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Neuropsychopharmacology > Revision 2 > Flashcards

Revision 2 Flashcards

1
Q

Describe the mechanism behind drug addiction and craving (major neurotransmitters and brain areas).

A

**CRAVINGS = **Glutamate (prefrontal cortex (anterior cingulate gyrus, amygdala)-> nucleus accumbans)

ADDICTION = Dopamine (Ventral Tegmental area, through nucleus accumbens and to prefrontal cortex — mesolmbic dopamine system), reward circuits.

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2
Q

What are the treatments for heroin and morphine addiction?

A

Heroin and Morphine are both opiates - act on MU opiate receptors in the Nucleus accumbens/VTA

  • Methadone - agonist mu receptors - a weaker version of heroin (less rush) [REPLACEMENT T]
  • Buprenorphine - partial agonist - like methadone, but even weaker! [REPLACEMENT T]
  • Naloxon - antagonist mu opiate receptor - compliance is a problem (can be combined with naloxone)
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3
Q

Describe Methadone…

A

Heroine/morphine treatment

agonist mu receptors - a weaker version of heroin (less rush) [REPLACEMENT T]

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4
Q

Describe Buprenorphine….

A

Treat heroin and Morphine

partial agonist - like methadone, but even weaker! [REPLACEMENT T]

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5
Q

Describe Naloxone ……

A

Treat heroin and morphine

antagonist mu opiate receptor - compliance is a problem (can be combined with buprenorphine)

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6
Q

What are the treatments for alcoholism?

A
  • Acamprosate - NMDA receptor antagonist (block glutamate) - reduce craving
  • Naloxon - antagonist on mu opiate receptors - stops rewards effect of alcohol
  • Disulfiram - forces abstinence by making alcohol use ver unpleasant
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7
Q

Describe Acamprosate…

A

Treats alcoholism

NMDA receptor antagonist (block glutamate) - reduce craving

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8
Q

Describe Naloxon…

A

Treats alcoholism
antagonist on mu opiate receptors - stops rewards effect of alcohol

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9
Q

Describe Disulfiram…..

A

Treats alcoholism

forces abstinence by making alcohol use very unpleasant

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10
Q

What are the treatments for nicotine?

A
  • Nicotine replacement therapies - weans addict off nicotine
  • Buproprion - Dopamine reuptake inhibitor, increase dopamine in nucleus assumes act as replacement
  • Varenicline - partial agonist for nicotine receptor - competes with fast acting nicotine
  • Nicobrevin - camphor, eucalyptus oil, monthly validate, quinine - wtf does this do
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11
Q

Describe Nicotine replacement therapies….

A

Treat nicotine addiction

weans addict off nicotine

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12
Q

Describe buproprion….

A

Treat nicotine addiction

Dopamine reuptake inhibitor, increase dopamine in nucleus assumes act as replacement

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13
Q

Describe Varenicline

A

Treat nicotine addiction

partial agonist for nicotine receptor - competes with fast acting nicotine

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14
Q

Describe Clonidine…

A

Treats withdrawal effects of opiods, cocaine and nicotine

Antagonist at alpha2 adrenoceptors (noradrenaline) - ( noradrenaline cell bodies in the locus coerteleus are thought to produce withdrawal symptoms)

Intolerable side effects (low blood pressure/drowsy)

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15
Q

Describe Psychostimulant replacement therapy (Benzotropines)…..

A

Treat cocaine addiction

Similar to methadone - but block the dopamine transporter.

Drug binds slowly to DAT and stay there for a long time - prevents cocaine from having its effect at DAT.

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16
Q

What are the general neurotransmitter mechnisms and brain areas(6) behind anxiety disorders?

A

Neurotransmitters

  • Increase noradrenaline
  • decrease serotonin

Brain areas

  • Amygdala (emotion/fear)
  • Hippocampus (memory and negative associations)
  • Thalamus (relay/alertness level)
  • Locus Coeruleus (in pons stress and panic)
  • Dorsal or Rostral Raphe Nuclei (produce serotonin in the brain stem)
  • Cerebral cortex (less focused information from environment)
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17
Q

How does panic disorder differ from other anxiety disorders?

A
  • peri acqueductal grey (defensivness)
  • hypothalamus (integrates autonomic/somatic responses and releases cortisol/adrenalin/emotional response)
  • frontal cortex/cingulate cortex (mind panic)
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18
Q

How do Phobias differ from other anxiety disorders?

