron has resting membrane potential of -70mV
Graded Potentials
= Small deviations from resting potential of -70mV
* hyperpolarization = membrane has become more negative
* depolarization =
membrane has become more positive (less negative)
Local Potentials:
= Local disturbances in membrane potential
-- aka: graded potentials caused by depolarizing of the inside of plasma membrane
-- happens when neuron is stimulated by chemicals, light, heat or mechanical disturbance.
-- depolarization decreases potential across cell membrane due to opening of gated Na+ channels
* Na+ rushes in down concentration and electrical gradients
* Na+ diffuses for short distance inside membrane producing a change in voltage called a LOCAL POTENTIAL
Local Potential (L/P or G/P)
vs
Action Potential (A/P)
* L/P are graded (vary in magnitude accord. to stimulus strength)
* L/P are decremental (get weaker the farther they spread)
* L/P are reversible as K+ diffuses out of the cell
* L/P can either excitatory or inhibitory
How do Graded Potentials Arise?
1. Source of stimuli:
-- mechanical stimulation of membranes with mechanical gated ion channels (pressure)
-- chemical stimulation of membranes with ligand gated ion channels (neurotransmitter)
2. Graded/post-synaptic/ receptor or generator potential
-- ions flow through ion channels and change membrane potential locally
-- amount of change varies with strength of stimuli
3. Flow of current (ions) is local change only
Action Potential
-- Series of rapidly occurring events that change and then restore the membrane potential of a cell to its resting state
-- Ion channels open, Na+ rushes in (depolarization), K+ rushes out (repolarization)
-- All-or-none principal = with stimulation, either happens one specific way or not at all (lasts 1/1000 of a second)
-- Travels (spreads) over surface of cell without dying out
Depolarizing Phase of Action Potential
-- Chemical or mechanical stimulus causes a graded potential to reach at least threshold (-55mV)
-- Voltage-gated Na+ channels open & Na+ rushes into cell
* in resting membrane, inactivation gate of sodium channel is open & activation gate is closed (Na+ can not get in)
* when threshold (-55mV) is reached, both open & Na+ enters
* inactivation gate closes again in few ten-thousandths of second
* only a total of 20,000 Na+ actually enter the cell, but they change the membrane potential considerably (up to +30mV)
--Positive feedback process
Re-polarizing Phase of Action Potential
* When threshold potential of
-55mV is reached, voltage-gated K+ channels open
* K+ channel opening is much
slower than Na+ channel
opening (which causing depolarization)
* When K+ channels finally do open, the Na+ channels have already closed (Na+ inflow stops)
* K+ outflow returns membrane potential to -70mV
* If enough K+ leaves the cell, it will reach a -90mV membrane potential and enter the after-hyperpolarizing phase
* K+ channels close and the membrane potential returns to the resting potential of -70mV
What is Refractory Period of Action Potential?
