Neurophysiology in ped neurology
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The human brain is incredibly complex, making it difficult to fully understand. Neurons are the basic functional units that transmit and process information in the brain and nervous system. They communicate via electrical and chemical signals. Imbalances in excitatory and inhibitory neurotransmission can lead to neuronal hyperexcitability and seizures. Changes to ion channels and receptors involved in excitation and inhibition can also contribute to seizures. Antiepileptic drugs work by various mechanisms that suppress neuronal excitability such as blocking sodium channels or enhancing GABA inhibition.
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Neurophysiology in ped neurology
- 2. IF THE HUMAN BRAIN WERE SO SIMPLE THAT WE COULD UNDERSTAND IT, WE WOULD BE SO SIMPLE THAT WE COULDNโT.
- 4. Neuron ๏ฎ The basic signaling unit of the nervous system is the neuron. ๏ฎ Neurons are found in the brain, spinal cord, and throughout the body ๏ฎ Neurons come in many shapes and sizes and perform many different functions.
- 6. NEURONS ๏ฎ Basic functional unit of N.S. ๏ฎ Specialized cell ๏ฌ All cells have same basic properties ๏ฎ information processing Transmits Integrates Stores ๏ฎ Regulation of behavior ~
- 10. ๏ฎ Axon carries information away from soma ๏ฎ Electrical signal ๏ฎ Axon terminal releases chemical message~ Stimuli ๏ฎ ~
- 11. Glia Neural Support Cells 10X100 billions Replaced all life
- 12. Four main types of glial cells ๏ฎ Astrocytes ๏ฎ Myelin producing oligodendrocytes and Schwann cells ๏ฎ Ependymal cells ๏ฎ Microglia.
- 13. 1- Astrocytes ๏ฎ Provide physical support/ nutrition ๏ฎ Regulating chemical content of ECF NTs & K+ concentration ๏ฎ N growth factors: synthesis & release ๏ฎ the scavenging of dead cells after an injury to the brain. ๏ฎ BBB role G
- 14. Brain Capillary Blood-Brain Barrier Astrocyte role Typical Capillary end feet fenestrations
- 16. THE BLOOD-BRAIN BARRIER BBB: Astrocyte Function ๏ฎ Maintains stable brain environment large fluctuations in periphery ๏ฎ Barrier to poisons ๏ฎ Retains neurotransmtters & other chemicals ๏ฎ Regulates nutrient supplies glucose, AA levels: active transport
- 17. 2-oligodendroglia / Schwann cells Myelin plus ๏ฎ Wrap around axon Saltatory Conduction ๏ฌ faster transmission ๏ฎ Bring nutrition support ๏ฎ Nerve Growth factor
- 20. Myelin ๏ฎ Brain/spinal cord: Oligodendrocyte ๏ฎ Peripheral nerves: Schwann cell ๏ฎ Function: Nerve signal travel faster and faster
- 21. 3- Ependymal cells ๏ฌ line walls of ventricles ๏ฌ role in neuron cell migration during development
- 22. ๏ฎ CSF production: ๏ฎ Origin: mainly from the choroid plexus in the lateral, third and fourth ventricles. ๏ฎ Process: an active process with sodium is pumped out then water ๏ฎ Rate of production: 20 ml /hour ๏ฎ Normal CSF volume: 50 cc in infancy and 150 cc in adult
- 26. CSF movements are due to hydrostatic gradient between the ventricular system (about 120 mm H2O)and venous channel(about90mm H2O). CSF MOVEMENT
- 28. *Average volume: Intracranial C.S.F 125ml Subarachnoid space 89 ml Lumbar sac 30 ml *Normal C.S.F Pressure Infants 40-50 mm H2O Children 40-100 mm H2O Older age 150 mm H2O >200 mm H2O is abnormal C.S.F pressure is about 40-50 mm H2O above intracranial venous pressure. C.S.F pressure falls with inspiration and rises With expiration
- 29. When does Hydrocephalus appear ? ๏ฎ 1- When there is over production of CSF. 2- When there is a blocking in the paths of the CSF circulation. 3- When not all the CSF produced is "eliminated".
- 30. ๏ฎ Microglia ๏ฌ Phagocytosis of dead nerve cells # ๏ฌ Produce nerve growth factors 4- Microglia
- 32. THE PLASMA MEMBRANE AND THE MEMBRANE POTENTIAL ๏ฎ The plasma membrane of neurons is made up of a lipid bilayer, a double layer of fatty molecules.