A
  • Cerebral cortex (less focused on environmental information)
  • Hippocampus (particularly strong negative associations)
  • Parietal/occipital/frontal lobe
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19
Q

How does general anxiety differ from other anxiety disorders?

A
  • Basal ganglia (increase vigilance, inadequate process of environmental info)
  • Cerebral cortex (inability to adequately execute responses appropriate to info from environment)
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20
Q

How does OCD differ from other anxiety disorders?

A
  • Uncontrolled communication between frontal, striatal and thalamic structures (lesions of frontal cingulate cortex breaks loop and helps OCD patients)
  • Substantia Nigra (dopamine system, repetition of habits), basal ganglia (increased dopamine reward habit formation)
  • **less cerebellar and sympathetic outflow than others disorders
  • increased DOPAMINE function in basal ganglia (nigrostriatal) produces repetition of habits.
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21
Q

How does PTSD differ from other anxiety disorders?

A

Amygdala becomes dominant and hippocampus shrinks (hippocampus can no longer provide helpful memories to overcome fear) - exacerbation of negative emotion linked to the memory of event

amgydala —-> hypothalamus = “increase cortisol
Hippocampus —>hypothalamus = “reduce cortisol”
Hypothalamus —-> piturity = release ACTH and increase cortisol
Cortisol levels tells hippocampus to tell amygdala to reduce cortisol messages

This mechanism dysfunctional when signals from amygdala outweigh those from hippocampus.

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22
Q

What was the general principle behind early treatments of anxiety?

A

If anxiety results from an overactive brain than
SILENCE BRAIN = Enhance inhibitory neurotransmission (IPSP) - enhance GABA receptor activation to enhance chloride ions CL-

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23
Q

Describe barbiturates….

A

Early treatment of anxiety disorders

Non-selective agonist of GABA receptor - lots of side effects (sedation/fatal overdose/highly addictive) - best used as anaesthetics

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24
Q

Describe Benzodiazepines (benzos)

A

Treats anxiety disorders

Selective GABA receptor agonists, enhance the effect of GABA on its receptor (therefore enahcned CL- and ISPS) - have their own binding site on the GABA receptor: BZ1 and BZ2

GABA-A receptor can bind both GABA and benzodiazepines to enhance receptor function on the dendrite of the neuron. (LETS THROUGH EXTRA CL-)

  • Reduce anxiety and agression
  • produce sedation (can be used for insomnia)
  • treatment is effective immediately (oral absorption is good)
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25
Q

More modern treatments of anxiety aim to….

A

Specifically decrease noradrenaline
• Specifically increase serotonin

NOT global treatments like barbiturates and benzodiazepines

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26
Q

What two types of specific treatments are generally used in anxiety disorders?

A

Selective Serotonin Reuptake Inhibitors (SSRI) (which block SERT)

and 5-HT1A agonists (which act like serotonin)

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27
Q

Describe SSRIs…..

A

Treat Anxiety and Depression

Block SERT (Serotonin transporter) preventing the reuptake of serotonin, therefore more serotonin remains in the synapse.

Delayed effect -
serotonin (5-H1A) receptors also exist presynaptically, serotonin that binds presynaptically signals for less serotonin to be produced. This process must be exhausted (presynaptic receptors must desensitise to serotonin or the agonist - then SSRI become effective.

28
Q

Describe 5-H1A agonists…..

A

Treat anxiety

Act like serotonin and bind to 5-HT1A metatrobic receptors having an overall inhibitory effect.

Delayed effect -
serotonin (5-H1A) receptors also exist presynaptically, serotonin that binds presynaptically signals for less serotonin to be produced. This process must be exhausted (presynaptic receptors must desensitise to serotonin or the agonist - then 5-H1A can become effective.

29
Q

Why is there a latency for SSRIs and 5-H1A agonists to work (2-3weeks)?

A

Serotonin (5-H1A) receptors also exist presynaptically, serotonin that binds presynaptically signals for less serotonin to be produced. This process must be exhausted (presynaptic receptors must desensitise to serotonin or the agonist - then SSRI and 5-H1A can become effective.