period of time during which neuron can't generate another action-potential
Types of Refractory Periods
1. Absolute refractory period
-- even very strong stimulus will not begin another AP
-- inactivated Na+ channels must return to the resting state before they can be reopened
-- large fibers have absolute refractory period of 0.4 msec and up to 1000 impulses per second are possible
2. Relative refractory period
-- a supra-threshold stimulus will be able to start an AP
-- K+ channels are still open, but Na+ channels have closed
Summary of Action Potential
* Resting membrane potential is -70mV
* Depolarization is the change from -70mV to +30 mV
* Repolarization is the reversal from +30 mV back to -70 mV)
Propagation of Action Potential
= An action potential spreads (propagates) over the surface of the axon membrane
* as Na+ flows into the cell during depolarization (voltage of adjacent areas is effected and their voltage-gated Na+ channels open)
* self-propagating along the membrane

-- The traveling action potential is called a NERVE IMPULSE
(Local) Anesthetics
-- Prevent opening of voltage-gated Na+ channels
-- Nerve impulses cannot pass the anesthetized region
-- i.e: Novocaine and lidocaine

Regional Anesthetics:
-- chemicals given @ spinal cord/plexus to affect several nerves (ie: epidural)
General Anesthetics:
-- affect synaptic transmission some ESPS (depolarized), some are IPSP (hyper-polarized) >>deals with perception
Continuous Conduction
vs
Saltatory Conduction
1. Continuous conduction (unmyelinated fibers):
step-by-step depolarization of each portion of the length of the axolemma
2. Saltatory conduction
-- depolarization only at nodes of Ranvier where there is a high density of voltage-gated ion channels
-- current carried by ions flows through extracellular fluid from node to node (conduction hops between node of Ranvier
Speed of Impulse Propagation
the propagation speed of a nerve impulse is not related to stimulus strength
>> larger, myelinated fibers conduct impulses faster due to the size and saltatory conduction
Fiber types
1. Type A fibers
-- largest (5-20 microns, 130m/sec)
-- myelinated somatic sensory and motor to skeletal muscle
2. Type B fibers
-- medium (2-3 micron, 15m/sec)
-- myelinated visceral sensory and autonomic pre-ganglionic fibers
3. Type C fibers
-- smallest (.5-1.5 micron, 2m/sec)
-- un-myelinated sensory and autonomic motor fibers
How do we differentiate a light touch from firmer touch?
(Encoding of Stimulus Intensity)
1. Frequency of impulses
-- firm pressure generates impulses at a higher frequency
2. Number of sensory neurons activated
-- firm pressure stimulates more neurons than does a light touch
Action Potentials in Nerve and Muscle
1. Entire muscle cell membrane versus only the axon of the neuron is involved
2. Resting membrane potential
-- nerve is -70mV
-- skeletal & cardiac muscle is closer to -90mV
3. Duration:
-- nerve impulse is 1/2 to 2 msec
-- muscle action potential lasts 1-5 msec for skeletal & 10-300msec for cardiac & smooth
3. Fastest nerve conduction velocity is 18 times faster than velocity over skeletal muscle fiber
Comparison of Graded & Action Potentials
1. Origin
-- GPs arise on dendrites and cell bodies
-- APs arise only at trigger zone on axon hillock
2. Types of Channels
-- AP is produced by voltage-gated ion channels
-- GP is produced by ligand or mechanically-gated channels
3. Conduction
-- GPs are localized (not propagated)
-- APs conduct over the surface of the axon
4. Amplitude
-- amplitude of the AP is constant (all-or-none)
-- amplitude of GP vary depending upon stimulus
5. Duration
-- The duration of the GP is as long as the stimulus lasts
6. Refractory period
-- AP has a refractory period due to the nature of the voltage-gated channels, and the GP has none.
Signal Transmission @ Synapses -- 2 Types of Synapses
1. Electrical
-- ionic current spreads to next cell through gap junctions
-- faster, two-way transmission & capable of synchronizing groups of neurons
2. Chemical
-- one-way information transfer from a presynaptic neuron to a postsynaptic neuron
* axodendritic: from axon to dendrite
