Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
199 Cards in this Set
- Front
- Back
1. How are proteins determined?
|
The unique characteristics of a protein are dictated by its linear sequence of amino acids.
|
|
2. General properties of AAs
|
1. A carboxylic acid group
2. An amino group attached to the α-carbon in an L configuration 3. A hydrogen atom 4. A unique side chain |
|
3. Zwitterions
|
At physiologic pH in solution, the free amino acids exist as ions in which the amino group is positively charged and the carboxylate group is negatively charged.
|
|
4. What determines the chemical properties of the amino acids?
|
The side chains determine the types of bonds and interactions each AA in a polypeptide chain can make with other molecules.
|
|
5. Nonpolar, Aliphatic
|
1. Glycine
2. Alanine 3. Proline 4. Valine 5. Leucine 6. Isoleucine |
|
6. Polar, Uncharged
|
1. Asparagine
2. Glutamine 3. Serine 4. Threonine |
|
7. Charged (Negative/Acidic)
|
1. Aspartate
2. Glutamate |
|
8. Charged (Positive/Basic)
|
1. Arginine
2. Lysine 3. Histidine |
|
9. Aromatic Nonpolar
|
Phenylalanine
|
|
10. Aromatic Polar
|
1. Tyrosine
2. Tryptophan |
|
11. Sulfur-containing
|
1. Methionine
2. Cysteine |
|
12. pKa of α-amino groups
|
pKa = 9.5
|
|
13. pKa of primary carboxylic acid
|
pKa = 2
|
|
14. What's significant about glycine?
|
The α-carbon is an asymmetric (chiral) carbon in all amino acids except in glycine
|
|
15. D or L in mammalian proteins?
|
The AAs in mammalian proteins are all L-amino acids.
Glycine is neither D nor L because it is achiral |
|
16. Side chain interactions
|
1. Hydrophobic regions
2. Electrostatic bonds 3. Hydrogen bonds 4. Disulfide bonds 5. Peptide backbone of other regions |
|
17. Important of side chain interactions
|
The chemical properties of the side chains determine how the protein folds, how it binds specific ligands, and how it interacts w/its environment
|
|
18. Useful classifications of side chains
|
1. pKa
2. Hydropathic index -scale used to denote the hydrophobicity of the side chain; the more positive the index, the greater is the tendency to associate with other non-polar molecules. |
|
19. pKa1
|
pKa of the carboxyl group
|
|
20. pKa2
|
pKa of the amino group
|
|
21. pKaR
|
pKa of the R group
|
|
22. Glycine
|
pKa1= 2.4
pKa2= 9.8 pKaR= Hydropathy= -0.4 |
|
23. Proline
|
pKa1= 2.0
pKa2= 11.0 pKaR= Hydropathy= -1.6 |
|
24. Alanine
|
pKa1= 2.3
pKa2= 9.7 pKaR= Hydropathy= 1.8 |
|
25. Leucine
|
pKa1= 2.4
pKa2= 9.6 pKaR= Hydropathy= 3.8 |
|
26. Valine
|
pKa1= 2.3
pKa2= 9.6 pKaR= Hydropathy= 4.2 |
|
27. Isoleucine
|
pKa1= 2.4
pKa2= 9.7 pKaR= Hydropathy= 4.5 |
|
28. Phenylalanine
|
pKa1= 1.8
pKa2= 9.1 pKaR= Hydropathy= 2.8 |
|
29. Tyrosine
|
pKa1= 2.2
pKa2= 9.1 pKaR= 10.5 Hydropathy= -1.3 |
|
30. Tryptophan
|
pKa1= 2.4
pKa2= 9.4 pKaR= Hydropathy= -0.9 |
|
31. Threonine
|
pKa1= 2.1
pKa2= 9.6 pKaR= 13.6 Hydropathy= -0.7 |
|
32. Serine
|
pKa1= 2.2
pKa2= 9.2 pKaR= 13.6 Hydropathy= -0.8 |
|
33. Aparagine
|
pKa1= 2.0
pKa2= 8.8 pKaR= Hydropathy= -3.5 |
|
34. Glutamine
|
pKa1= 2.2
pKa2= 9.1 pKaR= Hydropathy= -3.5 |
|
35. Cysteine
|
pKa1= 2.0
pKa2= 10.3 pKaR= 8.4 Hydropathy= 2.5 |
|
36. Methionine
|
pKa1= 2.3
pKa2= 9.2 pKaR= Hydropathy= 1.9 |
|
37. Aspartate
|
pKa1= 1.9
pKa2= 9.6 pKaR= 3.9 Hydropathy= -3.5 |
|
38. Glutamate
|
pKa1= 2.2
pKa2= 9.7 pKaR= 4.1 Hydropathy= -3.5 |
|
39. Histidine
|
pKa1= 1.8
pKa2= 9.3 pKaR= 6.0 Hydropathy= -3.2 |
|
40. Lysine
|
pKa1= 2.2
pKa2= 9.0 pKaR= 10.5 Hydropathy= -3.9 |
|
41. Arginine
|
pKa1= 2.2
pKa2= 9.0 pKaR= 12.5 Hydropathy= -4.5 |
|
42. Amino acids freq found on the surface of water soluble globular proteins
|
Aliphatic, polar, uncharged amino acids:
|
|
43. Amino acid that causes a kink in the peptide backbone
|
Proline
|
|
44. Amino acid freq found in bends or in tightly packed chains of fibrous proteins
|
Glycine
|
|
45. Important amino acid for forming disulfide bonds?
Why are disulfide bonds important? |
Cysteine can form a covalent disulfide bond with another cysteine molecule through oxidation of their sulfhydryl groups.
The resultant AA, cystine, is present in blood and tissues, and is not very water soluble. These bonds often play a role in holding two polypeptide chains together. |
|
46. Isoelectric point
|
The point at which the net charge on the molecules will not migrate in an electric field toward either a positive pole (cathode) or a negative pole (anode)
|
|
47. Electrophoresis
Net charge on a protein at a certain pH |
A technique used to separate proteins on the basis of charge
Net charge on a protein at a certain pH is a summation of all of the positive and negative charges on all of the ionizable amino acid side chains plus the N-terminal amino and C-terminal carboxyl groups. |
|
48. Is the substitution of a glutamate for a valine in sickle cell hemoglobin a conservative replacement?
What about the substitution of an aspartate for a glutamate? |
Glutamate for a valine is a nonconservative replacement because a negatively charge AA is substituted for a hydrophobic BCAA.
However, the substitution of an aspartate for a glutamate is a conservative replacement b/c the two AA have the same polarity and nearly the same size. |
|
49. Clinical case: Will Sichel
17-year-old male brought to ER with severe pain in lower back, abdomen and legs |
Low blood Hb level
Low hematocrit (% red blood cells) Radiograph (X-ray) of abdomen shows radiopaque stones in gall bladder Diagnosis: Sickle cell anemia - homozygous (confirmed by analysis of hemoglobin) Caused by a point mutation in his DNA that changes the sixth AA in the β-globin chain of Hb from glutamate to valine. |
|
50. The proteolytic digestive enzyme chymotrypsin cleaves the peptide bonds formed by the carboxyl groups of large, bulky, uncharged AAs.
Which AAs fall into this group? |
Chymotrypsin's highest activity is toward peptide bonds formed by the carboxyl groups of aromatic AAs:
Phenylalanine Tyrosine Tryptophan Isoenzymes of chymotrypsin also prefer: Leucine Methionine |
|
51. Origination of the CNS
|
Originates in the ectoderm and appears as the neural plate at the middle of the third week.
After the edges of the plate folds, the neural folds approach each other in the midline to fuse into the neural tube. |
|
52. Cranial and caudal pores close on what days?
|
Cranial: 25
Caudal: 27 |
|
53. Three layers of the Neural Tube:
|
1. Inner epithelial layer (ependyma)
2. Mantle layer 3. Marginal layer *The sulcus limitans separates the alar (dorsal) and basal (ventral) plates. |
|
54. What are the three primary brain vesicles formed by the cephalic end of the neural tube?
|
1. Prosencephalon (Forebrain)
2. Mesencephalon (Midbrain) 3. Rhombencephalon (Hindbrain) |
|
55. Secondary brain vesicles:
|
Prosencephalon:
1. Telencephalon* 2. Diencephalon* 3. Mesencephalon 4. Metencephalon** 5. Myelencephalon** *Part of prosencephalon **Part of rhombencephalon |
|
56. Brain flexures:
|
1. Cervical flexure at the junction of the hindbrain and the spinal cord
2. Cephalic flexure in the midbrain region 3. Pontine flexure between the metencephalon and the myelencephalon |
|
57. Derivatives of the Rhombencephalon
|
1. Medulla oblongata
2. Pons 3. Cerebellum 4. Fourth ventricle |
|
58. Derivatives of the Mesencephalon
|
Remains as the “midbrain”; cerebral aqueduct
|
|
59. Derivatives of the Prosencephalon
|
1. Diencephalon
-Optic cup and stalk -Pituitary -Hypothalamus -Thalamus -Epiphysis 2. Telencephalon -Forms the cerebral hemispheres |
|
60. Anterior and posterior pituitary gland derives from where?
|
Anterior pituitary: From an ectodermal outpocketing of the stomodeum immediately in front of the buccopharyngeal membrane, known as Rathke's pouch
Posterior pituitary: From a downward extension of the diencephalon, the infundibulum. |
|
61. Craniopharyngiomas
|
Are benign epithelial tumors derived from remnants of Rathke’s pouch and the junction of the infundibulum and pituitary.