30
Q

All anxiety disorders have an effect on (6 brain areas + broad effect)

A
  1. Amygdala (emotion/fear)
  2. Hippocampus (memory and negative associations)
  3. Thalamus (relay/alertness level)
  4. Locus Coeruleus (in pons stress and panic)
  5. Dorsal or Rostral Raphe Nuclei (produce serotonin in the brain stem)
  6. Cerebral cortex (less focused information from environment)
31
Q

What is the overall neuropathology of depression (brain areas and neurotransmitters)?

A
  • Prefrontal cortex - reduced glia, neuron size and volume
  • Hippocampus - reduced GABA interneurons and volume
  • Amygdala - overactivation

+

  • Depression Neurotransmitters - Overall reduction in serotonin, noradrenaline and dopamine [monomines]
  • Depressed patients have decreased metabolites monoamines in their cerebrospinal Fluid (CFS) - DEPLETION OF MONOAMINES (NORADRENALINE, DOPAMINE, SEROTONIN)
  • Noradrenaline - locus coeruleus and caudal raphe nuclei [catecholamines]
  • Dopamine - mesolimbic system and nigrostriatal system [catecholamines]
  • Serotonin - rostral raphe and causal raphe nuclei [indolamine], tryptophan lacking in diet can produce symptoms of depression because tryptophan is needed to make serotonin.
  • Increase beta adrenoceptors in the cortex

increase 5-HT receptors in limbic regions
Decreased serotonin metabolites in several brain regions

32
Q

Reducing _____ in the diet will produce symptoms of depression because it is important in the production of ______.

A

Tryptophan, Serotonin

33
Q

What are the neurotransmitter abnormalities underlying mania?

A
  • Increased noradrenaline
  • Increased dopamine
  • Increased serotonin
  • Decreased GABA (major - IPSP) - neurons and interneurons
34
Q

What was the general principle behind first generation anti-depressants (+ what where these drugs) and how was it a problem?

A

If monoamines neurotransmission is reduced in depression, enhancing it will treat the depression

Drugs that increase all monoamines (Serotonin, noradrenaline and dopamine) e.g., Tricyclic antidepressants (blocks reuptake of all monoamine) or Monoamine oxidase inhibitors (blocks the metabolism of active monoamines)

LOTS of side effects:

TCA - dry mouth, impaired vision, increased heart rate, difficulty peeing, memory and learning impairments, sedation, postural hypertension (blocks alpha 1 adrenoceptors) CARDIOTOXIC (blocks ability for heart to pump.

MAOI - tremors, excitment, insomnia, food & drug interactions, hypertension, cardiotoxic (less than TCA) - can’t eat foods containing tyramine because MAO is needed to break down tyramine and failure to do so can cause spikes in blood pressure.

35
Q

Describe TCAs….

A

First gen treatment of depression

Tricyclic antidepressants (blocks reuptake of all monoamine)

LOTS of side effects:

TCA - dry mouth, impaired vision, increased heart rate, difficulty peeing, memory and learning impairments, sedation, postural hypertension (blocks alpha 1 adrenoceptors) CARDIOTOXIC (blocks ability for heart to pump.

36
Q

Describe Monoamine Oxidase Inhibitors…..

A

First gen treatment for depression

Monoamine oxidase inhibitors (blocks the metabolism of active monoamines)

LOTS of side effects:

MAOI - tremors, excitment, insomnia, food & drug interactions, hypertension, cardiotoxic (less than TCA) - can’t eat foods containing tyramine because MAO is needed to break down tyramine and failure to do so can cause spikes in blood pressure.

37
Q

Describe SSRI (dep)….

A

Used to treat depression and anxiety.

Blocks the Serotonin transporter (SERT) and thus prevents the reuptake of serotonin leaving more serotonin in the synapse (–> IPSP) for binding at 5-HT1A receptor.

Side effects: nausea, vomitting, gastrointenstinal upset, insombia, tremor, headach. NOT cardiotoxic (safer if OD?), little memory/learning impair, better compliance

Possibly increases suicide rates in children/adolescents - should be used with caution in younger populations.

38
Q

Describe NRIs ….

A

Used to treat depression and anxiety.

Noradrenaline Reuptake Inhibitor - blocks adrenaline (norepinephrine) transporter (NET) leaving for adrenaline in the synapse for binding at alpha or beta adrenoceptors.

Side effects: LESS THAN TCAs and SSRIs! Not cardiotoxic.

39
Q

Describe SNRIs…..

A

Treatment for depression.

Blocks both serotonin (SERT) and Adrenaline (NET) transporters leaving more serotonin and adrenaline in the synapse for binding with 5-HT1A and alpha/beta adrenoceptors.