* axosomatic: from axon to cell body
* axoaxonic: from axon to axon
Chemical Synapses
-- Action potential reaches end bulb and voltage-gated Ca+ 2 channels open
-- Ca+2 flows inward triggering release of neurotransmitter
-- Neurotransmitter crosses synaptic cleft & binding to ligand-gated receptors
(the more neurotransmitter released, the greater the change in potential of the postsynaptic cell)
-- Synaptic delay is 0.5 msec
-- One-way information transfer
Nervous System Divisions
1. Central nervous system (CNS): brain and spinal cord
2. Peripheral nervous system (PNS): cranial and spinal nerves that contain both sensory and motor fibers
-- connects CNS to muscles, glands & all sensory receptors
Subdivisions of PNS
1. Somatic (voluntary) nervous system (SNS):
-- neurons from cutaneous and special sensory receptors to the CNS (voluntary effectors)
-- motor neurons to skeletal muscle tissue
2. Autonomic (involuntary) nervous systems
-- sensory neurons from visceral organs to CNS
-- motor neurons to smooth & cardiac muscle and glands:
a. sympathetic division (speeds up heart rate)
b. parasympathetic division (slow down heart rate)
3. Enteric nervous system (ENS)
-- involuntary sensory & motor neurons control GI tract
-- neurons function independently of ANS & CNS
Neurons
* Functional unit of nervous system
* Have capacity to produce APs (electrical excitability)
* Cell body
-- single nucleus with prominent nucleolus
-- Nissl bodies (chromatophilic substance)
-- abundant rough ER & free ribosomes for protein synthesis
-- neurofilaments give cell shape and support
-- microtubules move material inside cell
-- lipofuscin pigment clumps (harmless aging)
* Cell processes = dendrites & axons
* Amitotic (your cell is as old as you are)
Dendrites
-- Conducts impulses towards the cell body
-- Typically short, highly branched & unmyelinated
-- Surfaces specialized for contact with other neurons
-- Contains neurofibrils & Nissl bodies
Axons
-- Conduct impulses away from cell body
-- Long, thin cylindrical process of cell
-- Arises at axon hillock (trigger zone)
-- Impulses arise from initial segment (trigger zone)
-- Side branches (collaterals) end in fine processes (=axon terminals)
-- Swollen tips called synaptic end bulbs (synaptic terminals/ boutons) contain vesicles filled with neurotransmitters
Axonal Transport (Axoplasmic Flow Diffusion)
* Cell body is location for most protein synthesis
-- neurotransmitters & repair proteins
* Axonal transport system moves substances
1. slow axonal flow
-- movement in one direction only: away from cell body (remove waste)
-- movement at 1-5 mm per day
2. fast axonal flow
-- moves organelles & materials along surface of microtubules (200-400 mm per day)
-- transports in either direction
-- for use or for recycling in cell body
Axonal Transport & Disease
-- Fast axonal transport route by which toxins or pathogens reach neuron cell bodies
1. Tetanus (Clostridium tetani bacteria)
-- disrupts motor neurons causing painful muscle spasms
-- bacteria enter the body through a laceration or puncture injury
-- more serious if wound is in head or neck because of shorter transit time
Functional Types of Neurons
1. Sensory (afferent) neurons
-- receptors detect changes in body and external environment
-- this information is transmitted into brain or spinal cord
2. Interneurons (association neurons)
-- lie between sensory & motor pathways in CNS
-- 90% of our neurons are interneurons
-- process, store & retrieve information
3. Motor (efferent) neuron
-- send signals out to muscles & gland cells
-- organs that carry out responses called effectors
Functional Classification of Neurons
1. Sensory (afferent) neurons
-- transport sensory information from skin, muscles, joints, sense organs & viscera to CNS
2. Motor (efferent) neurons
-- send motor nerve impulses to muscles & glands
3. Interneurons (association) neurons
-- connect sensory to motor neurons
-- 90% of neurons in the body
Variation in Neuronal Structure
1. Multipolar neuron
-- most common
-- many dendrites/one axon
2. Bipolar neuron
-- one dendrite/one axon
-- olfactory, retina, ear
3. Unipolar neuron