- 33. Phospholipids <------- Phosphate head hydrophilic <------- Lipid tails hydrophobic
- 34. Phospholipid Bilayer Hydrophilic heads -----> Hydrophobic tails -----> water plus
- 35. Ungated channels: ๏ฎ H20 out & in H2O H2O
- 37. How does a nerve signal travel from one neuron to another?
- 38. the synaptic cleft. Synaptic Cleft
- 39. Synapse
- 41. Presynaptic Axon Terminal Postsynaptic Membrane Terminal Button Dendritic Spine the synaptic cleft.
- 48. Ca++ Exocytosis
- 49. 5. Activation
- 50. 6. Termination
- 52. 6. Termination by... Enzymatic degradation
- 55. Membrane Proteins ๏ฎ Channels ๏ฎ Pumps ๏ฌ active transport ๏ฎ Receptor protein sites ๏ฌ bind messenger molecules ๏ฎ Transducer proteins: ๏ฌ 2d messenger systems ๏ฎ Structural proteins ๏ฌ form junctions with other neurons ~
- 56. Membrane Proteins 3 OUTSIDE INSIDE 3 Na 2 K NON GATED GATED
- 57. Membrane Proteins: Ionophores ๏ฎ Ions Channels ๏ฎ Nongated always open ๏ฎ Gated chemically-gated electrically-gated mechanically-gated ~
- 58. Chemically-Gated Channels ๏ฎ Ionotropic direct control ---> fast ๏ฎ Metabotropic second messenger system indirect ---> slow ~
- 63. Metabotropic Channels ๏ฎ Receptor separate from channel ๏ฎ 2d messenger system ๏ฌ G proteins ๏ฌ cAMP ๏ฌ other types ๏ฎ Effects ๏ฌ Control channel ๏ฌ Alter properties of receptors ๏ฌ regulation of gene expression ~
- 64. G protein: direct control ๏ฎ NT is 1st messenger ๏ฎ G protein binds to channel ๏ฌ opens or closes ๏ฌ relatively fast ~
- 65. G protein: direct control R G GDP
- 66. G protein: direct control R G GTP Pore
- 67. ๏ฎ Open or close channels at resting Vm ๏ฎ NT = 1st messenger ๏ฎ Membrane-associated components ๏ฌ Receptor ๏ฌ Transducer ๏ฌ Primary effector ๏ฎ Intracellular ๏ฌ 2d messenger ๏ฌ Secondary effector ~ G protein: Protein Phosphorylation
- 68. G protein: Protein Phosphorylation Receptor trans- ducer primary effector external signal: nt 2d messenger secondary effector Receptor trans- ducer primary effector external signal: nt 2d messenger secondary effector GS norepinephrine cAMP protein kinase b adrenergic -R adenylyl cyclase
- 69. G protein: Protein Phosphorylation R G GDP A C PK
- 70. G protein: Protein Phosphorylation R A C PK G GTP ATP cAMP
- 71. G protein: Protein Phosphorylation R A C PK G GTP ATP cAMP P Pore
- 72. Resting membrane potential 3 2 -70 mV - Ca++
- 75. Action Potential
- 76. Na Channels ๏ฎ Essential for depolarization during action potential ๏ฎ Blocking fast channel inactivation leads to increased excitability ๏ฌ Induces paroxysmal depolarization shifts ๏ฌ Increasing synchrony
- 77. -70 -60 0 +40 -80 Time Depolarization Na+ influx C & E gradients drive Na+ into cell
- 80. -70 -60 0 +40 -80 Time Depolarization Na+ influx = 110 mV Amplitude - 70 mV to +40 mV
- 81. K Channels ๏ฎ Important for post-excitatory membrane re-polarization ๏ฎ M current controls sub-threshold membrane excitability ๏ฎ K Channel blockade produces epileptiform discharges in vitro ๏ฎ M current defect identified in benign neonatal familial convulsions
- 87. Ca Channels ๏ฎ Different types of channels (T, N, L, P, Q) ๏ฎ Ca currents contribute to the paroxysmal depolarization shift ๏ฎ May be responsible for long-term structural changes affecting excitability and synaptic efficacy ๏ฎ Participate in cytotoxicity ๏ฎ Activation of T-type channels is thought to underlie the abnormal thalamocortical rhythmicity associated with 3-Hz spike- and-wave in absence
