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Drugs that affect the NS > New Deck > Flashcards

New Deck Flashcards

1
Q

what are the modes of synthesis and release of of neuropeptide receptors?

A
  • hormone from non-neural sources : a metabolic product secreted by one cell-type that affects the function of another cell-type
  • synaptic NT/neuroendocrine mediator: released locally by exocytosis to activate post-synaptic R’s
  • protease-activated receptors (PAR) - GPCR wutg a tethered ligand that can be revleacd by proteolysis
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2
Q

how is neuropeptide bradykinin formed?

A
  • Precursor: (prepro) kininogens
    • liver derived
    • high and low MW forms in blood
  • Enzymes: (prepro) Kallikriens
    • cleaved kininogens

generation of kinins:
negatively charged surface (wound)–> activation of factor XII –>activates Kallikrein –> BK (from HMW-kininogen)

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3
Q

what is the agonist, antagonist and action of the B1-BK receptor?

A
  • agonist: Des-Arg8-bradykinin
  • antagonist: Des-Arg10-Hoe140
  • action: activation of PLC, painful
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4
Q

what is the agonist, antag, action of B2-BK receptor?

A
  • agonists: BK, kallidin
  • antagonist: Hoe140
    • contain Tic and Oci - similar to BK sequence
  • action: PLC > increase BV dilation and permeability> increase contraction (painful)
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5
Q

what are the actions of sub p?

A
  • contracts gut
  • stimulates cutaneous pain receptors relaxes vascular smooth muscle (NO), increases permeability
  • histamine rlease and exocrine secretions
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6
Q

how are substance P, NKB and NKA produced and what are group do they belong in?

A
  • TAC1 (gene) is processed to produce substance P and NKA
  • TAC3 gene product is process –> NKA

all = Tachykinins

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7
Q

how can substance P be analgesic?

A

release sub p –> neurogenic inflammation –> desen + analgesic

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8
Q

what are the agonists + antagonists for NK1R, NK2R and NK3R?

A

NK1R

  • agonist = sub P
  • antagonists = spanitde, aprenant

NK2R

  • agnoist = NKA

NK3R

  • agonists = NKB
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9
Q

what are protease-activated receptors?

A
  • GPCR’s (Gi, Gq)
  • activated by serine proteases - chop terminal to expose active portions
  • PAR1, 2, 4 = part of clotting process
  • PAR2 also part of pain senation
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10
Q

why are neuropeptides of limited use of drugs?

A
  • hard to make/ourify
  • poor oral absorption
  • degraded by peptidases
  • non-pep agonist/antagonists
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11
Q

what is the relationships between hypothalamus and pituitary?

A
  • neuroendocrine neurons secrete hormones into blood circulation
  • special cell bodies nerve ends near nodes
  • neuro surrounds endocrine structure –> more hormone release
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12
Q

what are the 2 types of neuroendocrine pathways?

A

neurohypophyseal - traverse H-P stalk

  • hypothalamus (subventricular nuc) –> posterior pit , hormone released from nerve ending

hypophyseaotropic - to H-P blood supply

  • hypothalamus (paraventricular nuc) –> anterior putuitary, hormone released into portal blood
  • short nerves, complex
  • vescular bed through portal system to anterior pit which stimulate releasing factors
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13
Q

what is the function of oxytocin?

A
  • induces uterine contractions during birth
  • induces milk letdown in lactating mothers
  • subject to classical conditioning
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14
Q

how does Arg vasopressin (AVP) function?

A
  • hypothalamus detects hypo-osmolarity and low BP
  • activation of cells in AVP-containing supraoptic nuclei causes release into posterior pituitary (PP) near PP circulation
  • pain, exercise and stress = AVP relase
  • acts in kidney at V2R to increase water reaborp and increase BP
  • dfects in AVP = diabetes
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15
Q

what are the clinical uses of AVP?

A
  • short duration
  • desmopressin = V2R agonists
    • for diabetes
  • Tolvapatan V2-selective non-peptide antagonists
    • for inapprop AVP secretion
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16
Q

how is V1a implicated in bahaviour of animals?