Less side effects than TCAs and SSRIs. Not cardiotoxic

40
Q

Describe tetracylic antidepressants….

A

Treatment for depression, similar to TCAs but work on NA AND 5-HT

41
Q

Describe atypical antidepressants….

A 
Trazodone, nefazodone - 5-HT uptake block (not good affinity)
sedative effects (not work for severe depression)
42
Q

Describe melatonergic antidepressant….

A

Works using melatonin to improve sleep in depressed people.

43
Q

Describe herbal antidepressants….

A

St John’s Wort (Hypericum officinalis)
Inhibits reuptake of NA, 5-HT and DA

44
Q

What are the neurotransmitter abnormalities behind mania?

A
  • Increased noradrenaline
  • Increased serotonin
  • Increased dopamine
  • Decreased GABA
45
Q

Treatments for mania try to ____ mood.

A

Stabalise

46
Q

Describe Lithum Salts…

A

Treatment for mania.

Stabalise neurons by reducing the ability of receptors to communicate with second messenger systems. (i.e., AFTER the adrenaline has binded to its receptors…it couples to G-proteins triggering a second messanger system to excite the neuron - which is blocked by lithium salts, so noradrenaline cannot produce and EPSP)

SIDE EFFECTS:

  • Gastrointenstinal (nausea, vommiting)
  • Neuromuscular (weakness and tremor)
  • Central nervous system (blurred vision, dizziness, somnolence)
  • Cardiovascular system (hypotension, ECG changes, circulatory collapse, polyuria, dehydration, lethargy.
47
Q

Describe anticonvulsants (two types)….

A

Treatment for mania.

e.g., carbamazepine and sodium valproate

Mood Stabilisers
• Prevent positive ion channels from opening (drugs keep sodium NA+ channels inactivated, so NA+ cannot get in and excite the neuron)
• Also inhibit second messenger systems (similar to lithium salts)
to stabilise the activity of neurons

Sodium valproate blocks calcium channels (Ca++)

Side effects:

Carbamazepine - cognitive impairments, drowsiness, vertigo, blurred vision, nausea, vomiting

Valproate (Well tolerated)[valproic acid] - gastrointestinal upset, sedation

48
Q

Describe Electroconvulsive threapy (ECT)…

A

Treatment for mania.

  • Pass electricity through the temporal lobes causing Seizure activity
  • (anaesthetic & muscle relaxants are given to prevent movement)
  • Relief from disorder is relatively fast (after first session) (Antidepressant drugs can take up to 2 weeks to be effective!)
  • Side effects can be impaired memory and temporary inability to create new memories (hippocampus)
49
Q

Describe exercise (as a therapy)…

A

For depression….

  • Decreases the symptoms of depression
  • Increases the release of monoamines
  • Increases ‘endorphins’ - natural opioid peptides
  • Not greatly ‘prescribed’ but mounting evidence that it may be a promising treatment
50
Q

What mechanism is thought to underly scizophrenia (general theory, neurotransmitters)?

A

Deficits in sensorimotor gating (unable to respond appropriately to environmental stimuli and deficits in theory of mind).

  • Dopamine - dopamine hypothesis
  • Serotonin - uncertain
  • Glutamate (an excitatory amino acid) may be involved
51
Q

What is the dopamine hypothesis of schizophrenia?

A

HYPOFRONTALITY - schizophrenia has abnormal mesocorticolimbic dopamine system.

  • Increased dopamine in the nucleus accumbens AND dorsal striatum (putamen and caudate nucleus) = positive symptoms [increased D2 pre- and post-synaptic receptors]
  • Decreased dopamine in the prefrontal cortex (hypofrontality) - both communicated with Ventral tegmental area. = negative and cognitive symptoms.
    • PFC (Decreased mesocortical dopamine)= working memory, sequencing, planning, executing behaviours
    • Nucleus accumbens (increased mesolimbic dopamine) = positive symptoms (psychoses) and euphoria (at the beginning) - at D2 receptors, increased number of these receptors.
    • MESOCORTICOLIMBIC DOPAMINE SYSTEM IS ABNORMAL IN SCHIZOPHRENIA
  • drugs that increase dopamine lvls in the nucleus accumbens exacerbate or produce positive psychotic symptoms (e.g., amphetamine, cocaine, dopamine receptor agonists)
  • drugs which block dopamine transmission alleviate some of the symptoms of scizophrenia (dopamine antagonists)
52
Q

First gen typical antipsychotics ‘neuroleptics’ are…..?

