Lecture notes
Neuroscience Conditions lectures
- Module
- Biochemistry
- Institution
- Imperial College London (ICL)
Neuro Lectures on Parkinson's and Alzheimers
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Parkinson’s and Prions Lecture 5&6 neuroscience.Intro:
- Symptoms are split into motor and non-motor.
- Motor relates to Parkinson’s tremor and rigidity. Slowness in movement execution as
well.
- Before the motor symptoms there are non-motor like sleep disorder, cognitive
defects, and depression.
- Unlike Alzheimer’s there is a pharmacological treatment.
Origins of PD:
- Genetic
- Juvenile-onset Parkinsonism
- Idiopathic – unknown causes
- Toxic and environmental – Insecticides and some recreational drugs that cause
mitochondrial damage due to the free radicals.
Dopamine Neuron:
- Dopamine is a neuromodulator – so that means it does not directly activate ion
channel receptors.
- Dopaminergic neurons – they secrete the dopamine degenerate in PD.
- These neurons are in one part of the brain – called Substantia Nigra and ventral
tegmental area.
- Dopamine is released non-specifically from neuronal varicosities (not at the synapse
like neurotransmitter) and it diffuses through large volume – this is called Volume
Transmission. So that means large areas of the brain are affected by dopamine.
So why is dopamine so important?
- Dopamine Receptors D1-5R are GPCRs.
- It activates the AC – so the cAMP as well.
- Changes K+ channel opening and closing by P
- Short term / long term.
- Vasodilation role.
- Dopamine’s role in physical role in motor control.
- Pleasure.
Behavioural Control of dopamine:
- Dopamine shortage: indecisive personality, unable to initiate movement.
- Dopamine excess: Arousal, ADHD, addiction.
- L-DOPA: Precursor to the dopamine. Only one enzyme is needed to transform to the
dopamine.
L-DOPA as a treatment:
- Cell downregulates the dopamine receptors so that means it becomes less sensitive.
- Transient elevation of PD symptoms before neurones eventually become insensitive
to L-DOPA.
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