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neuroscience psychology > lecture 4- neurotransmitters 2 > Flashcards

lecture 4- neurotransmitters 2 Flashcards

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1
Q

neurotransmitters- biogenic amines

A
  • dopamine
  • serotonin
  • histamine
  • adrenaline/ epinephrine
  • noradrenaline/norepinephrine
  • small molecule NTs
  • similar structures
  • widespread in the brain
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2
Q

serotonin in the CNS

A
  • 90% serotonergic signalling in the gut
  • 10% serotonergic neurons in the brain
  • produced in the pons and upper brainstem (raphe nuclei), it has projections to the forebrain
  • roles: regulation of mood, appetite and sleep, also involved in memory and learning
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3
Q

depression and monoamines

A
  • depressions key clinical features:
  • intense feelings of persistent sadness, helplessness and hopelessness
  • anhedonia (general lack of interest)
  • tiredness, lack of energy
  • abnormal sleep and eating patterns
  • cognitive impairments: concentration, memory, executive functions
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4
Q

the monoamine hypothesis

A
  • reserpine (hypertension medication)
  • reported side effect: symptoms of major depression (Michaels & Gibbon, 1963)
  • antagonist of monoamines
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5
Q

antidepressants

A
  • monoamine oxidase inhibitors (MAOIs)- inhibit the activity of the enzyme MAO that normally breaks down monoamine NTs- dopamine, noradrenaline and serotonin
  • tricyclic antidepressants (TCAs) block reuptake of noradrenaline and serotonin- increasing the levels if these two NTs in the synapse
  • SSRIs- selective serotonin reuptake inhibitors: first choice for treating depression
  • SNRIs- selective noradrenaline reuptake inhibitors
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6
Q

serotonin based treatments

A
  • selective serotonin reuptake inhibitors (SSRIs) block the channels that allow serotonin to be removed from the cleft
  • side effects are still seen:
  • due to the high levels of serotonin receptors in the GI tract, side effects of treatments can include weight less, nausea and diarrhoea
  • example of SSRIs, prozac, fluoxetine
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7
Q

depression = low serotonin?

A
  • agonists enhance serotonin action
  • thus depression = low serotonin? yes
  • moncrieff, 2022: meta-analysis
    • no strong evidence for lowered serotonin actions in depressed patients compared to controls
  • royal college of psychiatrists (2019)
    • stated that saying anti-depressants correct a chemical imbalance is an “over-simplification”
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8
Q

anti-depressants are effective for some patients:

A

-Cipriani et al (2018) review/meta-analysis of antidepressants found all studied drugs to be more effective than placebo
- three SSRIs (escitalopram, paroxetine & sertraline) found to have the highest response/lowest drop out rates

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9
Q

what other effects might SSRIs have?

A
  • beck (1967): cognitive mechanisms causing depression
    • negative automatic thoughts
    • negative schema
    • negative information processing biases
  • negative biases in processing
    • information recall
    • interpretating facial expressions
    • distraction by negative stimuli
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10
Q

SSRIs can influence cognitions

A
  • in depressed participants, following a single dose of SSRIs, we find:
  • enhanced recognition of facial expressions (Tranter et al., 2009)
    • particularly happiness
  • increased recall of positive stimuli in word memory tasks (Harmer et al., 2009)
  • no associated increase in self reported mood
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11
Q

acute effects

A
  • acute effects of antidepressants are found for processing emotional stimuli
  • reduced negative bias in attention and memory tasks, enhanced recognition of facial expressions
  • findings are consistent with cognitive theories of depression- negative ‘low level’ (perceptual & attentional) biases are related to ‘high level’ beliefs about self, world & others (Becks dysfunctional schemas)
  • importantly, acute cognitive effects occur with no reported change in mood
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12
Q