A
  • Phenothiazines (antagonise dopamine receptors)
  • Thioxanthines (antagonise dopamine receptors)
  • Butyrophenones & Diphenylbutylpiperidines (antagonise dopamine receptors - better affinity for D2 receptors)
53
Q

Describe phenothiazines and thioxanthines.

A

Treatments of schizophrenia, first generaltion typical antipsychotics ‘neuroleptics)

Main action is to antagonise dopamine receptors

Have antihistaminic (sedative), anticholinergic & adrenaline-like effects (i.e., sympathetic effects)

54
Q

Describe Butyrophenones & Diphenylbutylpiperidines:

A

Treatment for mania. First generation typical antipsychotics ‘neuroleptics’

Main action is to antagonise dopamine receptors - better afinity for D2 receptors

Mostly lack antihistaminic (sedative),
anticholinergic & adrenaline-like effects (ie ‘sympathetic’ effects)
No longer sold

55
Q

which dopamine receptor is implicated in schizophrenia?

A

D2

56
Q

Why were first generation typical antipsychotics poor for the treatment of schizophrenia?

A
  • The first generation typical neuroleptics antagonised both
  • Dopamine D1 and D2 receptors (and many other receptors!!)
    • no effect on negative or cognitive symptoms
    • ineffective in 30 % patients
    • exacerbate symptoms in some
    • 20 % relapse rate
    • 5-10% have intolerable side effects (due to many receptors involved)
    • cardiotoxicity
    • Extrapyramidal Side Effects (EPS)
57
Q

In schizophrenia, what is the role of D1 and D2 receptors - what happens when an antipsychotic antagonises both receptors?

A
  • Typical neuroleptics block the D1 and D2 family of receptors
  • D2 (D3, D4) receptors in the nucleus accumbens produce positive psychotic symptoms
  • D1 (D1, D5) receptors are very important for normal movement …extrapyramidial effects.
58
Q

What are extrapyrimidal side effects and how do they occur?

A

Drug induced movement disorders that include acute and tardive symptoms. Can be caused by first gen antipsychotics (neuroleptics).

Substantia nigra —-> dorsal striatal (putamen and caudal) [nigrostriatal] system can be blocked by neuroleptics resulting in symptoms similar to parkinsons disease). Lots of D1 receptors in this system.

The Nigrostriatal DA system is important for movement – Decreasing DA in nigrostriatal causes Parkinson’s Symptoms. i.e., Blocking D1 AND D2 receptors interrupts our ability to move.

Typical neuroleptics block the D1 family (+D5) and D2 (D3, D4) family of receptors. D2 receptors in the nucleus accumbens produce positive psychotic symptoms. D1 receptors are very important for normal movement

59
Q

Describe the pyramidal vs extrapyramidal movement system….

A

Pyramidal

Primary motor cortex M1, Premotor area, Supplementary motor area ——-> Spinal cord & Muscle Voluntary Movement

**Extrapyramidal**
Nigrostriatal dopamine (A9), Substantia Nigra, Caudate/Basal Ganglia ---\> Rythmic/Phasic Movement Subconscious: eg. Walking
60
Q

in order for neuroleptics to treat psychosis, what % of D2 receptors need to be blocked? and what is the problem with this?

A

80% blocking of D2 needed……D1 receptors get blocked to!!!

Results in extrapyrmidal side effects.

Parkinson’s like symptoms (reduced dopamine transmission in Caudate)
Acute dystonias (involuntary movements)
muscle spasms, protruding tongue
May cause development of Tardive Dyskinesia (20-40% over years)
Debilitating movement disorder - involuntary movements: jaw/lips/limbs

61
Q

Describe Benzamides…..

A

Treatment for psychoses/schizophrenia

Highly selective for D2 receptors - less extrapyramidal side effects

Still no effect on negative or cognitive symptoms - need to address prefrontal cortex deficits!

_______________________

Dopamine antagonists will not help a
 Reduction*of dopamine in prefrontal cortex
(*once thought increased)
 What role does serotonin play?

62
Q

What are the treatments for schizophrenia?