-- sensory from skin & organs to spinal cord
4. Anaxonic neuron
-- many dendrites/no axon
-- help in visual processes
Structural Classification of Neurons
Based on number of processes found on cell body:
1. multipolar = several dendrites & one axon
most common cell type
2. bipolar neurons = one main dendrite & one axon
found in retina, inner ear & olfactory
3. unipolar neurons = one process only(develops from a bipolar)
are always sensory neurons
Neuroglial Cells
* Half of the volume of the CNS
* Smaller cells than neurons
50X more numerous
* Cells can divide
-- rapid mitosis in tumor formation (gliomas)
* 4 cell types in CNS
-- astrocytes
-- oligodendrocytes
-- microglia
-- ependymal
* 2 cell types in PNS
-- schwann cells
-- satellite cells
Astrocytes
* Star-shaped cells
* Form blood-brain barrier by covering blood capillaries
* Metabolize neurotransmitters
* Regulate K+ balance
* Provide structural support
Oligodendrocytes
* Most common glial cell type
* Each forms myelin sheath around more than one axons in CNS
* Analogous to Schwann cells of PNS
Microglia (smallest)
* Small cells found near blood vessels
* Phagocytic role -- clear away dead cells
* Derived from cells that also gave rise to macrophages & monocytes
Ependymal Cells
* Form epithelial membrane lining cerebral cavities & central canal
* Modify cerebrospinal fluid (CSF)
-- Coroid Plexus produces CSF
Satellite Cells
* Flat cells surrounding neuronal cell bodies in peripheral ganglia
* Support neurons in the PNS ganglia
Schwann Cells
* Cells encircling PNS axons
* Each cell produces part of the myelin sheath surrounding an axon in the PNS
Axon Coverings in PNS
* All axons surrounded by a lipid & protein covering (myelin sheath) produced by Schwann cells
* Neurilemma is cytoplasm & nucleus of Schwann cell
(gaps are called nodes of Ranvier)
* Myelinated fibers appear white
-- jelly-roll like wrappings made of lipoprotein (myelin is 20% protein, 80% lipid)
-- acts as electrical insulator
-- speeds conduction of nerve impulses
* Unmyelinated fibers
-- slow, small diameter fibers
-- only surrounded by neurilemma but no myelin sheath wrapping
Myelination in PNS
* Schwann cells myelinate (wrap around) axons in the PNS during fetal development
* Schwann cell cytoplasm & nucleus forms outermost layer of neurolemma with inner portion being the myelin sheath
* Tube guides growing axons that are repairing themselves
Un-myelinated Axons
* Schwann cells hold small nerve fibers in grooves on their surface with only one membrane wrapping
Myelination in CNS
* Oligodendrocytes myelinate axons in the CNS
* Broad, flat cell processes wrap about CNS axons, but the cell bodies do not surround the axons
* No neurilemma is formed
* Little regrowth after injury is possible due to the lack of a distinct tube or neurilemma
Regeneration and Repair
1. Plasticity maintained throughout life
-- sprouting of new dendrites
-- synthesis of new proteins
-- changes in synaptic contacts with other neurons
2. Limited ability for regeneration (repair)
-- PNS can repair damaged dendrites or axons
-- CNS no repairs are possible
Neurogenesis in the CNS
1. Formation of new neurons from stem cells was not thought to occur in humans
-- in 1992 a growth factor was found that stimulates adult mice brain cells to multiply
-- in 1998 new neurons found to form within adult human hippocampus (area important for learning)
2. Factors preventing neurogenesis in CNS
-- inhibition by neuroglial cells, absence of growth stimulating factors, lack of neurolemmas, and rapid formation of scar tissue
Repair Within the PNS-- part I
1. Axons & dendrites may be repaired if
-- neuron cell body remains intact
-- schwann cells remain active and form a tube
-- scar tissue does not form too rapidly
2. Chromatolysis
-- 24 to 48 hours after injury, Nissl bodies break up into fine granular masses
Repair Within the PNS -- part II
3. Between 5 to 5 days:
-- Wallerian degeneration occurs (breakdown of axon & myelin sheath distal to injury)
-- retrograde degeneration occurs back one node
4. Within several months, regeneration occurs
-- neurolemma on each side of injury repairs tube (schwann cell mitosis)