- 88. Synaptic Events ๏ฎ Action Potential reaches axon terminal ๏ฎ Chemical substance released Neurotransmitter (NT) ๏ฎ Diffuses across synapse ๏ฎ Binds to receptor protein EPSP or IPSP ~
- 91. CRITERIA ๏ฎ NT found in axon terminals ๏ฎ NT released by action potentials
- 92. Lock & Key Model ๏ฎ NT binds to receptor NT = key Receptor = lock ๏ฎ Receptor changes shape determines if EPSP or IPSP receptor subtypes
- 93. Receptor A ๏ฎ ligand binds to receptor ๏ฎ activation: + or - NT
- 94. Receptor B Receptor A ๏ฎ Same NT can bind to different -R by different part of NT NT
- 95. NT Specificity of drugs Drug A Drug B Receptor B Receptor A
- 97. Mechanisms of Seizures ๏ฎ Defective balance between excitatory and inhibitory neurotransmission +VE -VE + -
- 98. What causes neuronal hyperexcitability? ๏ฎ Changes in Excitatory receptors Excitatory amino acid receptors Enhancement: NMDA, AMPA ๏ฌ Excitatory AA : Glutamate, aspartate +VE Changes in ion channels
- 99. Na Ca K
- 100. Excitatory amino acid (EAA) receptors ๏ฎ EAA: glutamate and aspartate ๏ฎ Two main receptor types: AMPA/kainat e and NMDA
- 101. NMDA receptor ๏ฎ Sustains long- lasting depolarization events ๏ฎ NMDA agonists induce epilepsies in animals ๏ฎ Structural changes have been seen in surgical specimens ๏ฎ Involved in long term potentiation
- 102. GABA receptors ๏ฎ Activation leads to membrane hyperpolarizati on via inflow of Cl and outflow K ๏ฎ Decreased neuronal firing
- 103. the synaptic cleft.
- 104. Gamma-aminobutyric acid ๏ฎ GABA - GABAergic ๏ฎ Major NT in brain inhibitory system ๏ฎ Receptor subtypes GABAA - controls Cl- channel GABAB - controls K+ channel ๏ฎ Precursor = glutamate ~
- 105. What causes neuronal hyperexcitability? ๏ฎ Changes in Inhibitory receptors GABA โ A receptors ๏ฌ inhibitory AA : GABA -VE ๏ฎChanges in ion channels Plus
- 106. GABA receptors ๏ฎ There are two classes of GABA receptors: GABAA and GABAB.
- 107. GABA receptors ๏ฎ Activation leads to membrane hyperpolarization via inflow of Cl and outflow K ๏ฎ Decreased neuronal firing
- 108. GABA ๏ฎ GABA is one of the main inhibitory NTs in the brain. GABAergic neuron dysfunctions lead to seizures
- 109. Glutamate GABA glutamic acid decarboxylase GABA Synthesis
- 110. GABA Synthesis & Reuptake ๏ฎ From Krebs cycle metabolism of glucose in mitochondria ๏ฎ From Glial cells GABA ---> Glutamate ---> Glutamine Glutamine into neurons ๏ฎ After release GABA back into glia ~
- 111. LEVETIRACETAM FIRST OF A NEW CLASS OF AEDS Lynch, PNAS 2004 For internal use only
- 112. What causes neuronal hyperexcitability? ๏ฎ Changes in ion channels 1- Na ions channels 2- K ions channels 3- ca ions channels
- 113. Na Channels ๏ฎ Essential for depolarization during action potential ๏ฎ Blocking fast channel inactivation leads to increased excitability ๏ฌ Induces paroxysmal depolarization shifts ๏ฌ Increasing synchrony
- 114. Ca Channels ๏ฎ Ca currents contribute to the paroxysmal depolarization shift ๏ฎ Activation of T-type channels is thought to underlie the abnormal thalamocortical rhythmicity associated with 3-Hz spike- and-wave in absence (absence seizures) ๏ฎ Different types of channels (T, N, L, P, Q)
- 115. K Channels ๏ฎ Important for post-excitatory membrane re-polarization ๏ฎ K Channel blockade produces epileptiform discharges in vitro