Presents with raised intracranial pressure, hydrocephalus, pituitary dysfunction, visual loss and diabetes insipidus. |
|
62. Significance of alar, basal, floor, and roof plates?
|
The alar and basal plates separate sensory from motor nuclei in the “brain”.
They are separated by the "sulcus limitans" Floor and roof plates serve as connecting plates between the two sides. |
|
63. Role of SHH
|
SHH ventralizes the neural tube in the spinal cord region and induces the floor and basal plates
Also, it is secreted by the prechordal plate and notochord, and ventralizes the forebrain and midbrain areas. |
|
64. Role of Bone morphogenetic proteins (BMP) 4 & 7?
|
Expressed in nonneural ectoderm, maintain and upregulate expression of PAX3 and PAX7 in the alar and roof plates.
Also, they induce and maintain expression of dorsalizing genes. |
|
65. Development of the basal plate in the spinal cord
|
1. Spinal accessory nucleus
2. Motor columns 3. IML (T1-L2) 4. Sacral parasympathetic columns |
|
66. Development of the alar plate in the spinal cord
|
1. Visceral receptive area
2. Substantia gelatinosa |
|
67. Development of the basal plate in the medulla
|
1. Hypoglossal nucleus (CN XII)
2. Inferior salivatory nucleus 3. Dorsal vagal (CN X) 4. Nucleus ambiguous |
|
68. Development of the alar plate in the medulla
|
1. Solitary nucleus
2. Spinal trigeminal (CN V) 3. Vestibular and cochlear (CN VIII) |
|
69. Development of the basal plate in the pons
|
1. Abducens nucleus (CN VI)
2. Superior salivatory nucleus 3. Trigeminal nucleus (CN V) 4. Facial nucleus (CN VII) |
|
70. Development of the alar plate in the pons
|
1. Chief sensory of CN V
2. Mesencephalic |
|
71. Development of the basal plate in the midbrain
|
1. Oculomotor nucleus (CN III)
2. Edinger-Westphal nucleus 3. Trochlear (CN IV) |
|
72. Development of the alar plate in the midbrain
|
Form the anterior and posterior colliculi as relay stations for visual and auditory reflex centers, respectively
|
|
73. Rhombomeres
|
Located in the hindbrain
Give rise to motor nuclei of CN: IV, V, VI, VII, IX, X, XI, XII |
|
74. Cranial nerves sensory ganglia originate from?
|
Ectodermal placodes and neural crest cells
|
|
75. Layers of the cortex
|
Cortical neurons migrate from the subventricular zone.
1. Molecular layer 2. External granular layer 3. External pyramidal layer 4. Internal granular layer 5. Internal pyramindal layer 6. Multiform layer The six layers of the cerebral cortex are formed in an “inside-out” fashion. As a result, the oldest neurons are in the deepest layers and the newest neurons are in the most superficial layers. |
|
76. Meningocele
|
Meninges + CSF
|
|
77. Meningomyelocele
|
Meninges + CSF + spinal cord
|
|
78. Excitatory neurotransmitter in muscle fibers
|
Acetylcholine
-synthesized in the cytoplasm of the terminal, but is absorbed quickly in many small synaptic vesicles and then the enzyme acetylcholinesterase destroys acetylcholine a few ms after it has been released from the synaptic vesicles. |
|
79. What is the effective stimulus for causing acetylcholine release from the vesicle?
|
Entry of calcium ions through voltage-gated calcium channels
|
|
80. Acetylcholine gated ion channels
|
Located almost entirely near the mouths of the subneural clefts lying immediately below the dense bar areas where the acetylcholine is emptied into the synaptic space.
Made up of five subunit proteins, two alpha and one of beta, delta, and gamma proteins. |
|
81. Passage of ions thru the Acetylcholine gated ion channels
|
Far more sodium ions flow through the acetylcholine gated ion channels than any other ions.
For two reasons: 1. Only two positive ions in large concentrations: sodium and potassium 2. Very negative potential on the inside of the muscle membrane pulls the positively charge sodium ions to the inside of the fiber, while simultaneously preventing efflux of the positively charged potassium ions when they attempt to pass outward. |
|
82. Principle effect of the acetylcholine gated ion channels
|
Allows large numbers of sodium ions to pour to the inside of the fiber creating a local positive potential change which initiates an action potential.
|
|
83. Curare
|
Blocks the gating action of acetylcholine on the acetylcholine gated ion channels by competing for acetylcholine receptor sites.
|
|
84. Botulinum toxin
|
A bacterial poison that decreases the quantity of acetylcholine release by the nerve terminals
|
|
85. Safety factor and fatigue
|
Safety factor:
Each impulse that reaches the NMJ causes about 3x as much end plate potential as that required to stimulate the muscle fiber. Fatigue: Stimulation of the nerve fiber at high rates for several minutes often diminishes the number of ACh vesicles so much that impulses fail to pass into the muscle fiber |
|
86. Acetylcholinesterase splits ACh into?
|
1. Acetate ion
2. Choline -resorbed actively into the neural terminal to be recycled |
|
87. Drugs that stimulate the muscle fiber by ACh-like action
|
1. Methacholine
2. Carbachol 3. Nicotine *These drugs are not destroyed by ACh-ase or are destroyed slowly |
|
89. Drugs that stimulate the NMJ by inactivating ACh-ase
|
1. Neostigmine
2. Physostigmine 3. Diisopropyl fluorophosphate - military potential as a nerve gas All inactivates ACh-ase Causes muscle spasm |
|
90. Myastenia gravis
|
Causes muscle paralysis b/c of inability of the NMJ to transmit enough signals from the nerve fibers to the muscle fibers.