A
  • First gen antipsychotics ‘neuroleptics’
    • Non-selective dopamine antagonists that block D2 AND D1 receptors
      • Cardiotoxic + extrapyrimidal SEs
      • treats only psychoses component of schizophrenia (excess dopamine in basal ganglia)
      • Does not help negative and cognitive effects caused by lack of dopamine in prefrontal cortex.
  • Typical antipsychotics that are highly selective for D2 receptors
    • less extrapyrimidal SE, but still not treat cognitive and negative effects.
  • Newer atypical antipsychotics also act as 5-HT2 (serotonin) antagonists - blocks serotonin which increases dopamine release in the nucleus accumbens and prevents lack of dopamine in prefrontal cortex.
    • e.g., Dibenzazepine - blocks D4 and D2 (dopamine) and blocks 5-HT2, muscarinic, histamine & adrenergic receptors. THEREFORE attentuates both positive and negative symptoms. but 3% develop agranulocytosis (suppression of white blood cells - immunity)
63
Q

What is the role of serotonin in schizophrenia?

A

Taking LSD (Acid) agonist at 5HT2 receptors - produce both positive and negative symptoms - suggests that serotonin has a role in schizophrenia.

Serotonin modulates the mesocorticolimbic dopamine system - encourages the dopamine deficit in the prefrontal cortex?

Serotonin can also increase dopamine release - 5-HT2A receptors. Encourages increased dopamine in the nucleus accumbens.

In Schizophrenia:
Serotonin levels in prefrontal cortex are unaltered
Prefrontal cortex serotonin receptor levels are altered
Drugs activating 5-HT2 receptors produce schizophrenia-like symptoms
Serotonin modulates dopamine systems
Newer Atypical Antipsychotics also act as 5-HT2 antagonists
5-HT2 antagonism helps with the negative symptoms of schizophrenia

64
Q

Describe Dibenzazepine….

A

second gen atypical antipsychotic for schizophrenia

Dibenzazepine: Clozapine (Clopine/Closyn/Clozaril)
Blocks both dopamine D4 and D2
(*elevated D4 receptors in schiz - yet specific D4 antag not effective)
Blocks 5-HT2, muscarinic, histamine & adrenergic receptors

Attenuates both positive and negative symptoms
No Extrapyramidal Side Effects
3% will develop agranulocytosis
 Life-threatening suppression of white blood cells (immunity)
 Clozapine is only used if two other neuroleptics are unsuccessful

65
Q

What is the glutamate hypothesis of schizophrenia?

A

Current antipsychotics concentrate on mixed 5-HT/D2 antagonists, evidence suggests that glutamate may also be involved.

Glutamate is an excitatory amino acid with inotropic [NMDA, AMPA, Kainate] and metabotrophic receptors. Phencyclidine (PCP) is an antagonist at NMDA receptors (as is ketamine) PCP can induce psychosis in humans with one dose.

In schizophrenia - NMDA receptors don’t work properly in prefrontal cortex, AMPA/Kainate receptors reduced in hippocampus.

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Treatments - novel antipsychotics that increase

activation of NMDA receptors by binding to glycine site so that Glutamate is more effective at opening ion channel.

e.g., Novel antipsychotic - NMDA receptor modulators, improves the negative symptoms of schizophrenia.

Glycine and D-serine (full agonist at glycine site - longer acting)….improves negative symptoms, psychosis and cognition.

+ future treatments may also modulate AMPA (inotropic) glutamate receptors to improve attention memory, distractibility and cognition.

66
Q

Antipsychotics try to….(4 things)

A

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  • Reduce Dopamine effect at D2 receptors (D2 antagonist)
  • Reduce Serotonin effect at 5-HT2 receptors (5-HT2 antagonist)
  • Increase Glutamate neurotransmission (NMDA & AMPA receptors)
  • Stabilise dopamine neurons (GABA-A agonists)
67
Q

how can anticonvulsants/antimania drugs be used to treat schizophrenia?

A

Activation of GABA-A Receptors May Also Treat Psychosis

Activation of GABA-A receptors reduces dopamine cell firing

So Pharmacotherapies could also include:

Benzodiazepines Sodium Valproate

These anticonvulsants/antimania drugs stabilise neurons .

Mood Stabilisers
• Prevent positive ion channels from opening
• Also inhibit second messenger systems (similar to lithium salts) to stabilise the activity of neurons
Lithium carbonate (Lithicarb/Quilonum) also used as antipsychotic

Neuropsychopharmacology (5 decks)

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