A
  • montane (polygomous) vs. prarie (mono) voles
  • V1a receptor extensice expression in prarie voles
  • species differences in behaviour due to variations in expression
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17
Q

describe the hypothalamus –> tissue pathway.

A

hypothalamus>>releasing hormone>> ant pituitary>> trophic hormone >> peripheral gland >> horone >> target tissue>> effect

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18
Q

describe the hypothalamic-pituitary-adrenal stress cascade.

A
  • includes corticotrophin release factor (CRF, hypothalamus)
  • adrenocorticotrophic hormone (ACTH, anterior pit)
  • cortisol (adrenal cortex)

HPA axis

  1. paraventriculr nucleus release CRF
  2. stimulates anterior pit release ACTH
  3. ACTH stimulates adrenal cortex to release GC’s
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19
Q

what are the features of corticotrophin?

A
  • produced in paraventricular nucleus
  • critcal stress response hormone
  • apart from endocrine actions: autonomic activation, increase BP + HR, behavioural effects and inhibits food intake
  • important NT in locus coeruleus
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20
Q

what are the 4 CRF receptors?

A
  • CFR-1 : cortex and cerebellum
  • CRF-2α: lateral septum and hypothalamus
  • CRF-2γ: amygdala
  • CRF-2β: skeletal muscle and heart etc
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21
Q

what are antagonists of CRF-1 and CRF-2?

A

CFR-1 = antalarmin

CRF-2 = astressin-B

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22
Q

dicuss the general role of groth hormones and what is the result of a deficiency or XS.

A
  • primary hormone responsible for growth
  • activtes GH receptors to induce IGF synthesis and secretion in liver –> protein synthesis and lipolysis
    • increase bone growth
    • decr. fat
  • mediated by stress, nutrition, sleep etc levels of GHRH/somatostatin
  • deficiency –> dwarfism
  • XS –> gigantism
    • pituitary adenoma
    • diagnosis - increase GH IGF-1
    • treated with microsurgery , radiotherapy
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23
Q

what are the positive symptoms of schizophrenia? are they treated?

what are the cognitive symptoms?

A
  • hallucinations
  • delusions
  • thought disorders - disorganised
  • movement disorders

anti-psychotics only treat negative symptoms

cognitive:

  • less ability to make decisions
  • problems with working mem
  • problems with focussing
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24
Q

what is the evidence for DA, 5-HT and Glu (PCP) that these systems –> schizophrenia??

A

DA

  • activating DAergic system can induce psychoses.
  • blocking D2 R decreases psychotic symptoms in some ppl

5-HT

  • activating serotonergic sys can induce psychoses

Glu (PCP)

  • blocking ion-channel of NMDAR can cause behaviours similar to those in schiz
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25
Q

what type of receptors showed a marked decrease in some schiz patients?

A
  • M1R decreased in all regions, in particular hippocampus caudate-putamen and DLPFC
    • consequence is abnormarl GP recruitment of M1
  • no evidence that drugs affected the number of M1Rs
  • 25% patients lost 75% of cortical M1Rs
  • No change in M2, M3 or M4Rs
  • M1R = cholinergic

= muscarinic receptor deficient (MDR)

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26
Q

what is the correlation with MRD and anti-psychotic drug resistance?

A
  • 25% have lost 75% of cortical M1Rs
  • 25% on average given higher levels of anti-psychotic drugs –> resistant group?
    *
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27
Q

***what are 2 peices of evidence supporting the MRD theory in schizophrenia?

A

drugs havent caused decrease

  • patients with low M1R are more agitated therefore more likely to be give BZD
  • GABA system does not appear to affect MRs

microRNAs - one targeting M1, one does not

  • level of microRNA increases in patients who have lost M1Rs as microRNA blocks translation
  • loss of mRNA by blocking it with microRNA
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28
Q

what are 2 drugs that restore cognition in MRD schiz patients?