-- axonal buds grow down the tube to r
Gray and White Matter
* White matter = myelinated processes (white in color)
* Gray matter = nerve cell bodies, dendrites, axon terminals, bundles of unmyelinated axons and neuroglia (gray color)
-- In the spinal cord = gray matter forms an H-shaped inner core surrounded by white matter
-- In the brain = a thin outer shell of gray matter covers the surface & is found in clusters called nuclei inside the CNS
Excitatory Cholinergic Synapse
* Nerve signal opens voltage-
gated calcium channels
* Triggers release of ACh which crosses synapse
* ACh receptors trigger opening of Na+ channels producing local potential (postsynaptic potential)
* When reaches -55mV, triggers AP
Inhibitory GABA-ergic Synapse
* Nerve signal triggers release of GABA (GamaAminoButyric Acid) which crosses synapse
* GABA receptors trigger opening of Cl- channels producing hyper-polarization
* Postsynaptic neuron now less likely to reach threshold
Excitatory Adrenergic Synapse
* Neurotransmitter is NE (Norepinephrine)
* Acts through 2nd messenger systems (cAMP: cyclic AMP)
* Receptor is an integral membrane protein associated with a G protein, which activates adenylate cyclase, which converts ATP to cAMP
* cAMP has multiple effects
-- synthesis of new enzymes
-- activating enzymes
-- opening ligand gates
-- produce a postsynaptic potential
Cessation & Modification of the Signal
1. Mechanisms to turn off stimulation
-- diffusion of neurotransmitter away from synapse into ECF where astrocytes return it to the neurons
-- synaptic knob reabsorbs amino acids and monoamines by endocytosis & breaks them down with monoamine oxidase
-- acetylcholinesterase (AChE) degrades ACh in the synaptic cleft (choline reabsorbed & recycled)
2. Neuromodulators modify synaptic transmission
-- raise or lower number of receptors
-- alter neurotransmitter release, synthesis or breakdown
>> nitric oxide stimulates neurotransmitter release
Neural Integration
1. More synapses a neuron has the greater its information-processing capability
-- cells in cerebral cortex with 40,000 synapses
-- cerebral cortex estimated to contain 100 trillion synapses
2. Chemical synapses are decision-making components of the nervous system
-- ability to process, store & recall information is due to neural integration
3. Neural integration is based on types of postsynaptic potentials produced by neurotransmitters
Post-synaptic Potentials
1. Excitatory postsynaptic potentials (EPSP)
-- a positive voltage change causing postsynaptic cell to be more likely to fire (result from Na+ flowing into the cell)
-- glutamate & aspartate are excitatory neurotransmitters
2. Inhibitory postsynaptic potentials (IPSP)
-- a negative voltage change causing postsynaptic cell to be less likely to fire (hyper-polarize) >>result of Cl- flowing into the cell or K+ leaving the cell.
-- glycine & GABA are inhibitory neurotransmitters
3. ACh & norepinephrine vary depending on cell
Excitatory & Inhibitory Potentials
* The effect of a neurotransmitter can be either excitatory or inhibitory
1. a depolarizing postsynaptic potential is called an EPSP
-- it results from the opening of ligand-gated Na+ channels
-- the postsynaptic cell is more likely to reach threshold
2. an inhibitory postsynaptic potential is called an IPSP
-- it results from the opening of ligand-gated Cl- or K+ channels
-- it causes the postsynaptic cell to become more negative or hyper-polarized
-- the postsynaptic cell is less likely to reach threshold
Removal of Neurotransmitter
1. Diffusion
-- move down concentration gradient
2. Enzymatic degradation
-- acetylcholinesterase (AChE)
3. Uptake by neurons or glia cells
-- neurotransmitter transporters
-- Prozac = serotonin reuptake
inhibitor
Spatial Summation
Summation of effects of neurotransmitters released from several end bulbs onto one neuron (at once), multipolar neuron
Temporal Summation
Summation of effect of neurotransmitters released from 2 or more firings of the same end bulb in rapid succession onto a second neuron (over time/ in succession)
Three Possible Responses
1. Small EPSP occurs
-- potential reaches -56 mV only