Antibodies that attack the ACh-gated sodium ion transport proteins have been found in the blood of patients w/this disease. The end plate potentials that occur in the muscle fibers are mostly too week to stimulate the muscle fibers. Can be treated w/neostigmine. |
|
91. Resting membrane potential in muscle fibers
|
about -80 to -90 mV
|
|
92. Duration of action potentials in muscle fibers
|
1 to 5 ms in skeletal muscle; about five times as long as in large myelinated nerves
|
|
92. Velocity of conduction in muscle fibers
|
3 to 5 m/s
about 1/13 the velocity of conduction in the large myelinated nerve fibers |
|
93. Transverse T tubules
|
These transmit action potentials all the way thru the muscle fiber.
Cause a release of calcium ions inside the muscle fiber in the vicinity of the myofibrils, and these ions cause contraction. This is called excitation-contraction coupling |
|
94. Important fact about T tubule location
|
They are open to the exterior of the muscle fiber and thus they communicate w/the extracellular fluid surrounding the muscle fiber; they are internal extensions of the cell membrane.
|
|
95. Sarcoplasmic reticulum
|
Composed of two major parts:
1. Large chambers call terminal cisternae that surround the T tubules 2. Long longitudinal tubules that surround all surfaces of the actual contracting myofibrils. Contains calcium channels and calcium pumps to concentrate or sequester calcium ions around the myofibrils. |
|
96. Calsequestrin
|
A protein inside the sarcoplasmic reticulum that can bind up to 40 times more calcium than the calcium pump.
|
|
97. Somatic portion of the sensory system
|
Transmits sensory info from the receptors of the entire body surface and form some deep structures.
This info enters the CNS thru peripheral nerves and is conducted immediately to multiple sensory areas in: 1) spinal cord 2) reticular substance of the medulla, pons and mesencephalon 3) cerebellum 4) thalamus 5) areas of the cerebral cortex |
|
98. Motor functions of the nervous system
|
1. Contraction of appropriate skeletal muscles throughout the body
2. Contraction of smooth muscle in the internal organs 3. Secretion of active chemical substances by exocrine and endocrine glands. |
|
99. Effectors
|
The muscles and glands are called effectors b/c they are the actual anatomical structures that perform the functions dictated by the nerve signals.
|
|
100. Areas that can control skeletal muscles
|
1. spinal cord
2. reticular substance of the medulla, pons and mesencephalon 3. basal ganglia 4. cerebellum 5. motor cortex The lower regions control automatic muscle responses to sensory stimuli while the higher regions control deliberate muscle movements controlled by thought processes of the brain. |
|
101. Most important function of the nervous system
|
Process incoming information in such a way that appropriate mental and motor responses will occur.
To do this, the the nervous system needs to channel and process information via its "integrative function" |
|
102. What determines the directions in which nervous signals travel?
|
The synapses perform a selective action, often blocking weak signals while allowing strong signals to pass, but at other times selecting and amplifying certain weak signals and often channeling these signals in many directions.
|
|
103. Where does most of the storage of information occur?
|
Most storage occurs in the cerebral cortex.
The basal regions of the brain and spinal cord can store small amounts of information as well |
|
104. Facilitation
|
Each time certain types of sensory signals pass through sequences of synapses, these synapses become more capable of transmitting the same type of signal the next time.
|
|
105. Three major levels of the nervous system
|
1. The spinal cord
2. The lower brain / subcortical level 3. The higher brain / cortical level |
|
106. Spinal cord level
|
Neuronal circuits in the cord can cause:
1. walking movements 2. pain reflexes 3. reflexes that stiffen the legs against gravity 4. reflexes that control local blood vessels, GI movements, or urinary excretion |
|
107. Lower brain / subcortical level
|
Controls the subconscious activities of the body in the medulla, pons, mesencephalon, hypthalamus, thalamus, cerebellum, and basal ganglia.
