Week 11 and 12 Flashcards
(32 cards)
Monoamine dopamine transmitters
- Dopamine
- Adrenaline (Epinephrine)
- Noradrenaline (Norepinephrine)
- Serotonin (5-hydroxytryptamine)
Which response system is noradrenaline associated with? and what does it do in the brain
ANS
o Arousal and mood (reward and pleasure from food, sex, drugs etc.)
o Regulation of BP in the brain stem
o Long term memory
Main action of Serotonin (5-hydroxytryptamine)
- Mood
- Sexual
- Sleep
- Appetite
- Pain
- Motor function
- Autonomic and endocrine functions
Therapeutic targeting of serotonin function
- Antidepressants (SSRI’s and older drugs)
- Antipsychotics (second generation i.e. The newer ones)
- Antimigraine drugs
- Anxiety
- Obsessive-compulsive disorder
- Alzheimer’s
Dopamine main functions
- Very important in reward pathway and in behavioural drives
- Initiation, planning and execution of movements
- Control of prolactin release (inhibits it from the pituitary gland)
4 pathways of dopamine from S. Nigra
o Nigrostriatal (control of movement)
o Mesocortical (forebrain, pleasures and planning/executive function)
o Mesolimbic (midbrain to deeper part of forebrain - limbic and motivational system)
o Tuberoinfundibular (projects down to the pituitary - controls release of prolactin)
Therapeutic targeting of dopamine function
- Psychosis
- Parkinson’s Disease
Boosting Levels of Monoamines
- Monoamines (neurotransmitters) cross the synaptic cleft from the pre-synaptic neuron to attach to the receptors on the post-synaptic neuron. This stimulates a response.
- To end that signal (repolarisation), the neurotransmitters must be removed from the receptors to prevent continuous signalling. There are two ways this is done:
a. Re-uptake using active pumps into the pre-synaptic cleft
b. Enzymes that break down the neurotransmitters that are left hanging around in the synaptic cleft
i. Monoamine Oxidase (MAO)
ii. Catechol-o-methyl transferase (COMT)
If you get a drug which inhibits any of these components, you’re going to raise the level of the monoamines in the synaptic cleft.
Acetylcholine functions
Used as the communication between motor neurons and skeletal muscle allowing them to twitch
* Transmission at skeletal mm
* ANS - parasympathetic responses
* In the brain
o Short term memory
▪ People who suffer from dementia (particularly Alzheimer’s) suffer from degeneration of
ACh containing neurons in the hippocampus o Arousal and sleep
o Motivation and reward
Therapeutic targeting of ACH
- Dementia
o Treatment pharmacologically is new
o Success with mild and recently diagnosed dementia - Parkinson’s
o Use is falling - taking a backseat to the dopaminergic agents
GABA Therapeutic uses
“Calming down”
* Inhibitory neurotransmitter
* Makes neuron less likely to respond to excitatory influences
Therapeutic targeting of GABA function
* Anticonvulsants
* Anxiolytics
o Anxiety disorders
Glutamate therapeutic uses
- Excitatory neurotransmitter
- Excitotoxicity - over presence of glutamate causing death of cells post stroke/epilepsy Therapeutic targeting of Glutamate function
- Stroke (neuroprotectives)
- Anticonvulsants
Drugs for treatment of anxiety
Anxiolytic Drugs
Benzodiazepines uses and side effects
- Most common form of treatment for anxiety
- Act by binding to GABA-A receptor and increasing its activity
o Side effect - sedating - Hypnotic (put your to sleep), sedative, mm relaxant, anticonvulsant (epilepsy, but not long term),
amnesic (forget events) - Used for anxiety, insomnia, mm spasms, epilepsy, short endoscopic procedures, withdrawal from other
CNS depressants e.g. Alcohol
Benzodiazepines MOI
- Binding site on this channel where the GABA binds (GABA-a receptor)
- Opens chloride channel - chloride ions flow in to the cell from the outside (they are negatively charged)
o Hyperpolarises the cell (negative on the inside) o Less likely to be depolarises
o This is how GABA acts - Benzodiazepine works on the same channel and when bound, makes it more likely the channels will remain open for a longer period of time allowing more GABA to enter and stimulate more of a response
- Alcohol works the same way
How does tolerance of benzodiazepines occur?
o Increased GABA influx - over the long term the GABA transmission levels have increased so the system responds to that by removing some of the receptors
▪ Increase dose of Benzodiazepine as a result - if you stop taking the drug, the capacity for GABA inhibition reduces meaning you have a dangerous low level of GABA inhibition resulting in an over-excitation of the CNS
▪ Can result in convulsions - withdrawal symptoms
Buspirone (5HT and DA, not GABA benefits over typical anti-anxiety drugs
less sedation
Main symptoms of depression
- Misery, psychological pain
- Pessimism
- Low self-esteem
- Guilt
- Indecisiveness
- Lack of motivation
- Thought disorders
- Depersonalisation
other symptoms to depression
- Autonomic symptoms: sweating, CV symptoms, headaches, tightness in chest, feeling of choking
- Psychomotor retardation or acceleration (mental and physical functions)
- Diurnal rhythm disturbance (sleep-wake cycles)
- Insomnia, sometimes hypersomnia
- Loss of libido
two forms of depression
uni and bipolar
symptoms of mania
- Excessive euphoria
- Excessive self-confidence
- Pressure of speech
- Impulsiveness
- Grandiose ideas
- Irritability
- Impatience
- Aggression
Treatment of Unipolar Depression drugs
SSRI (most common), TCA’s , MAOI’s (least common)
SSRIs: specific serotonin reuptake inhibitors (-oxetine) MOI
= reuptake inhibitor
TCAs: tricyclics (-amine) MOi
= reuptake inhibitor
o Overdose possible