A
  • xanomelin - M1 agonists, improved cog deficiency
  • allosteric M1 modulators
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29
Q

why are neurons so susceptible to neurotoxins?

A

adult DCNS neurons are post-mitotic

  • do not divide - is lost it is for good
  • neuronal stem cells mostly inact in adult - not many born (exp olfacotry + hippo)
  • dead neurons are replaced by glial cells -scar formation

many CNS neurons are extremely large

  • very large SA - big target, more exposure to toxins
  • energy intensive, dep on high O2 supply
  • many neurons use Fe3+ for NT synthesis -formation of ROS

polarised cell mebranes

  • activated by depol - release NT, IC Ca2+
  • damage often causes prolonged depol - disrupts neuronal function
30
Q

describe general features of apoptosis

A
  • programmed cell death
  • extrinsic and intrinsic signal activate proteases
  • plasma membrane blebbing occurs
  • apoptotic neurons display “eat me” signals on surface
  • mac’s move in to dispose of cell in orderly manner without eliciting an inflammatory response
31
Q

what are the general features of necrosis?

A
  • unprogrammed cell death
  • often elicits inflam response
  • caused by enzymes released from lysosomes that digests cell
  • cell swell
  • damage to neuron may compromise lysosome membrane direcetly or set off chain reaction
  • may harm nearby cells
  • removal of cell debris is difficult as cells dont have “eat me “ signals to attact phagocytes to engulf neuron
32
Q

what are typical apoptotic triggers?

A
  • absence of survival factors
  • DNA damage
  • oxidative stress
  • death receptor ligands
33
Q

what are typical necrosis triggers?

A
  • hypoxia, ischemia
  • depletion of ATP
  • prolonged membrane depolarisation
  • disrupted Ca2+ control
  • activatin of proteases
  • damage to membrane
  • local imflammation/ damage to neighbouring cells
34
Q

draw a flow chart of the sequence of events following an ischemic insult.

A
  • NOS produces NO and RNS (reactive nitrogen species) + ROS –> cell membrane lipid and protein oxidation and DNA base modification
35
Q

what aare the critical periods of sensitivity to toxins in development?

A
  1. post-fertilisation
  2. pre-implanatation
  3. implantation –> gastrulation
  4. organogenesis
  5. foetal period
36
Q

how can tobacco smoke and alcohol cause morbidity in children?

A
  • as brain develops ethanol can cuase FAS –> dysmorphorism, intellectual defects
  • tobacco smoke –> developmental disease and morbidity
    • nicotine = teratogen
    • teratogen exposure –> all or nothing efefct in pre-embryonic phase
37
Q

how do folate deficiency and medication effect prenancies?

A
  • medications taken during 3-8 week phase have the greatest potential to induce gross malformations by affecting organogenesis
    • type of malformation dep on which organs are most susceptible at the time
  • folate deficiency is associated with neural tube defects (closure)
    • anti-seizure med’s are folate antag’s (methotrexate, 5-fluruorcil)
  • folate function as carbon donor in formation of serine from glycine - affects purine and pyrimidine bases and tRNA(indirect)
38
Q

what are potential toxic mechanism that may interfere with developent?

A
  • altered energy source
  • altered nucleic acd function/integrity
  • change memrbane characterisitcs
  • enzyme inhibition
  • mutation
39
Q

describe how severd axons can be recovered.

A
  • PNS axons can regenerate to re-establish some lost connections
  • some limited CNS axon sprouting but little axon regeneration
  • dendrites can regenerate to reform new connections
  • recrutiment of alternate undamaged neurons to perform new functions (if regen not successful)
40
Q

what is the Parkingson’s hypothesis?

A
  • it is product of DA that promotes cell death
  • XS DA –> ROS
  • DA forms quinone with Cys residues on proteins (cell damage)
  • requried Fe3+ for synthesis
  • metabolised by MAO-B = ROS
  • DA neuron in high density
41
Q

describe MPTP toxin and how it produces its effects.