Initiates wakefulness, or arousal |
|
108. Higher brain / cortical level
|
Stores memories, essential for thought processes, but cannot function by itself.
|
|
109. Brain and computers
|
The brain is a central processing unit; it is analogous to computers
|
|
110. Synaptic functions of neurons
|
Impulses may be:
1) blocked in its transmission from one neuron to the next 2) changed from a single impulse into repetitive impulses 3) integrated with impulses from other neurons to cause highly intricate patterns of impulses in successive neurons. |
|
111. Two major types of synapses
|
1. Chemical synapses
-almost all synapses used for signal transmission in the CNS are chemical -utilize neurotransmitters 2. Electrical synapses -direct open fluid channels that conduct electricity from one cell to the next via gap junctions -used in smooth muscle and cardiac muscle |
|
112. Important property of chemical synapses
|
They transmit signals in a "one-way" direction; that is, from the presynaptic neuron to the postsynaptic neuron.
It allows signals to be directed toward specific goals. |
|
113. Differences in neurons
|
1. size of the cell body
2. length, size, and number of dendrites 3. length and size of the axon 4. number of presynaptic terminals |
|
114. Two important structure in the terminal boutons
|
1. Transmitter vesicles
-contain transmitter substance that excites or inhibits the postsynaptic neuron 2. Mitochondria -provide ATP which in turn supplies the energy for synthesizing new transmitter substance. |
|
115. Two important components of receptor proteins
|
1. A binding component that protrudes outward from the membrane into the synaptic cleft where it binds the neurotransmitter
2. An ionophore component that passes all the way thru the postsynaptic membrane to the interior of the post synaptic neuron. |
|
116. Two types of ionophores
|
1. Ion channel
2. Second messenger activator that is not an ion channel but instead is a molecule that protrudes into the cell cytoplasm and activates one or more substances inside the postsynaptic neuron. |
|
117. Cation channels
|
Usually allow sodium ions to pass when opened, but sometimes potassium and or calcium ions as well.
Lined with negative charges which attract the positively charged ions and repel chloride ions and other anions. |
|
118. Anion channels
|
Allow mainly chloride ions to pass when the channels open wide enough.
Sodium, potassium, and calcium cations are blocked, mainly b/c their hydrated ions are too large to pass. |
|
119. Excitatory transmitter
|
One that opens cation channels
Depolarizes |
|
120. Inhibitory transmitter
|
One that opens anion channels.
Hyperpolarizes |
|
121. G-proteins
|
Most common type of second messenger proteins. Consists of three parts:
1. an alpha component that is the activator portion of the G-protein 2. a beta component* 3. a gamma component* *both attached to the alpha component and also to the inside of the cell membrane adjacent to the receptor protein. On activation by a nerve impulse, the alpha portion separates from the beta and gamma portions and then is free to move w/in the cytoplasm of the cell. |
|
122. Functions of the separated alpha components of the G-protein
|
1. Opening specific ion channels thru the postsynaptic cell membrane
2. Activation of cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP) in the neuronal cell. 3. Activation of one or more intracellular enzymes 4. Activation of gene transcription |
|
123. Things that cause excitation
|
1. Opening of sodium channels to allow large #'s of positive electrical charges to flow to the interior of the postsynaptic cell.
2. Depressed conduction through chloride or potassium channels, or both. 3. Various changes in the internal metabolism of the postsynaptic neuron. |
|
124. Things that cause inhibition
|
1. Opening of chloride ion channels through the postsynaptic neuronal membrane
2. Increase in conductance of potassium ions out of the neuron 3. Activation of receptor enzymes that inhibit metabolic functions. |
|
125. Difference between small-molecule, rapidly acting transmitters and neuropeptides
|
Small-molecule, rapidly acting transmitters cause acute responses of the nervous system while neuropeptides usually cause more prolonged actions.
|
|
126. Examples of small-molecule, rapidly acting transmitters
|
1. ACh
2. Norepinephrine 3. Epinephrine 4. Dopamine 5. Serotonin 6. Histamine 7. GABA 8. Glycine 9. Glutamate 10. Aspartate 11. NO |
|
127. Examples of Neuropeptides or growth factors
|
1. Hypothalamic releasing hormones
2. Pituitary peptides -Vasopressin -Oxytocin -Prolactine -Luteinizing hormone 3. Peptides that act on the gut -Gastrin -Insulin -Glucagon |
|
128. Areas that secrete acetylcholine
|
1. Terminals of the large pyramidal cells from the motor cortex
2. Several different types of neurons in the basal ganglia 3. Motor neurons that innervate the skeletal muscles 4. Preganglionic neurons of the autonomic nervous system 5. Postganglionic neurons of the parasympathetic nervous system 6. Some postganglionic neurons of the sympathetic nervous system. |
|
129. Where is norepinephrine secreted?
|
The terminals of many neurons whose cell bodies are located in the brain stem and hypothalamus.
Specifically, norepinephrine secreting neurons in the locus ceruleus in the pons send nerve fibers to the widespread areas of the brain to control wakefulness and mood. Also secreted by most postganglionic neurons of the sympathetic nervous system, where it excites some organs but inhibits others. |
|
130. Where is dopamine secreted?
|
Secreted by neurons that originate in the substantia nigra. The termination of these neurons is mainly in the striatal region of the basal ganglia.
