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EXP NEURO > Neuropharm and neurosci > Flashcards

Neuropharm and neurosci Flashcards

1
Q

define neuropharmocology:

A
  • study function of neurons, systems that they drive

- not only applied to neurons in brain, also neurons leading to peripheral control of organs/mm

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2
Q

define pharmacology:

A
  • drug interaction w receptors/ binding sites

- effect on brain and body

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3
Q

NT release: procedure

A
  • NT exists in presyn, released (exocytosis)
  • release of AP
  • acts on receptor (biological effect)
  • inactivation (unbound NT transported into presyn terminal) reuptake= endocytosis
  • application of exogenous chemical (agonist or antagonist of NT)
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4
Q

receptor activation: ionotropic receptors

A
  • ligand gated ion channels
  • composed 5 subunits
  • binding of NT to subunit, causing to move and create channel
  • +ve and -ve ions flow into cell
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5
Q

receptor activation: metabotropic receptors mechanism

A
  • activate ion channels/ 2º messenger system
  • need metabolic process through G protein to cause effect
  • receptor binds activating G protein, GDP replaced w GTP
  • G protein splits, activates effector proteins - 2º messenger systems or ion channels
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6
Q

define: agonist

A
  • direct communication
  • binds to receptor, effect of neuron
  • works like NT
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7
Q

define: antagonist

A
  • direct communication
  • binds to receptor but not effect of neuron
  • stops NT from having effect
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8
Q

define: positive allosteric modulator (PAM)

A
  • enhances function of agonists at receptor
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9
Q

define: negative allosteric modulator (NAM)

A
  • reduces function of agonist at receptor
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10
Q

we use neuropharm to: list (4)

A
  • investigate how NT interact within particular circuits in the brain
  • determine how peripheral neurons work, what brain regions/ NT drive them
  • understand how NT/ neuropeptides work in brain to drive behaviour
  • drive hormone release by brain structures/ NT
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11
Q

hormone release: list glands (2)

A
  • pineal

- pituitary

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12
Q

hormone release: pineal hormone

A
  • melatonin
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13
Q

hormone release: pituitary reg by? (region)

A
  • regulated by hypothalamus
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14
Q

hormone release: ant pituitary controlled by

A
  • parvocellular secretory cells of hypothalamus
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15
Q

hormone release: ant pituitary releases (6)

A
  • ACTH
  • FSH
  • LH
  • TH
  • GH
  • prolactin
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16
Q

hormone release: list post pituitary hormones (2)

A
  • vasopressin

- oxytocin

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17
Q

hormone release: oxytocin reg by, released where?

A
  • magnocellular neurosecretory cells of hypothalamus

- released into blood vessels of post lobe of pituitary gland

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18
Q

hormone release: oxytocin periphery regulates (3)

A
  • myometrial contractions (contracts uterus during childbirth)
  • contracts myoepithelial cells in mammary glands for milk expression (breastfeeding/ lactation)
  • increases sperm no. and contractions needed for ejaculation
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19
Q

oxytocin: effects in brain (5)

A

social neuropeptide:

  • social interactions btw peers
  • formation of monogamous pair bonding
  • sexual arousal and orgasm
  • maternal behaviour
  • social memory and anxiety reduction (anxiolytic)
20
Q

oxytocin (OXY): location in the brain

A
  • magnocellular neurosecretory cells of hypothalamus
  • magnocellular cells are in PVN (paraventricular nucleus), SON (supraoptic nucleus) and accessory nucleus of hypothalamus
21
Q

oxytocin: SON- function and spread

A
  • mostly volume transmission and neuron to neuron contact
22
Q

oxytocin: PVN- function and travels to

A
  • classical neuron to neuron contact and vol transmission (less than in SON)
  • oxytocin receptors in brain aka OT receptors
23
Q

pharmacology of amphetamines: function

A
  • increase extracellular monoamines
  • reverse monoamine and vesicular transporters (VMAT)
  • methamphetamine reverses DAT, VMAT
24
Q

pharmacology of amphetamines: eg. ecstacy

A
  • type of amphetamine

- reverses SERT (serotonin transporter)

25
Q

oxytocin (OXY) in METH taking and relapse: summary (2)

A
  • oxytocin reduced motivation to consume methamphetamine
  • reduced relapse to meth-seeking behaviour

where in brain is oxytocin inhibiting behavioural effects of meth?