- 116. AED
- 117. 118 AED Modes of action 1 Suppress action potential ๏ฎ Sodium channel blocker or modulator ๏ฎ Potassium channel opener* ๏ฎ Ca channels and transmitter release
- 118. 119 Modes of action 2 Enhance GABA transmission ๏ฎ GABA uptake inhibitor ๏ฎ GABA mimetics 3 Suppression of excitatory transmission ๏ฎ 4- SVA inhibitor
- 119. 120 Sodium channels ๏ฎ Main target for many drugs ๏ฎ Sodium channels are responsible for the rising phase of the action potential in excitable cells and membranes ๏ฎ Examples: Phenytoin Carbamazepine Oxcarbazepine Lamotrigine
- 120. 121 Potassium channels ๏ฎ Very diverse group of ion channels ๏ฎ Responsible for resting potential ๏ฎ Influences excitability of neurones ๏ฎ Determine potential width
- 121. 122 Calcium channels ๏ฎ T type ๏ฌ Ethosuximide, zonisamide ๏ฎ L type ๏ฌ Barbiturates, felbamate ๏ฎ N type ๏ฌ Lamotrigine, barbiturates , oxcarbazepine ๏ฎ P/Q type ๏ฌ Lamotrigine, oxcarbazepine
- 122. 123 Calcium channels ๏ฎ Four main types ๏ฌ L, P/G, N; high voltage ๏ฌ T; low voltage Mono amines modulate the circuit Nifedipine blocks L
- 123. 124 GABA A and GABA B ๏ฎ Inhibitory neurotransmitter ๏ฎ GABA A post synaptic; 7 classes ๏ฌ Dependent upon chloride and bicarbonate ions ๏ฎ GABA B pre and post synaptic
- 124. 125 GABA A Transmission ๏ฎ Barbiturates (+ open Cl channels) ๏ฌ primidone ๏ฎ Benzodiazepines (GABA mimic) ๏ฌ Clobazam, clonazepam, diazapam ๏ฎ Tiagabine ๏ฎ Vigabatrin ๏ฎ VPA ( decrease its uptake)
- 125. 126 Glutamate ๏ฎ Major excitatory transmitter ๏ฌ Mainly intracellular ๏ฎ Three receptor types ๏ฌ NMDA Associated with sodium and calcium ions Magnesium ions block Other messengers act at NMDA site ๏ฌ AMPA and kainate receptors ๏ฌ metabotropic
- 127. Other (unique) LEVETIRACETAM Lynch, PNAS 2004 For internal use only
- 128. 129 Sites of action ๏ฎ Valproate, vigabatrin, tiagabine increase GABA by inhibiting reuptake and preventing breakdown within the cell ๏ฎ Benzodiazepines bind to GABA receptors ๏ฎ Phenobarbital opens chloride channels ๏ฎ Topiramate blocks sodium channels and is a GABA agonist at some sites
- 129. 130
- 130. 131 Other modes of action ๏ฎ Gabapentin, has similar structure to GABA ๏ฎ Phenytoin,carbamazepine,oxcarbazepin e, lamotrigine, act on sodium channels ๏ฎ Ethosuximide, reduces calcium currents ๏ฎ Levetiracetam, has neuroprotective effect ๏ฎ Topiramate, acetazolamide, are carbonic anhydrase inhibitors ๏ฎ Zonisamide has weak carbonic anhydrase activity
- 131. 132 Thank you
- 132. 133 1- GABA(A) receptor agonist i)Barbiturates: Barbexaclone ยท Metharbital ยท Methylphenob arbital ยท Pentobarbital ยท Phenobarbital. Primidone ii)Benzodiazepines: Clobazam ยท Clonazepam ยท Clorazepate ยท Diazepam# ยท Flutoprazepam ยท Lorazepam ยท Midazolam ยท Nimetazepam ยท Nitrazepam ยท Temazepam
- 133. 134 2- OTHER GABA agents Aromaticallylic alcohols (Stiripentol)
- 134. 135 3- Carbonic anhydrase inhibitor: Sulfa drugs Acetazolamide ยท Ethoxzolamide ยท Sult iame ยท Zonisamide
- 135. 136 4- Channel blockers 1)Primarily sodium: #Hydantoins:Ethotoin ยท Fosphenytoin ยท Mephenytoin ยท Phenytoin #Carboxamides: Carbamazepine # ยท Eslicarbazepine acetate ยท Oxcarbazepine ยทRufinamide 2)Primarily calcium #Succinimides:Ethosuximide # ยท Mesuximide ยท Phensuximide 3)Unknown/ungrouped: #Phenyltriazines: Lamotrigine #Oxazolidinediones:Ethadione ยท Paramethadione ยท Trimethadione Ureas Phenacemide ยท Pheneturide #MonosaccharidesTopiramate