The effect of dopamine is usually inhibition |
|
131. Where is glycine secreted?
|
Secreted mainly at synapses in the spinal cord.
It is believed to always act as an inhibitory transmitter |
|
132. Where is GABA secreted?
|
Secreted by nerve terminals in the spinal cord, cerebellum, basal ganglia, and many areas of the cortex.
It is believe to always cause inhibition. |
|
133. Where is glutamate secreted?
|
Secreted by the presynaptic terminals in may of the sensory pathways entering the CNS, as well as many areas of the cerebral cortex.
It probably always causes excitation |
|
134. Where is serotonin secreted?
|
Secreted by the nuclei that originate in the median raphe of the brain stem and project to many brain and spinal areas, especially to the dorsal horns of the spinal cord and to the hypothalamus.
Acts as an inhibitor of pain pathways in the cord, and an inhibitor of the higher regions of the nervous system. |
|
135. Where is nitric oxide secreted?
|
NO is especially secreted by nerve terminals in areas of the brain responsible for long-term behavior and for memory.
It is synthesized almost instantly as needed, and it then diffuses out the presynaptic terminals over a period of seconds. Does not greatly alter the membrane potential but instead changes intracellular metabolic functions that modify neuronal excitability for second, minutes, or longer. |
|
136. Synthesis of neuropeptides
|
Not synthesized in the cytosol of the presynaptic terminals, instead they are made as integral parts of large protein molecules by ribosomes in the neuronal cell body.
Goes thru the ER, Golgi apparatus, packaged into vesicle, transported to the tips of axons via axonal streaming. Process takes a while and hence the reason for a smaller amount of substance released compared to small-molecule transmitters. |
|
137. Resting membrane potential of the neuronal soma
|
-65 mV
|
|
138. At resting potential, where are the sodium ions?
|
Sodium ion concentration is high in the extracellular fluid, but low inside the neuron
|
|
139. At resting potential, where are the potassium ions?
|
Potassium ion concentration is high inside the neuronal soma but low in the extracellular fluid
|
|
140. At resting potential, where are the chloride ions?
|
Chloride ion concentration is high in the extracellular fluid but low inside the neuron
|
|
141. If chloride ions are can easily pass through the permeable neuronal membrane, why does the concentration stay low inside the cell?
|
The -65 mV resting potential repels the negatively charge anions.
|
|
142. Nernst potential
|
A potential that exactly opposes movement of an ion; potential will be negative (-) for positive ions and positive (+) for negative ions.
Reported in mV and abbreviated as EMF |
|
143. Nernst potential equation
|
EMF = ± 61 * log ([inside]/[outside])
|
|
144. Uniform distribution of electrical potential inside the soma
|
Any change in potential in any part of the intrasomal fluid causes an almost exactly equal change in potential at all other points inside the soma.
This is important b/c it plays a major role in summation of signals. |
|
145. EPSPs and IPSPs are types of...?
|
postsynaptic excitatory and inhibitory events
|
|
146. Presynaptic inhibition
|
Caused by release of an inhibitory substance on the outsides of the presynaptic nerve fibrils before their own endings terminate on the postsynaptic neuron.
In most cases, the inhibitory transmitter is GABA which has a specific effect of opening anion channels. This type of inhibition occurs in many of the sensory pathways in the nervous system. |
|
147. Spatial summation
|
The effect of summing simultaneous postsynaptic potentials by activating multiple terminals on widely spaced areas of the neuronal membrane.
|
|
148. Temporal summation
|
Successive discharges from a single presynaptic terminal, if they occur rapidly enough, can add to one another.
|
|
149. Facilitation of neurons
|
Often the summated postsynaptic potential is excitatory but has not risen high enough to reach the threshold for firing by the postsynaptic neuron.
When this happens, the neuron is said to be facilitated; it will reach threshold more easily. |
|
150. Importance of dendrites in spatial summation
|
The dendrites receive a large spatial area around the motor neuron.
Also, between 80-95% of all the presynaptic terminals of the anterior motor neuron terminate on dendrites compared to only 5 to 20% terminating on the neuronal soma. |
|
151. Can dendrites transmit action potentials?
|
Most fail to transmit action potentials b/c their membranes have few voltage-gated sodium channels. However, they do transmit electronic current down the dendrites to the soma.
|
|
151. What is the drawback of dendritic transmission of electric current?
|
Dendrites are long, and their membranes are thin and at least partially permeable to K+ and Cl- making them "leaky" to electric current.
This is called decremental conduction. The farther the EPSP is from the soma of the neuron the great will be the decrement and the less will be the excitatory signal that reaches the soma. |
|
152. Can dendrite summate EPSPs and IPSPs?
|
Yes, they can in the same way that the soma can.
|
|
153. Fatigue of synaptic transmission
|
When EPSPs are repetitively stimulated at a rapid rate, the # of discharges by the postsynaptic neuron is at first very great, but the firing rate becomes progressively less in succeeding milliseconds or seconds.