A
  • MPTP - toxin affect neuron cell body
  • produces Parkinson’s symtomes
  • depletes DA terminals
  • lipid-soluble, cross BBB
  • enters astrocytes, converted to MPP+ by MAO-B
  • MPP+ accumulates in DAergic cells of substantia nigris cia DAT re-uptake system
  • MPP+ enters mitchondria, block respiration –> energy depletion –> neuronal death
42
Q

what are some potential targets for PD treatments (from MPTP pathway)?

A
  • MAO-B inhibitors - block MPTP–> MPP+
  • DAT blockers - block MPP+ uptake
  • PARP-1 knockout mice have decreased sensitivity to MPTP+, suggesting PARP inhibitors may be used in treatment of PD
43
Q

describe toluene neurotoxcity.

A
  • accumulates in membrane of oligodendrocytes and disrupts the myelin sheath in CNS white-matter
  • De-myelinated neurons are slower, AP arrive out of synch
  • lipid soluble
44
Q

describe n-Hexane neurotoxicity.

A
  • damages neurofilaments and cross-linked cytoskeleton proteins which disrupts AP at nodes of Ranvier
  • axon pathology shows from distal –> proximal end
45
Q

what are the affects of chronic and acute toxin exposure in CNS?

A

Acute

  • low exposure - alterations of cognitive and psychomotor functions (reverible)
  • high - headaches, ataxia, nauses, euphoria (mostly reversible)
  • very high - coma, loss of consciousness, deah

Chronic: impairment of memory and learning skills, irritability, personality change

46
Q

what occurs in chronic abuse of n-hexane and nitous oxide?

A
  • peripheral neurological defects
  • sensorimotor polyneuropathy (n-hex)
  • demyelinating polyneuropathy (nitrous oxide)
  • extreme weakness (nit) may be related to inactivation of vitamine B12
47
Q

what are the type of axonal transport and what are some toxins affecting it?

A
  • axonal transport: MT (fast) and neurofilaments (slow)

toxin s

  • colchicine - binds tubulin and prevents polymerisation
  • vincrisstine - prevents MT formation
  • nocodazole - causes depolymerisation of MTs
  • mercury - bind beta sub’s of tubulin and disrupts MT formation and transport
48
Q

what pathologies does lead poisioning lead to?

A
  • metals are frequently bound to proteins for transport, storage and limit their redox reactivity
  • lead can replace Ca2+ in bone because both exist as 2+ state and have similar radii so can fit into same pocket
  • pathology: oedema of brain to extravasion of fluid from capillaries, neuronal death and gliosis
  • recovery: epilepsy, mental retardation, blindness
  • lead have pronounced effects on development of CNS and produces cognitive impairments, affects glu-transmission and DAergic function (critical for learning and mem)
49
Q

what is the mechanism leading to lead toxicity?

A
  • competes/sub’s Ca2+ and disrupts Ca2+ homeostasis
  • stimulates Ca2+ release from mitochondria
  • damages mitocondia and membranes
  • accumulates in brainastrocyes etc. (glials)
  • absorption of Pb from GI tract greater in children, Pb crosses intestinaly cells via Ca2+ uptake systems (upreg in kids)
  • highest concentration in hippo, cerebellum and cerebral cortex
  • once deposityed lead to eliminated very slowly - half life of 2 years in brain
50
Q

describe the acute, chronic and developmental affects of ethanol toxicity.

also describe the metabolism.

A
  • acute - CNS depression, vasodilation, hypoglycaemia
  • chronic - fatty liver, alchoholic hepatitis, cirrhosis
  • developmental - low birth weight, poor muscle coordination, mental deficiency
  • metabolism - by alcohol dehydrogenase (ADH) - toxicity due to metabolite acetealdehyde and formic acid
51
Q

what are the different types of neurotrophins and their functions?