26
Q

c-fos: function

A
  • immediate early gene
  • neurons activated, gene upregulated
  • increase in manufacture of protein c-Fos
  • c-Fos immunohistochemistry labels excited cells in brain
27
Q

OXY: brain regions affected (2)

A
  • nucleus accumbens (NAc)

- subthalamic nucleus (STh)

28
Q

addiction circuit: NT assoc (3)

A
  • glutamate
  • dopamine (DA)
  • GABA
29
Q

OXY: administration affect which summary

A
  • OXY administration, systemically or into NAc/ STh sig reduced CPP reward/ relapse to meth-seeking behaviour
  • local effect of oxy partially reverse by selective OTR antagonist when administered into NAc or STh
  • effect of systemic oxy not reversed by systemic pretreatment w OTR antagonist

oxy admin reduced relapse to meth use through receptor mechanisms other than OTR (oxy receptors)

= possibly vasopression V1a receptors

30
Q

vasopressin: periphery function (3)

A
  • aka ADH
  • diuresis (increases urine production) ADH release retains fluid in body (V2 receptors)
  • regulates blood vol and ion (salt) conc.
  • causes constriction of blood vessels to increase BP (V1 receptors)
31
Q

vasopressin: in the brain- location, highest lvls, function

A
  • also in SON, PVN neurons
  • highest lvls of Vaso receptor binding in bed nucleus stria terminalis, central amygdala and nucleus accumbens
  • effect on brain depends on receptor subtype activated
32
Q

vasopressin: V1a activation

A
  • prosocial effects

does oxy activate V1a receptors to reduce meth relapse?

33
Q

vasopressin: V1b activation

A
  • anxiety, fear, aggression
34
Q

vasopressin receptor on oxy: summary

A
  • effect of oxy to reduce meth relapse reversed by V1a receptor antagonist (admin sys or locally into NAc)

= suggests oxy admin is effective in reducing meth use through V1a receptor dependent mechanism

35
Q

molecular neuropharmacology: FSCV aka

A
  • fast scan cyclic voltammetry
36
Q

molecular neuropharmacology: FSCV function

A
  • electrochemical technique used to look in real time at conc. of NT released within circuit
  • can measure electroactive NT (dopamine, NAd, serotonin)
37
Q

molecular neuropharmacology: dopamine function

A
  • important for motor, cognitive functions

- regulating reward processes

38
Q

FSCV: features and mechanism

A
  • carbon fibre microelectrode inserted into brain region of interest
  • stimulator + cannula
  • voltage applies to electrode, holds -ve potential and then to +ve potential (oxidation) then -ve (reduction)
  • application of charge in triangular waveform repeated every 100ms
  • change in current during oxi-redox process measured
39
Q

FSCV: pros

A
  • good spatial resolution

- good temporal resolution

40
Q

Acetylcholine and addiction: type and location

A
  • NT and neuromodulator

cell bodies located in:

  • magnocellular basal forebrain system (medial septum, nucleus basalis of meynert, diagonal band of broca)
  • brainstem system (pedunculopontine tegmental nucleus, laterodorsal tegmental nucleus)
41
Q

Acetylcholine and addiction: list (2) receptors, locations and function (5)

A
  • projections all around brain, also effect vol transmission
  • muscarinic (metabotropic) and nicotinic (ionotropic) receptors
  • involved in attention, memory, learning, mm movement and REM sleep
42
Q

Acetylcholine and addiction: reward and addiction processes

A
  • cholinergic input from pedunculopontine tegmental nucleus (PPTG) and laterodorsal tegmental nucleus (LDTG) stimulates dopamine release from VTA
  • following exposure to drugs, cues assoc to drugs, increased acitivity in both PPTG and LDTG ACh neurons (increase firing of dopaminergic neurons in VTA)
43
Q

cocaine administration summary:

A
  • cocaine admin (experimenter given/ self-administered) increases dopamine firing in VTA and NAc pathway in animals previously exposed to cocaine
  • cholinergic input from brainstem cholinergic sys stimulates dopamine firing in VTA
  • in cocaine withdrawn animals, cholinergic input to VTA drives dopaminergic firing, not glutamate
  • cholinergic activation of muscurinic receptors of VTA drive global reward processes, whilst activation of nicotinic receptors in VTA drive drug reward processes
44
Q

overall summary: neuropharm

A
  • neuropharm allows researchers to directly manipulate neural sys to see how they are activated/ inhibited and how this affects systems neurosci (behaviour, CVS etc.)
  • help understanding how drugs abuse work, treat diff disorders and diseases
45
Q

which (2) brain regions involved in memory of how good is drug use?

A
  • hippocampus

- amygdala

46
Q

OXY antagonist: reverses effect of OXY in what brain regions (2) and partially/completely?

A
  • NAc: partially reversed

- STN: partially reversed

47
Q

cocaine withdrawn animals: cholinergic input to VTA drives dopaminergic/glutamate/both firing?

A
  • only dopaminergic firing

EXP NEURO (10 decks)

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