Is important b/c areas of the nervous system can become overexcited; i.e. seizures. |
|
154. Mechanism of fatigue in synaptic transmission
|
Mainly exhaustion or partial exhaustion of the stores of transmitter substance int he presynaptic terminals.
Also results from: 1. progressive inactivation of many of the postsynaptic membrane receptors 2. slow development of abnormal concentrations of ions inside the postsynaptic cell. |
|
155. Effect of alkalosis on neuronal excitability
|
Normally, alkalosis greatly increases neuronal excitabilty.
Thus, when one hyperventilates, the overbreathing blows of CO2 and therefore elevates the pH of the blood and increases neuronal excitability. |
|
156. Effect of acidosis on neuronal excitability
|
Acidosis greatly depresses neuronal activity.
In very sever diabetic or uremic acidosis, coma virtually always develops. |
|
157. Strychnine
|
Best known agent that increases the excitability of neurons.
It inhibits the action of some normally inhibitory transmitter substances. Results in severe muscle spasms. |
|
158. Anesthetics and neuronal excitability
|
They increase the neuronal membrane threshold for excitation and thereby decrease synaptic transmission at many points.
B/c they are lipid soluble, it is also plausible that they may change the physical characteristics of the neuronal membranes. |
|
159. Synaptic delay
|
The minimal period of time required for all these events to take place is about 0.5 ms:
1. Discharge of transmitter by presynaptic neuron 2. Diffusion of the transmitter to the postsynaptic membrane 3. Action of the transmitter on the membrane receptor 4. And etc... |
|
160. Four different stages of development in which children are prey to disorders *that we have data on
|
1. The neonatal period (first 4 weeks of life)
2. Infancy (first year) 3. Age 1 to 4 years 4. Age 5 to 14 years |
|
161. Three leading causes of death during the first 12 months of life
|
1. Congenital anomalies
2. Disorders relating to gestation and low birth weight 3. SIDS |
|
162. Disruptions
|
Result from secondary destruction of an organ or body region that was previously normal in development; thus they arise from an extrinsic disturbance in morphogenesis.
Ex: amniotic bands that encircle, compress or attach to developing parts of the fetus |
|
163. Three groups of anomalies that are genetic in origin
|
1. Those associated w/karyotypic aberration
2. Those arising from single gene mutations 3. Multifactorial inheritance |
|
164. Chromosomal syndromes
|
Characterized by congenital anomalies; the great prevalence of these cytogenic aberrations arises as defects in gametogenesis and so are not familial
*except for a form of Down syndrome associated with a Robertsonian translocation |
|
165. Single gene mutations
|
May underlie major congenital anomalies, which as expected, follow mendelian patterns of inheritance.
Of these, approx 90% are inherited in an autosomal dominant or recessive pattern, while the remainder segregates in an X-linked pattern. |
|
166. Gene involved in developmental patterning and holoprosencephaly
|
sonic hedgehog (SHH)
|
|
167. At risk period for rubella infection
|
Extends shortly before conception to the 16th week of gestation; the hazard being greater in the first 8 weeks.
Leads to rubella embryopathy |
|
168. At risk period for cytomegalovirus
|
The highest at-risk period is the second trimester of pregnancy.
|
|
169. Diabetic embryopathy
|
Maternal hyperglycemia-induced fetal hperinsulinemia results in increased body fat, muscle mass, and organomegaly; cardiac anomalies, neural tube defects, and other CNS malformations
|
|
171. Teratogens and genetic defects may act at sever steps involved in normal morphogenesis, which are:
|
1. Proper cell migration
2. Cell proliferation 3. Cellular interactions 4. Cell-matrix association 5. Programmed cell death 6. Hormonal influences and mechanical forces. |
|
172. Relationship between retinoic acid and TGF and FGF?
|
TGF and FGF are both involved in morphogenesis; abnormal expression of TGF and FGF have been found in the developing palate in those animals exposed to retinoic acid.
Thus, retinoic acid can lead to cleft palate and cleft lip. However, a retinoic acid derivative, all-trans-retinoic acid, is essential for normal development and its absence results in a constellation of malformations; thus the need for Vitamin A. |
|
173. HOX genes
|
Homeobox genes; involved in transcriptional regulation
Have a 180 nucleotide motif which has DNA binding properties; these genes have been implicated in the patterning of limbs, vertebrae, and craniofacial structures. Interacts w/many other genes |
|
174. PAX genes
|
A 384 base pair sequence family of developmental genes.