- 136. 137 5- Indirect GABA agents ๏ฎ Carboxylic acids/ Fatty acid derivatives i)GABA transaminase inhibitor: Valproic acid# (Sodium valproate & Valproate semisodium) ยท Valpromide ยท Valnoctamide ii)GABA reuptake inhibitor: Tiagabine ๏ฎ GABA analogs ยท Gabapentin Pregabalin ยท Progabide ยท Vigabatrin
- 137. 138 6- Unknown/multiple/ unsorted i)Carbamates: Emylcamate ยท Felbamate ยท Meprobam ate ยท Carisbamate ii)Pyrrolidines:Brivaracetam ยท Levetirac etam ยท Nefiracetam ยท Seletracetam iii)Propionates:Beclamide ยท Lacosamid e iv)Aldehydes: Paraldehyde v)Bromides: Potassium bromide ยท Sodium bromide
- 138. 139 inhibitors excitatory 1- GABA2 1- Ca + channels 2- enhanced GABA level 2- Na + channels 3- K+ channels 3- glutamate
Editor's Notes
- the body. Scientists estimate conservatively that there aremore than 100 billion neurons in the brain and about 1 billion neurons in the spinal cord+ glia all around
- Most cells in the body have geometric shapesโthey are squarish, cubical, or spherical. Pyramidal tract is an exampleA single neuron can have anywhere from 1 to 20 dendrites, each of which can branch many times. Dendrites receive messages from other neurons and carry them toward the cell body.
- Soma= neuron stimuli to neuron forReceives information and Integrates informationElectrical signal= action potentialsCONNECTIONSThe nervous system is an intricate network of neurons (nervecells) and their connections. Surrounding the neurons areglia, which play many supportive roles in the nervous system.Neurons receive and process chemical messages fromother neurons and then send electrical signals down theiraxons to trigger the release of neurotransmittersโchemicalmessengersโthat go out to other neurons. The electricalcurrent that travels down the neuronal axon is made up of aseries of action potentials, which are generated by the openingof voltage-gated Na+ channels in the axon membrane.
- Glia are special cells that play a supporting role in the nervous system. They outnumber neurons by about 10 to 1 in the brain, where they make up at least half of the brainโs volume. The number of glia in other parts of the nervous system has not yet been determined. Unlike neurons, glia are replaced constantly throughout life. Like neurons, glia have many extensions coming off their cell bodies. Unlike neurons, however, most glia do not transmit electrical impulses. A recent discoveryโthat a subtype of oligodendrocyte precursor cells (OPSs) generate electrical signalsโchallenges the traditional view that no glial cells can do so. These special glial cells notonly generate electrical impulses but also receive input from neuronal axons.
- 1-Astrocytes surround neurons and provide structural support to hold neurons in place. 2-They provide nutritional support by contacting nearby blood vessels and transporting glucose and other nutrients from the bloodstream.3- uptake of neurotransmitters from the synapse, regulation ofthe extracellular potassium (K+) concentration, 4- synthesis and release of nerve growth factors (that help repair damaged nerves outside the brain and spinal cord.5-the scavenging of deadcellsafter an injury to the brain.
