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(@?^u=>M 禰{h鹖偅u<╈DAR ( @D烪1曼殪K鹢N幂@#骡乤茷/桃坨@#乔聺tX邊=簹$/(x {W<(墷=45璄L脩鲂v刿睥 CM}烔 (< 技琚0囤S慦橄睽灬(衳 (ˊ>w+殃狗*(瑢c焻á4QP繸_螙餮E#孟棈#k镋@箣B芗(q鐍4iaE3泐(9)媂蹗P K涾Sá忯51~|h1w8:_遼?GU齏繒|埝玺N濛t!赀呾v睨QE^樽檞鳹笍Mi他栂稔a:;vz?]}钜4Q^/湛篌灍痧 鶬m爪鹥縘鳊折;m犋鳽谶軪士/懙蚪傀 緥褓/缍摘+枳 3 n/鉔*咹虻竢ш縼C茁戙E @s fuP[媝キP篲猃T嵖緤(4iE^v( 蜥鱎>^鸔E努-鱎kiEL惃譾9袳C鏡<á~玅EJ( / 0DArialNew 埞埞&鸱0z[ 0"D媅SOalNew 埞埞&鸱0z[ 0 DTimes New Roman鸱0z[ 0@ .  @n?" dd@  @@`` d餦饦D#    /餢R$髉VAjv 棰`叄孏R$忆i稪{醟獛%4孏 0咥臕@簱蚌蕷;斍蕷;g4[d[d z[ 0牺ppp@ <4ddddL 0埞& ___PPT10D媅SOes New 埞埞し尫0しz[ 0湻DTimes New Romanし尫0しz[ 0湻 pp @Treatment of Parkinson s disease Overview of CNSAct presynaptically by influencing the production, storage, or termination of action of neurotransmitters. Other agents may activate or block postsynaptic receptor.Neurotransmission in the CNSSimilar to autonomic nervous system The circuitry of the CNS is much more complex than the autonomic nervous system Contains powerful networks of inhibitory neurons that are constantly active More than 10 neurotransmitters&tSynaptic potentialsReceptors at most synapses are coupled to ion channels. Depolarization or hyperpolarization of the postsynaptic membrane, depending on the specific ions that move and the direction&<JZExcitatory pathways%Excitatory postsynaptic potential(EPSP) are generated by the following 1. stimulation of an excitatory neuron causes the release of neurotransmitter molecules 2. The influx of Na+ causes a weak depolarization 3. Pass a threshold, and an all-or-none action potential is generated. "HZZ&Inhibitory pathways Results in a hyperpolarization of the postsynaptic membrane. Inhibitory postsynaptic potentials (IPSP) are 1. releases neurons releases neurotransmitter molecules, such as -aminobutyric acid (GABA) or glycine. Increase in the permeability of specific ions, such as, potassium and chloride ions 2. the influx of chloride and efflux of potassium cause a weak hyperpolarization or IPSP that moves the postsynaptic potential away from its firing threshold. 8lcoA"t  O >Overview of parkinson s disease  Parkinson's disease (PD) is a progressive disorder of the nervous system. With an annual incidence of approximately 20 new cases per 100,000 people. PD is generally age-specific; it is estimated that approximately 1% of the population over age 60 has PD.   Etiology~Is correlated with a reduction in the activity of inhibitory dopaminergic neurons in the substantia nigra and corpus striatum.>=      ` 秽33櫃櫶` 枛S檉3檉` 櫶烫33痝` 搛枛嵠f` www3烫PP` ZXdbmo` \咭3緔`英` 3f3ff` 3f汶3F奒f疱` hk]www蜒悙灗蘤檐` ff>>\`Y{ff櫶` R>&- 呃寋p廮/檀尀>?" dd@,|?" dd@   " @ ` n?" dd@   @@``PR    @ ` ` p>> 瘊饞(  鹗  6鑛  `}  餖US鸔dkY憦蚹Hrh槝7h_  瘘  0 樆  `  饎8US鸔dkY憦蚹Hr噀,g7h_ ,{孨 ,{ N ,{踁 ,{擭  鹦  0; ^ `  餢*鹨  0h樆 ^   餤*鹨  0椿 ^ `  餤*餒  0師藿h ? 秽33櫃櫶80___PPT10.#r@ *  貫緥!jg$ 饘 $(  餽  S 8蓟>  餽  S 炕 `    餒  0師藿h ? 秽33櫃櫶80___PPT10.#r皬A*$  饘0 $(  餽  S (b `} b 餽  S b ` b 餒  0師藿h ? 秽33櫃櫶80___PPT10.#rp谡?$  饘p$(  餽  S M `}  餽  S ; `  餒  0師藿h ? 秽33櫃櫶80___PPT10.#r($  饘 $(  餽  S PF `}  餽  S 豑 `  餒  0師藿h ? 秽33櫃櫶80___PPT10.$r鸯$  饘$$(  $餽 $ S \- `}  餽 $ S 糵 `  餒 $ 0師藿h ? 秽33櫃櫶80___PPT10.%rG%$  饘($(  (餽 ( S 0 `}  餽 ( S ? `  餒 ( 0師藿h ? 秽33櫃櫶80___PPT10.&r牬2$  饘,$(  ,餽 , S > `}  餽 , S 靅 `  餒 , 0師藿h ? 