dopamine

A
  • produced from tyrosine -> DOPA -> dopamine
  • dopamine is involved in multiple pathways in the brain
  • it is a key importance in many functions, including reward, movement and the release of hormones
  • four pathways:
    -nigrostriatal
    • tuberoinfundibular
    • mesocortical
    • mesolimbic
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13
Q

dopamine: the tuberoinfundibular pathway

A
  • arcuate nucleus of the hypothalamus to the pituitary gland
  • influences the release of hormones into the blood stream
  • eg growth hormone, adrenocorticoids, prolactin (production of milk)
  • pituitary gland further controls hormone release
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14
Q

dopamine: the nigrostriatal pathway

A
  • substantia nigra to striatum
  • involved in the basal ganglia loop and the initiation of movement
  • the pathway affected in Parkinson’s
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15
Q

dopamine: the mesocortical pathway

A
  • ventral tegmentum to frontal lobes
  • involved in motivation and emotional responses
  • decreased levels of dopamine in this pathway are thought to be associated with the negative symptoms of skits
  • apathy, listlessness, poverty of speech
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16
Q

dopamine: the mesolimbic pathway

A
  • ventral tegmentum to the limbic system, via, nucleus accumbens, amygdala, hippocampus and medial prefrontal cortex
  • associated with feelings of reward and desire
  • implicated in addition and depression
  • hyperactivity of dopamine associated with the positive symptoms of schizophrenia (eg delusions, hallucinations)
17
Q

schizophrenia

A
  • a psychotic disorder involving disturbances of thought, emotion and behaviour
  • literally ‘split mind’-
    • ‘fragmented thinking’
    • a disconnect between a persons subjective experiences and objective reality
18
Q

symptoms of skits

A
  • positive symptoms = presence of abnormal experiences and behaviour (eg hallucinations, delusions, disorganized speech and behaviour)
  • negative symptoms= absence of normal experiences and behaviour (eg lack of emotion, apathy, anhedonia, social withdrawal, poverty of speech)
  • cognitive symptoms= broad impairments in attention, working memory, episodic memory, executive functions
19
Q

the dopamine hypothesis of skits

A
  • link between dopamine and skits?
  • dopamine agonists (eg amphetamine, cocaine)
    • produce skits like symptoms in previously healthy individuals
    • worsen symptoms in people who have been diagnosed with a psychotic disorder
  • the dopamine hypothesis of skits: psychosis (positive symptoms) are caused by excessive levels of dopamine)
20
Q

dopamine agonists

A
  • amphetamine & cocaine: increase release and/or block reuptake of dopamine
    • chronic abuse can cause skits-like symptoms (paranoia, delusions, hallucinations, stereotyped repetitive & compulsive behaviours) in non-schizophrenics
    • amphetamine psychosis first described in 1950s
  • L-dopa: dopamine precursor
    • used to treat Parkinson’s disease since early 1960s
    • high doses can cause skits like symptoms in patients
21
Q

dopamine antagonists

A
  • anti-psychotics used to treat positive (ie psychotic) symptoms like hallucinations and delusions
    • chlorpromazine/thorazine
    • haloperidol
  • but little or no effect on negative on negative symptoms, and can actually make these worse
  • block dopamine receptors (specifically type D2) preventing their activation
22
Q

what about negative symptoms

A
  • original formulation of the dopamine hypothesis didnt address negative symptoms
  • current versions regard skits as a disorder of dopamine regulation
  • positive symptoms are linked to excessively high levels of dopamine, especially in basal (‘deep’) forebrain areas
  • negative symptoms may reflect abnormally low levels of dopamine (&reduced brain activity) in PFC - this would explain why antipsychotic drugs can worsen negative symptoms
23
Q

dopamine regulation

A
  • one version of this idea (eg Davis et al, 1991) sees dopamine under-activity in prefrontal cortex as the primary deficit in skits
  • this then leads to reduced inhibitory control over dopamine producing neurons in basal forebrain areas (‘mesolimbic system’)
  • ‘runaway’ dopamine release in basal forebrain/ mesolimbic areas then leads to positive symptoms
24
Q

