Neurotransmitters, Parkinson’s disease and depression
Autonomic nervous systems Sympathetic: Promotes a "fight or flight" response, corresponds with arousal and energy generation, and inhibits digestion Parasympathetic: Promotes a "rest and digest" response, promotes calming of the nerves return to regular function, and enhancing digestion.
Pathology Dopaminergic cells, (nerve cells which primarily secrete dopamine) suffer cell death in Parkinson's disease. These cells are highly concentrated in the substantia nigra and striatum. Both of which are in the basal ganglia. They are darkly pigmented.
Effect of dopamine The current model of the motor circuit describes dopamine’s role as ‘anti-inhibitory’. Even though dopamine may be inhibitory or excitatory. The lack of dopamine results in greater effort or hypokinesia since the frequency/number signals that reach the motor endplate may be inhibited.
Treatments Artificially replacing dopamine: L-dopa – topic 6 Dopamine antagonists - similar structure to dopamine, bind to receptors. Better for younger patients and early PD stages. MAO-B (monoamine oxidase-B) inhibitors inhibit the metabolization of dopamine in the basal ganglia. Also for early stages.
Depression Symptoms include melancholy; fatigue or insomnia; loss of appetite or overeating; lack of motivation. The theories for the cause depression are the monoamine hypothesis and the circadian rhythm.
Treatment Serotonin is a monoamine and the main reason behind the monoamine hypothesis is due to the efficacy of treatments that lead to increased levels of serotonin. However the hypothesis is criticised due to antidepressants that do not work through the monoamine system and the latency between serotonin levels increasing and increased mood. MDD also does not show evidence of issues in monoamine levels. SSRIs are the most commonly used antidepressant globally and work by inhibiting serotonin reuptake. MAO-A inhibitors reduce the oxidation of monoamines such as serotonin, ultimately increasing levels of serotonin.