2. An impulse is generated
-- threshold was reached
-- membrane potential of at least -55 mV
3. IPSP occurs
-- membrane hyper-polarized
-- potential drops below -70 mV
Strychnine Poisoning
* In spinal cord, Renshaw cells normally release an inhibitory neurotransmitter (glycine) onto motor neurons preventing excessive muscle contraction
* Strychnine binds to and blocks glycine receptors in the spinal cord
*Massive tetanic contractions of all skeletal muscles are produced
-- when the diaphragm contracts & remains contracted, breathing can not occur
Neurotransmitter Effects
1. Neurotransmitter effects can be modified
-- synthesis can be stimulated or inhibited
-- release can be blocked or enhanced
-- removal can be stimulated or blocked
-- receptor site can be blocked or activated
2. Agonist (work with)
-- anything that enhances a transmitters effects
3. Antagonist (work against)
-- anything that blocks the action of a neurotransmitter
Small-Molecule Neurotransmitters (part I)
1. Acetylcholine (ACh)
-- released by many PNS neurons & some CNS
-- excitatory on NMJ but inhibitory at others
-- inactivated by AChE (acetylcholinesterase)
2. Amino Acids
-- glutamate released by nearly all excitatory neurons in the brain (inactivated by glutamate specific transporters)
-- GABA is inhibitory neurotransmitter for 1/3 of all brain synapses (Valium is a GABA agonist -- enhancing its inhibitory effect)
Small-Moleculle Neurotransmitters (part II)
3. Biogenic Amines
-- modified amino acids (tyrosine)
* norepinephrine: regulates mood, dreaming, awakening from deep sleep
* dopamine: regulating skeletal muscle tone
* serotonin: control of mood, temperature regulation, & induction of sleep
-- removed from synapse & recycled or destroyed by enzymes (monoamine oxidase or catechol-0-methyltransferase)
Small-Molecule Neurotransmitters (part III)
4. ATP and other purines (ADP, AMP and adenosine)
-- excitatory in both CNS & PNS
-- released with other neurotransmitters (ACh & NE)
5. Gases (nitric oxide or NO)
-- formed from amino acid arginine by an enzyme
-- formed on demand and acts immediately
**diffuses out of cell that produced it to affect neighboring cells
**may play a role in memory & learning
-- first recognized as vasodilator that helps lower blood pressure
Neuropeptides
* 3-40 amino acids linked by peptide bonds
* Substance P: enhances our perception of pain
* Pain relief
-- enkephalins: pain-relieving effect by blocking the release of substance P
-- acupuncture may produce loss of pain sensation because of release of opioids-like substances such as endorphins or dynorphins
Neuronal Circuits
* Neurons in the CNS are organized into neuronal networks
* A neuronal network may contain thousands or even millions of neurons.
* Neuronal circuits are involved in many important activities
-- breathing
-- short-term memory
-- waking up
Types of Neuronal Circuits
1. Diverging -- single cell stimulates many others
2. Converging -- one cell stimulated by many others
3. Reverberating -- impulses from later cells repeatedly stimulate early cells in the circuit (short-term memory)
4. Parallel-after-discharge -- single cell stimulates a group of cells that all stimulate a common postsynaptic cell (math problems)
Multiple Sclerosis (MS)
* Autoimmune disorder causing destruction of myelin sheaths in CNS and PNS
-- sheaths becomes scars or plaques
-- 1/2 million people in the U.S
-- appears between ages 20 and 40
-- females twice as often as males
* Symptoms include muscular weakness, abnormal sensations or double vision
* Remissions & relapses result in progressive, cumulative loss of function
Epilepsy
* The second most common neurological disorder
-- affects 1% of population
* Characterized by short, recurrent attacks initiated by electrical discharges in the brain
-- lights, noise, or smells may be sensed
-- skeletal muscles may contract involuntarily
-- loss of consciousness
* Epilepsy has many causes, including;
-- brain damage at birth, metabolic disturbances, infections, toxins, vascular disturbances, head injuries, and tumors
Pre-Synaptic Inhibition
One presynaptic neuron suppresses another one.
