Scanziani bipn 140

Scanziani bipn 140 - CellularNeurobiologlel‘f’N140 K2)...

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Unformatted text preview: CellularNeurobiologlel‘f’N140 K2) Name- - 0 \U l MW 73° - Diem) 1) (10 points) (a) What is the difference between temporal and spatial summation? Which is likely to come into play at neurons in the cortex. Why? . '3" 3 (cmé‘orol EctAAMLt’ff an .15 rf I“! {LAM/La, 43 d? R, PC .I LLVL 5 a-{ if U {— SFUCJ“ ! 'f ‘L-J’ -‘U_/“‘- Spurol‘ca‘ 1 A // {fob-(q ‘m: (I w I ' ' ‘ ' ' "1‘1 -’(/Htf(f"(r" .1". D .6 Ja Jug-f QM“ mud. 02w x , x f , ., “‘1 (“UHF J”./’1‘0F'r’ v n}? (if?! iv”? (0/ -i—{,)( jfwc. c‘ f c ;m«,'- lax/1 --L.- - — (b) Which at the vertebrate neuromuscularjunction‘? Why? ' i f'r‘---‘-POr'c- ( (i5 5i?“ I" I :5 "‘ "-‘ 4- WV "TC—M‘Jré ti" 0? (WU-war" .,-‘. 2) (10 points) What is the metabolism of acetyicholine (ACh), i.e. where and how is it made, destroyed, and remade? (Name the players; don’t need molecular structures.) _ plififla. pic is \(A‘fltfl ‘( a, f'lftqu -‘ -‘\ (ha Raf/Mfr.) ‘C (1-!rft'z_ “Hi x m. 13-, {fll-‘mi [(‘nu. (1C. #4 4/6/10 3) (10 points) (a) What would be the consequences at both the molecular and behavioral level of blocking glutamic acid decarboxylase (GAD) in the brain? Why? - - >.-’ (iii 1p, (:11 D KP: 1:.‘U'514C J C— i “J ('3! G . “L M44 5 9% Adieu-0"- ' I 'f' ' “JV "H. "a! I' i i . i-'-'r i, { " I A] I a " 6“ rt" F} r I I (b) What about blocking acetylcholinesterase (AChase) instead? Why? ' _. . J 4 ‘ .; . n: "I! "5: / I / . .. . Ki .. IN“ ‘ -'- r- 'r z 1- «a4 W " 1 fr.“ [/ch L- i; "I.-' I {Kg/«C, rI ' /‘- c‘ ‘ Cellular Neurobiology ! BIPN 140 Name_ (c) What might be a good pharmaceutical strategy for compensating a chronically diminished (though not absent) GAD level in the brain? Why? fa/ér 4) (10 points) Diagram a dendritic spine. What does it doI and why is that of value for new uss stem functio ? _ . - f y / 'jl-Lrnai [UCCJ- f ('i’ "FL" "Al 2/,” - Pic. ff"? :11“. Fife? - 5'\ (:3 'C r; :E’valai .( l. ,_. h; 7L \ I L/ [Wine /6/ # 2 . 1 I .r __,d_.—-—. ‘ r -! L p»: 1:5 . 5) (10 points) (a) How do nicotinic acetylcholine receptors differ s ructurally from AMPA receptors? (Might be quickest to draw diagrams.) at; Q 1\ {Or’ {I} , lg l I I L m3} '1 I ' f, A 1'; Cellular Neurobiology l BlPN 140 Name (c) How does the reSponse generated by nicotinic receptors differ from the response generated by metabotropic receptors? f Mir/1f O“ f! t-(‘T‘rf {CI { pt, VIII—I arc". { "s I r E (“HI-LC (IT d PK ("'4 f (0' let" r C: /I L, . V . J J ‘ -,- |r 4'1: ,.,‘\ f n 4' /"'I'{‘ / {i r i. . I. [1 . bf} ‘ VC’I ‘ /’ {._ .i _ i,‘ (Jr r( '({-r x l"- liL ;' n. c ~r- r (u. m 1 '91-: if: <’ C.-""- r” / "€— r/ I: 6) (10 points) (a) In the mammalian brain, glutamate acts on ligand-gated ion channels to produce rapid excitatory PSPs. What ions flow, and why are the PSPs excitatory? .. _ 'H '1 / a] (r [Of-LC}, c. I ) ‘LI *q FE (Kilt/H" {Z’r{ F ‘24 If. I; Ill!“ - '_ _' I! [,1‘. {"1 ,-I ('"A’U'Ip “f if: f (b) You have found a strange animal in which stimulating the glutamatergic nerve terminal to release glutamate elicits a rapid hyperpolarization in the postsynaptic neuron. Name two mechanisms that might account for this. / i-I .. ..- » '( xiii 3" 'I'“ I \ <1 th :Ajlc'f xtml ‘4 ‘7‘“ r...