- THE BLOOD-BRAIN BARRIERAstrocytes also contribute to the formation of the blood-brainbarrier. Processes from astrocytes called โend feetโ adhere to theblood vessels of the brain and secrete chemical signals that induce(cause) the formation of tight junctions between the endothelialcells that line the blood vessels. As a result, substances from theextracellular fluid cannot move easily into these cells. The smallpores called fenestrations and some of the transport mechanismsthat are present in peripheral blood vessels are absent in the membranesof the cells that line the brainโs blood vessels.The blood-brain barrier keeps most substances other thanoxygen, glucose, and essential amino acids from entering the brainfrom the bloodstream. It protects the brain from toxins, peripheralneurotransmitters, and other substances that would interfere withthe brainโs functioning. Most large molecules cannot cross this bloodbrainbarrier. Small fat-soluble molecules and uncharged particlessuch as carbon dioxide and oxygen, however, diffuse easily across thisbarrier. Glucose and essential amino acids are transported across byspecial transporter proteins. Toxins that can diffuse across the bloodbrainbarrier include nerve gases, alcohol, and nicotine
- Oligodendrocytes are found in the brain and spinal cord,whereas Schwann cells are found in the peripheral nervoussystem. Both cell types have fewer extensions than astrocytes.Their main function is to provide the myelin sheath that coversmyelinated axons. Like astrocytes, they also help bringnutritional support to neurons. Schwann cells secrete growthfactors that help repair damaged nerves outside the brain andspinal cord.Myelin is the covering of glial extensions that wrap aroundthe axon of a neuron in as many as 100 layers. Each oligodendrocytemay wrap a different process around one segment ofthe axon of up to 50 different neurons. In the nerves outsidethe brain and spinal cord, Schwann cell processes wrap around
- Saltatory: combines both types of currentspeed without loss of signal Current passes through a myelinated axon only at the nodes of Ranvier. Voltage-gated Na+ channels are concentrated at these nodesAction potentials are triggered only at the nodes and jump from one node to the next . Much faster than conduction along unmyelinated axons
- Myelin is the covering of glial extensions that wrap around the axon of a neuron in as many as 100 layers. Each oligodendrocyte may wrap a different process around one segment of the axon of up to 50 different neurons. In the nerves outside the brain and spinal cord, Schwann cell processes wrap around one short segment of the axon of just one neuron. The layers of myelin provide additional electrical insulation that helps the nerve signal travel faster and farther
- Ependymal cells are glial cells that line the ventricles, thefluid-filled cavities of the brain. Unlike other glial cells, they donot have processes coming off the cell body. They secrete cerebrospinalfluid, the liquid that fills the ventricles and the spinalcanal. Cerebrospinal fluid acts as a shock-absorbing cushionto protect the brain from blows to the head. In effect, this fluidmakes the brain float inside the skull. The cerebrospinal fluidalso removes waste products from the brain.
- Small cells called microglia migrate from the blood intothe brain. They act as the cleanup crew when nerve cells die.They also produce chemicals called growth factors that helpdamaged neurons to heal. When you view a damaged area ofthe brain under a microscope, you can see glial cells clusteredin the places where dead cells were removed.
- May add a more lipid from myelin sheath
- Phospholipids arethe most common lipid found in the cell membrane.
- Becausethe phosphate-containing โheadโ of a phospholipid moleculeis attracted to water (hydrophilic) and the fatty acid-containing โtailโ is repelled by water (hydrophobic), the phospholipid molecules spontaneously form a bilayer with the fatty acid tails in the middle (Figure 1.4). This bilayer forms a barrier between the water outside the cell and the water inside the cell. It also keeps substances that are dissolved in water, such as ions, from crossing the cell membrane. Very few substances other than gases can cross the lipid bilayer easily.
- Some channels areopen all the time to let particular ions move back and forth.These channels are said to be ungated.
- Between the tip of each axon terminal and the point on the target neuron (usually a dendritic spine or the cell body) to which the axon sends a nerve signal, there is a tiny gap. It measures about 10 to 20 nanometers (3.94 to 7.87 in) across and iscalled the synaptic cleft.
- The synapse is the junction of a neuron with anotherneuron or a muscle fiber..Neurotransmitters carry the nerve signal as a chemical messageacross the synaptic cleft from the first (presynaptic) neuron to thesecond (postsynaptic) neuron. The neurotransmitter molecules bind toreceptors in the membrane of the postsynaptic neuron
- Few ions and molecules besides water and small unchargedmolecules, such as oxygen and carbon dioxide, can easily pass throughthe lipid bilayer of the cell membrane. Other substances needed forcell function must cross the cell membrane through special transporterproteins that span the lipid bilayer. These transporter proteins are highlyselective, allowing only a particular ion or molecule to pass.
- On presynaptic terminal. Binds NTsame as postsynaptic receptors different receptor subtypeDecreases NT release & synthesis Metabotropic receptor :alters protein synthesis ~
- ION PUMPS AS NA AND K PUMP
- ligand-gated
- specialmembrane protein, known as the sodium-potassium pump,helps control the Na+ and K+ concentrations by using energyto pump three Na+ ions out for every two K+ ions it allowsin. The area just inside of the plasma membrane is about 70millivolts, or mV (a millivolt is one thousandth of a volt),more negative than that of the extracellular fluid just outsidethe cell membrane. This electrical charge is called the restingpotential of the membrane. The interior of the cell membraneis said to be โpolarized.โ
- * And GABA release