秽33櫃櫶80___PPT10.(r犗# 痤8饐(  8餘 8 C &AparkinS餒 8 0師藿h ? 秽33櫃櫶80___PPT10.(r餼at$  饘<$(  <餽 < S \膸 `}  餽 < S 鼧 `  餒 < 0師藿h ? 秽33櫃櫶80___PPT10.(r小 S餕 D疸(  D餳 D C 餈A(Brain_Cross_Section<5; D <赞 鹣iCross-section of the human brain showing the substantia nigra, the region affected by Parkinson's diseasejj,- -餒 D 0師藿h ? 秽33櫃櫶80___PPT10.)rpr4RFr!#%'"*N,-0 ? 2  ( / 0DArialNew 埞埞&鸱0z[ 0"DArial宋体Times New Roman 默认设计模板"Treatment of Parkinson’s diseaseOverview of CNSNeurotransmission in the CNSSynaptic potentialsExcitatory pathwaysInhibitory pathways !Overview of parkinson’s disease 幻灯片 8 Etiology 幻灯片 10 幻灯片 11 etiology( in summary) Strategy of treatmentDrugs used in PDMechanism of action CarbidopaActionsTher_缿鉢bweiwei'alNew 埞埞&鸱0z[ 0"D媅SOalNew 埞埞&鸱0z[ 0 DTimes New Roman鸱0z[ 0@ .  @n?" dd@  @@`` 疖"M     !"#/餢R$髉VAjv 棰`叄孏R$忆i稪{醟獛%4孏 0咥臕@簱蚌蕷;斍蕷;g4[d[d z[ 0揀ppp@ <4ddddL 0埞& ___PPT10D媅SOes New 埞埞し尫0しz[ 0湻DTimes New Romanし尫0しz[ 0湻 pp@Treatment of Parkinson s disease Overview of CNSAct presynaptically by influencing the production, storage, or termination of action of neurotransmitters. Other agents may activate or block postsynaptic receptor.Neurotransmission in the CNSSimilar to autonomic nervous system The circuitry of the CNS is much more complex than the autonomic nervous system Contains powerful networks of inhibitory neurons that are constantly active More than 10 neurotransmitters&tSynaptic potentialsReceptors at most synapses are coupled to ion channels. Depolarization or hyperpolarization of the postsynaptic membrane, depending on the specific ions that move and the direction&<JZExcitatory pathways%Excitatory postsynaptic potential(EPSP) are generated by the following 1. stimulation of an excitatory neuron causes the release of neurotransmitter molecules 2. The influx of Na+ causes a weak depolarization 3. Pass a threshold, and an all-or-none action potential is generated. "HZZ&Inhibitory pathways Results in a hyperpolarization of the postsynaptic membrane. Inhibitory postsynaptic potentials (IPSP) are 1. releases neurons releases neurotransmitter molecules, such as -aminobutyric acid (GABA) or glycine. Increase in the permeability of specific ions, such as, potassium and chloride ions 2. the influx of chloride and efflux of potassium cause a weak hyperpolarization or IPSP that moves the postsynaptic potential away from its firing threshold. 8lcoA"t  O >Overview of parkinson s disease  Parkinson's disease (PD) is a progressive disorder of the nervous system. With an annual incidence of approximately 20 new cases per 100,000 people. PD is generally age-specific; it is estimated that approximately 1% of the population over age 60 has PD.   Etiology~Is correlated with a reduction in the activity of inhibitory dopaminergic neurons in the substantia nigra and corpus striatum.>=      Substantia nigra striatum Fire tonically, rather than in response to specific muscular movements or sensory input. GABA dopamine >6  x  etiology( in summary) Destruction of cells in the substantia nigra results in the degeneration of neurons responsible for secreting dopamine in the neostriatum.