In contrast to HOX genes, however, their expression patterns suggest they act singly. Mutations in PAX genes cause human malformations i.e. Waardenburg syndrome, aniridia, renal-coloboma syndrome. |
|
175. AGA
|
Appropriate for gestational age
weight falls between the 10th and 90th percentiles |
|
176. SGA
|
Small for gestational age
weight falls below 10th percentile Caused by fetal growth restriction (FGR) |
|
177. LGA
|
Large for gestational age
Weight falls above 90th percentile |
|
178. Prematurity
|
Defined by a gestational age less than 37 weeks (and also weigh less than 2500 gm)
|
|
179. Risk factors for prematurity
|
1. Preterm premature rupture of placental membranes (PPROM)
2. Intrauterine infections 3. Uterine, cervical, and placental structural abnormalities 4. Multiple gestation |
|
180. Consequences of fetal growth restriction
|
1. Hyaline membrane disease (respiratory distress syndrome)
2. Necrotizing enterocolitis 3. Sepsis 4. Intraventricular hemorrhage 5. Long term complications, including developmental delay. |
|
181. FGR
|
At least one third of infants who weigh less than 2500 gm are born at term and therefore are undergrown rather than immature.
Can be detected before delivery by US. Caused by: fetal factors, placental factors, and maternal factors. |
|
182. Fetal factors that reduce the growth potential
|
1. Chromosomal disorders
2. Congenital anomalies 3. Congenital infections -The TORCH group Infants who are SGA b/c of fetal factors are usually characterized by symmetric growth restriction, meaning that all organ systems are similarly affected |
|
183. TORCH
|
Toxoplasmosis
Other viruses, such as syphillis Rubella Cytomegalovirus Herpes virus |
|
184. Placental factors that reduce the growth potential
|
1. Uteroplacental insufficiency
2. Umbilical-placental vascular anomalies 3. Placenta abruptio 4. Placenta previa 5. Confined placental mosaicism Placental causes of FGR tend to result in asymmetric growth retardation with relative sparing of the brain |
|
185. Confined placental mosiacism
|
Results from viable genetic mutations occurring after zygote formation. If it occurs early, it results in generalized constitutional mosaicism of the fetus and placenta.
Conversely, if the mutation occurs later, a genetic abnormality limited to the placenta results. |
|
186. Maternal factors that reduce the growth potential
|
1. Preeclampsia
2. Chronic hypertension 3. Narcotics abuse 4. EtOH intake 5. Malnutrition |
|
187. Preterm lungs
|
The alveoli are small and the septa are considerably thicker than in the adult.
Development of alveoli continues after birth and the full adult stage is reached at age 8. The immature lungs are grossly unexpanded, red, and meaty. |
|
188. Preterm kidneys
|
In the preterm infant, the formation of glomeruli is incomplete. The deep glomeruli are well formed, however, and renal function is adequate to permit survival.
|
|
189. Preterm brain
|
Incompletely developed in the preterm infant.
Brain substance is easily torn, there is poorly developed myelination of the nerve fibers. Homeostasis is not perfect, and the preterm infant has difficulty maintaining a constant body temp. |
|
190. Preterm liver
|
Suffers from a lack of physiologic maturity in the preterm infant.
Have a transient period of physiologic jaundice within the first post natal week. |
|
191. Apgar score
|
Method of clinically evaluating the physiologic condition and responsiveness of newborn infants.
Infant may be evaluated at 1 min and at 5 min. A total score of 10 indicates an infant in the best possible condition |
|
192. What does the Apgar specifically measure?
|
1. Heart rate
2. Respiratory effort 3. Muscle tone 4. Response to catheter in nostril 5. Color |
|
193. What is the most common and most important birth injury?
|
Intracranial hemorrhages
Genreally related to excessive molding of the head or sudden pressure changes in its shape as it's subjected to the pressure of forceps or sudden precipitate expulsion. May arise from tears in the dura or from rupture of the vessels that traverse the brain. |
|
194. Caput succedaneum and cephalhematoma
|
Progressive accumulation of interstitial fluid in the soft tissues of the scalp giving rise to a usually circular area of edema, congestion, and swelling at the site where the head begins to enter the uterine canal.
Hemorrhage may occur in the scalp, producing a cephalhematoma. |
|
195. How are fetal and perinatal infections acquired?
|
Through one of two routes:
1. Transcervically (ascending) 2. Transplacentally (hematologic) |
|
196. Transcervical infections
|
The fetus eithers inhales infected amniotic fluid into the lungs shortly before birth or by passing through an infected birth canal during delivery.
Can cause: 1. Pneumonia 2. Sepsis 3. Meningitis |
|
197. Transplacental infections
|
Most parasitic and viral/bacterial infections gain access to the fetal bloodstream via the chorionic villi.
|
|
198. Fifth disease
|
Caused by the parvovirus B19 which can induce spontaneous abortion, stillbirth, hydrops fetalis, and congenital anemia.
|
|
199. What are the similar clinical and pathologic manifestations of the TORCH group of infections?
|
1. Encephalitis
2. Fever 3. Chorioretinitis 4. Hepatosplenomegaly 5. Pneumonitis 6. Myocarditis 7. Hemolytic anemia 8. Vesicular or hemorrhagic skin lesions |