A
  • nerve growth factor (NGF) - promotes survival of sympathetic neurons (PNS), sensory neurons (PNS), cholinergic neurons (CNS
  • brain-derived neurotrophiv factor (BDNF) - promotes survival of sensory neurons, motor neurons, DAergic neurons in CNS
  • Neurotrophin-3 (NT-3) - promotes surival of sensory neurons (CNS)
  • NT-4/5
52
Q

what are the sources of neurotrophins?

A
  • target-derived: NGF in targets on sympahetic neurons, BDNF in muscles
  • paracrine sources: BDNF up-regulated in Schwann cells after axonal lesion
  • autocrine: BDNF in dorsal root ganglion promotes dorsal root ganglion survival
53
Q

what are the 2 classes of neuotrophin receptors?

A
  • Trk family, receptor TK’s - high affinity binding
  • p75 - low affinity binding
54
Q

describe the general features of the Trk receptors and with NT’s bind each receptor

A
  • survival/differentiation signals
  • trkA, trkB, trkC
  • EC ligand binding domain
  • single TM domain
  • cytosoic TK activity

NGF–> trkA

BDNF and NT-4/5 –> trkB

NT-3 –> trkC (small amount to others)

55
Q

describe the neurotrophin binding trk

A
  1. neurotrophin binds 2 trk molecule
  2. NT-trk complex bind 2nd
  3. homodimerisation of receptor
  4. activation of intrinsic TK domain
  5. autophosphorylation of specific Tyr
  6. recruitment of SH2-fomain containing proteins from cytosol e.g. PLCγ
56
Q

describe the function of p75.

A
  • forms complex with trk or signals itself (Apoptosis)

apoptosis

  • antisense to p75 causes age-dependent survival/apoptosis rat sensory neurons
  • NGF –> apoptosis rat retinal neurons expressing p75 not trkA
  • p75 KO –> loss of sympathetic and sensory neurons
57
Q

describe the features of CNFT.

A

ciliary neurtophic factor (CNFT)

  • a cytokine related to IL-6
  • promotes surival of motor neurons, ciliary neurons, sympathetic neurons
  • not found in neuronal targets, present in schwann cells
  • acts as lesion factor. damage –> release and CNFT surrounds nerve to protect it
58
Q

describe the features of CNFT receptors

A
  • no intrinsic TK domain
  • recruits IC TK upon ligand binding
  • CNFT receptor complex:
    • Gp130 + CNTFRα (no IC domain) + LIFRβ→ multimerisation (with ligand)
    • complex recruits kinases e.g. JAK/TYK which phosphorylate complex
59
Q

how can BDNF and CNFT be used therapeuticly?

A
  • in neurodegenerative diseases e.g. motor neuron disease (MND), PD
  • characterised by loss of neuron populaitons
  • BDNF and MND preclinical evidence
    • ability to prevent peripheral nerve degen following axotomy
    • arrest of disease in some mouse models
  • shown to have lack of benefit (pharmacokinetics, disease related)
  • CNFT also shown to decrease neuronal death - withdrawn due to toxicity
60
Q

what are some other functions for neurtrophins (apart from treating neurodegenerative diseases)

A

NGF and pain

  • provokes pain –> hyperalgesia
  • inhibition of NGF decreases pain and hyperalgesia
  • NGF antag’s = analgesics?
  • side effects - peripheral neuropathy etc

BDNF used to treat depression and schizophrenia

61
Q

what is the mechanism of action of MDMA?

A
  • blocks catecholine reuptake transporters therefore prolonging DA in synapses
  • activates limbic system - euphoria as well as rebound depression after DA depleted
  • activates BG - hyperactivity, rebound hypoactivity
  • increase DA at D1 and D2 receptors (satiety and craving)
  • serotonin R’s involved in feeling warmth/love with MDMA,
    • decrease serotonin receptors with chronic use (down reg)
62
Q

ar the general features of the Toll-like receptors?

A
  • TLR and IL-1 signalling - detect pathogens
  • macrophages have an abundance of TLR transcripts as wella s glial cells (in brain)
  • activation of TLR drive pro-inflammatory cytokines
  • MyD88 = adaptor protein
    • all require MyD88 except TLR3
63
Q

what is the role of MyD88-dependent TLR signalling in stroke.