> R  Strategy of treatmentzTherapy is aimed at restoring dopamine in the basal ganglia and antogonizing the excitatory effect of cholinergic neurons.@ / Drugs used in PD levodopa(L-dopa) and carbidopa $ Mechanism of actionLevodopa: replenish the dopamine deficiency. Dopamine itself does not cross the blood-brain barrier. Levodopa is readily transported into the CNS and is coverted to dopamine in the brain. But side effects in the periphery.6_,> Carbidopa A dopamine decarboxylase inhibitor that does not cross the blood-brain barrier Diminishes the metabolism of levodopa in the GI tract and peripheral tissues, T(ActionsCLevodopa decreases the rigidity, tremors, and other symptoms of PD <Therapeutic usesBLevodopa in combination with carbidopa is a potent and efficacious$ Absorption and metabolismoLevodopa has extremely short half-life(1 to 2 hours) Taken on an empty stomach, typically 45 min before a meal.hAdverse effects@Peripheral effects: anorexia, nausea, and vomitting Hypotension*  CNS effectsHVisual and auditory hallucinations and dyskinesia Depression and anxiety'  Interactions jThe vitamin pyridoxine(V6) increases the peripheral breakdown of levodopa and diminishes its effectiveness&kA" Bromocriptine `Is a dopamine receptor agonist Produces little response in patients who do not react to levodopaX $  饘`P$(  P餽 P S 腯 `}  餽 P S h_ `  餒 P 0師藿h ? 秽33櫃櫶80___PPT10.*r漳$  饘`$(  `餽 ` S <~ `}  餽 ` S 笑 `  餒 ` 0師藿h ? 秽33櫃櫶80___PPT10.,r谤j$  饘X$(  X餽 X S 躮 `}  餽 X S 漤 `  餒 X 0師藿h ? 秽33櫃櫶80___PPT10.+r惤Z$  饘d$(  d餽 d S 豷 `}  餽 d S x进 `  餒 d 0師藿h ? 秽33櫃櫶80___PPT10.,r d運$  饘h$(  h餽 h S tw `}  餽 h S P% `  餒 h 0師藿h ? 秽33櫃櫶80___PPT10.-rP$  饘l$(  l餽 l S D狰 `}  餽 l S 斜 `  餒 l 0師藿h ? 秽33櫃櫶80___PPT10..r$  饘p$(  p餽 p S   `}    !"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHIJKLMNOPQRSTUVWXYZ[\]^_`abcdefghijklmnopqrstuvwxyz{|}Root Entry崄d汷嗞)嗻0r Pictures Current User)SummaryInformation(PowerPoint Document(~DocumentSummaryInformation8媅SOalNew 埞埞&鸱0z[ 0 DTimes New Roman鸱0z[ 0@ .  @n?" dd@  @@`` t餷皎L)     /餢R$髉VAjv 棰`叄孏R$忆i稪{醟獛%4孏 0咥臕@簱蚌蕷;斍蕷;g4[d[d z[ 0揀ppp@ <4ddddL 0埞& ___PPT10D媅SOes New 埞埞し尫0しz[ 0湻DTimes New Romanし尫0しz[ 0湻 ppW@Treatment of Parkinson s disease Overview of CNSAct presynaptically by influencing the production, storage, or termination of action of neurotransmitters. Other agents may activate or block postsynaptic receptor.Neurotransmission in the CNSSimilar to autonomic nervous system The circuitry of the CNS is much more complex than the autonomic nervous system Contains powerful networks of inhibitory neurons that are constantly active More than 10 neurotransmitters&tSynaptic potentialsReceptors at most synapses are coupled to ion channels. Depolarization or hyperpolarization of the postsynaptic membrane, depending on the specific ions that move and the direction&<JZExcitatory pathways%Excitatory postsynaptic potential(EPSP) are generated by the following 1. stimulation of an excitatory neuron causes the release of neurotransmitter molecules 2. The influx of Na+ causes a weak depolarization 3. Pass a threshold, and an all-or-none action potential is generated. "HZZ&Inhibitory pathways Results in a hyperpolarization of the postsynaptic membrane. 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