-- Neuron I releases inhibitory neurotransmitter GABA
prevents voltage-gated calcium channels from opening in neuron S so it releases less or no neurotransmitter onto neuron R and fails to stimulate it.
Neural Coding
* Qualitative information (salty or sweet) depends upon which neurons are fired
* Qualitative information depend on:
-- strong stimuli excite different neurons (recruitment)
-- stronger stimuli causes a more rapid firing rate
>>CNS judges stimulus strength from firing frequency of sensory neurons (600 APs /sec instead of 6 APs/sec)
Learning & Memory
* Learning is acquiring new knowledge
* Memory is retaining that knowledge:
1. short-term memory:
-- recall phone number while dialing
-- depends upon electrical events (reverberating circuits)
2. long-term memory
-- frequent retrieval of specific information helps with memory consolidation (learning)
-- structural or biochemical changes occurs (ie: increase in dendrites, enlarge end bulbs, increase in presynaptic terminals or formation of additional membrane receptors)
* Recently acquired memory lost first with coma or shock treatments
Memory & Synaptic Plasticity
* Memories are not stored in individual cells
* Physical basis of memory is a pathway of cells (aka: memory trace/engram)
-- new synapses or existing synapses have been modified to make transmission easier (synaptic plasticity)
* Synaptic potentiation
-- process of making transmission easier
-- correlates with different forms of memory (immediate, short term, and long term memory)
Immediate Memory
* Ability to hold something in your thoughts for just a few seconds
* Feel for the flow of events (sense of the present)
* Our memory of what just happened “echoes” in our minds for a few seconds
-- reverberating circuits
Short Term Memory
1. Lasts from a few seconds to several hours
-- quickly forgotten if distracted with something new
2. Working memory allows us to keep something in mind long enough search for keys, dial the phone
-- reverberating circuits
3. Facilitation causes memory to longer lasting
-- tetanic stimulation (rapid, repetitive signals) causes Ca+2 accumulates & cell becomes more likely to fire
4. Post-tetanic potentiation (to jog a memory)
-- Ca+2 level in synaptic knob has stayed elevated long after tetanic stimulation, so little stimulation will be needed to recover that memory
Long Term Memory
* May last up to a lifetime
* Types of long-term memory
1. Declarative: retention of facts as text/words
2. Procedural: retention of motor skills (ie:keyboard)
* Physical remodeling of synapses with new branching of axons or dendrites
* Molecular changes called long-term potentiation
-- Tetanic stimulation causes ionic changes (Ca+2 entry)
1. neuron produces more neurotransmitter receptors
2. synthesizes more protein used for synapse remodeling
3. releases nitric oxide signals presynaptic neuron to release more neurotransmitter
Alzheimer Disease
* 100,000 deaths/year
* 11% of population over 65; 47% by age 85
* Symptoms
-- memory loss for recent events, moody, combative, lose ability to talk, walk, and eat
* Diagnosis confirmed at autopsy
-- atrophy of gyri (folds) in cerebral cortex
-- neurofibrillary tangles & senile plaques
* Degeneration of cholinergic neurons & deficiency of ACh and nerve growth factors
* Genetic connection confirmed for some forms
Parkinson's Disease
* Progressive loss of motor function beginning in 50’s or 60’s -- no recovery
-- degeneration of dopamine-releasing neurons in substantia nigra (prevents excessive activity in motor centers/ basal ganglia)
-- involuntary muscle contractions (pill-rolling motion, facial rigidity, slurred speech, illegible handwriting, slow gait)
* Treatment is drugs and physical therapy
-- dopamine precursor can cross blood-brain barrier
-- deprenyl (MAO inhibitor) slows neuronal degeneration
-- surgical technique to relieve tremors