A
  • MyD88-signalling may be protective
    • KO MyD88 so all TLR not working (exp TLR3) –> massive stroke compared to control
    • unexpected because TLR plays role in inflammation–> death
  • in vitro - determinal, in vivo MyD88 signalling is protective
  • damaged brain signals for mediators invasion
  • TLR det release of cytokines and factors

MyD88 in haematopoietic cells det infarct volume

  • haematopoietic cells play protective role in brain after stroke using TLRs and MyD88 sig
  • MyD88 in haema cells det cellular infiltration and therefore infarct volume
  • MyD88 -/- means no invasion, large infarct

IL-10 (is AI cytokine) decreases damage of stroke, it is under control of MyD88. T-regulatory cell release it

64
Q

describe embolism formation

A
  • embolism break off and entery artery
  • most likely occludes mid-cerebral artery
  • MCA pefuses a lot of area in the brain
65
Q

what are ways to many the risk factors of stroke?

A
  • hypertension: ACEI with diuretics
  • lipid lowering: elevated LDL increases risk of stroke
  • diabetes type II: co-morbidity, increases risk
66
Q

draw a flow chart of the events following a stroke (ischemic event)

A

energy failure ⇒ ATPase Na+/K+ not functioning ⇒ depolarisation ⇒ Glu release ⇒ Ca2+/Na+ entry

⇒Ca2+ activates enzymes (NOS)⇒free radicals ⇒mediator release, DNA damage, mitochondiral damage⇒VISCIOUS CYCLE

⇒Na+ causes swelling

67
Q

describe the free radical reactions in stroke

A
  • lipid peroxidation (arachondic acid cycle, from phospholipid bilayer)
  • free radicals influence signal transduction and therefore how cell behaves
  • many processes occur - targeting one will not prevent the damage
  • high levels of Gpx in brain, low lebels of CAT
  • Gpx -/- mice: massive infarct size, lots of H2O2, oxidative stress plays huge role in injury
68
Q

discuss the effects of NFKB in stroke.

A
  • NFKB = major TF in oxidiative stress
  • oxidants –> more NKFB –> more adhesion molecules i.e. mediators (e.g. ICAM) = BAD
  • NKFB up-regulated; ICAM up-reg; Leukocytes roll and adhere more avidly –> bigger stroke
    • higher in smokers, drinkers
69
Q

discuss the role of leukocytes in stroke.

A
  • not as detrimental as previously though
  • post-ischmeic WT has more leukocyte recruitment in venules then Gpx -/- (more oxidative stress)
  • evidence that they may not be damaging as thought - MAb’s that target selectins and ICAM so leukocytes cannot adhere
70
Q

what is the acute treatment of a stroke?

A
  • T-PA i.v. is beneficial for ischemic strokes - 3 hour window
  • early admission to hospital with stroke unit is critical
  • hypothermia:
    • may decrease damage from excitotoxins, inflammation, free rad’s and necrosis
    • shivering can be detrimental - but muscle relaxants may also stop breathing
    • development of safer endovascular heat exchangers + anti-shivering protocols which avoid sedation
  • steroid - no imporvement in trials
  • Glu-NMDA antags - all trials failed
71
Q

what is the secondary prevention for strokes?

A
  • prevention of strokes for those who have already suffered one
  • anti-platelet/anti-thrombotic agents:
    • aspirin decreases risk
    • Clopidogrel superior to aspirin?
    • dipyimadole in patients who have failed aspirin
    • combination?
  • athersclerosis - anti platelet
  • cardioembolic - warfarin
  • surgical prevention: carotid endarterectomy in patients with extracranial carotid artery disease - trials
    • intracranial stenosis - trials
  • prevention = most cost effective
  • understanding subtye of stroke imp in development 2o prevention stratergies

Drugs that affect the NS (3 decks)

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