‘ j tic-.UV ‘ ‘ "' X {/1 \_ HUI C(fi "L. 5,. IrI-“flqu ‘ w I iii-.5 (0‘ (C CI'H' C) ‘2‘} 1'61'i Ir i ’r .f .\ E#___________———— .v- /| (c) What might be the mechanism if the hyperpolarization had been slow (time course of seconds)? I n _, _ . J: I ‘Vfl I H X47 ’(iit‘ it?” ('[)7{("5 r""' ‘{ b-J " “er ' (“Pita-r a; I r {If- c: l. ‘, I/ _ \ I'r’. I: 7) (10 points) (a) What is a “silent synapse"? ‘] .' | I I - F T If 5 l I, ' I H /.._ f x N M i) A t a I r .- l .1 o a Cellular Neurobiology I BIPN 140 Name (In) How were they discovered (illustrate with curr nt traces)? (c) What purposes are they likely to serve? 1 ‘ ' / .. ., .1; _ r I I I" . , 1‘ '2 (“J k ‘l a} J“) ' i ' -. L. U 4‘ L J r ‘ r i "‘ if r J,/ +3, I ,- 1 ( I If f C I { (f If, - If . . l . L - ‘__ m It.) M.- ) I ‘3 I! i / 8) (10 points) How does hippocampal LTD (in CA1 neurons) differ from cerebellar LTD (in Purkinje neurons) in the way it is triggered, the intracellular pathways and second messengers coming into play, and the final molecular events accounting for LTD? (Diagram if convenient.) If ’ :2 (l. ~/-—' "I _. I _, r3 .- \ -(. (‘4' ll-lklli’ofl'lr'rfl' l x ., a. .l Jim ’ 4‘- lw “ f?" ,2 ‘ ii 417' H rlUr.:'[‘J"< 'l I . y I. I I i ’ ’ II n .m. ‘ r {'.'(‘)l(_‘1.."' "if" F) [U r l [ l r ,1!) 2: 1 . _A"/_ Cellular Neurobiology i BiPN 140 Name 9) (10 points) (a) For Spike Timing-Dependent Plasticity, draw the temporal relationship between EPSP amplitude and the interval (quantitative) between pre- and postsynaptic Spikes. Label the axes of your diagram. a , Al “’5‘” | _i_. I}; t" 4' (b) Why is the interval so brief when trying to achieve LTP, i.e. what limits it? ‘ I-grzf' f («‘1‘ I I J ‘ I ' ’ if: _ ‘2 i " x. .- FLL' ‘.I i 3C"? I 'c'- [ t - f I I r r (0) Why so brief for LTD? .[.'I | /.y L“ ‘[ Cé‘ffl‘ r-IHHI; ‘I: lE‘r I, . . . . . _. F "ulh . [fl '1’ (‘1 i [To 10) EXTRA CREDIT (10 points) (a) In the paper by Frey and Morris, they tetanized (stimulated hard) one set of inputs (S1) to a neuron (N1) in hippocampal CA1 and then shortly after applied a protein synthesis inhibitor and stimulated a second set of inputs ($2) to the same neuron (N1). Why did they do that? What did they find? . Li: - LI." J 'r'l ‘ y ‘I I .\ J:- -' =2 I l 'I(, I: \/ (“in 'i- 7‘ l ‘4 [IV I '. 1-:5 '\/Ir "- I ' i] '. . I" _ , _ I. is {27); L I -'i r in"? i flol/ bi: wilt-gr;— .. I - . .. .1." L(‘x_.'( K JH\ - ._. ‘ -— , f .r Jr) ii: p .1611” -,L-- E / / .1_ir-( 1.r’)i-. / . W, I - J I in. r Ii,l \lr'r-l I] ‘: 43‘. If ' .5 - r /_ , |'| 1’2. ire-t, ll F 2-1 « ._.-fh- J ‘Irlll. L 1 l" i ’ L Ceilular Neurobiology f BIPN 140 Name (h) Then they repeated the experiment, this time also testing a second neuron (N2) which had been deprived of S1 input by surgery throughout the experiment while the 82 input remained intact. Why did they do that, and what did they find? hf A] {cry/é): I It \( I -' T / 6/( ml,“ I “Tim L . ,...-r_::.:- i _/ -' ‘ ‘I . ’ ‘ : _ L1(1‘(" Le 5 I. ‘flipt...'{" i-‘r-clh \I’ L3313i * <_“ w H? ‘r‘vj‘ (a... "i (XVI I )jLI‘t‘ ({ ,I ( w"; 'l- f! ...
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This note was uploaded on 11/16/2008 for the course BIPN 140 taught by Professor Unknown during the Winter '06 term at UCSD.

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Scanziani bipn 140 - CellularNeurobiologlel‘f’N140 K2)...

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