complementary therapies

A
  • antipsychotic drugs dont necessarily prevent hallucinations or delusional thoughts
  • but can make them feel less important and less distressing
  • psychotherapy (eg CBT) may be required to actually change delusional beliefs
  • but this is more likely to succeed if combined with an antipsychotic to weaken ‘attachment’ to delusional beliefs
  • treatment for negative symptoms may involve medication, but has also been found to benefit from CBT
25
Q

the side effects of dopamine treatments

A
  • due to widespread dopaminergic synapses, any treatment involving these receptors will have the potential for side effects
  • agonists of dopamine: drugs for parkinsons treatment can cause hallucinations, psychosis; impulse control disorders-compulsive gambling, shopping, binge eating (acting on the mesolimbic and mesocortical pathways)
  • antagonists of dopamine: Anti-psychotics can cause parkinsonism (parkinsons like symptoms); tremors and dystonia (acting on the nigrostriatal pathway)

increased secretion of prolactin, leading to galactorrhea (unusual secretion of breast milk) (acting on the tuberoinfundibular pathway)

26
Q

definition of a neurotransmitter

A

-needs to be present in the presynaptic terminal
- needs to be released when an action potential arrives and calcium moves into the synapse
- needs to be something on the post synaptic membrane that it can bind to, a specific receptor that it fits with

27
Q

unconventional neurotransmitters

A
  • these NTs are not stored in the pre-synaptic terminal
  • they are not released by exocytosis and may not be released from the terminal at all
  • they may be used in retrograde signalling: the post-synaptic cell signals back to the pre-synaptic cell
28
Q

endocannabinoids

A
  • produced ‘on demand’ from the cell membrane (not stored in vesicles)
  • retrograde signalling: post synaptic cells signal to pre synaptic neurons
    • their release reduces the amount of conventional neurotransmitters released for a short period
    • allows post synaptic cell to control its ‘incoming traffic’
  • role in synaptic plasticity (Vaughan & Christie, 2005)
  • involvement in memory, regulation of appetite, homeostasis
29
Q

endocannabinoids cont

A
  • anandamide (ANA)
  • endocannabinoid synthesised in the body
  • binds to cannabiniod receptors CB1 and CB2 in the CNS and PNS
  • effects on hunger, sleep, memory, identification of novelty
30
Q

agonists of cannabinoid receptors

A
  • cannabinoid receptors are the molecular target of the tetrahydrocannabinol (THC), the psychoactive component of marijuana
    • CB1 receptors in the neocortex: effects on perception
    • CB1 receptors in the basal ganglia: effects on motor behaviour
    • CB1 receptors in the hippocampus: effects on short-term memory
    • CB1 receptors in the hypothalamus: effects on appetite
31
Q

uses of THC

A
  • anti-emetic properties (inhibits vomiting) are useful in the treatment of cancer patients on chemotherapy (Fride et al., 2006; Mechoulam et al., 2006)
  • eases symptoms (eg muscle stiffness) in multiple sclerosis (Zajicek et al., 2012)
  • recent review into possibility of using THC to treat mental health conditions suggests that this aspect is not well supported (black et al., 2019)
  • risks of developing schizophrenia with adolescent use, slowing in cognitive functions (Borgelt et al., 2013) (causality debated here)
32
Q

antagonists of cannabinoid receptors

A
  • rimonabant
    • blocks CB1 receptor
    • affects appetite, reducing food intake
    • initially used as a weightloss drug
    • withdrawn worldwide in 2008 due to a psychiatric side effects
      increases in depression, anxiety
33
Q

antagonists of cannabinoid receptors cont

A
  • CBD aka cannabidiol
  • as an antagonist at CB1 receptors, there is interest in using CBD to treat psychosis (Bhattacharyya et al., 2015, 2018)
  • some evidence that CBD might interact with certain medications (Levinsohn and hill, 2020)

neuroscience psychology (6 decks)

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