problems with synapses Flashcards
symptoms of parkinsons
stiffness of muscles
tremor of muscles
slowness of movement
poor balance
walking problems
also may be: depression and difficulties with speech and breathing
cause of parkinson’s
dopamine-secreting neurones in the basal ganglia die
these neurones usually release dopamine in the motor cortex
so the motor cortex receives little dopamine and there is a loss of control of muscular movements
slowing loss of dopamine from brain
MAOB inhibitors used treatment for parkinson’s
selegiline
monoamine oxidase (MAO) is the enzyme responsible for breaking down dopamine in the brain
thereby inhibiting it increases the availability of dopamine
L-dopa
converted into dopamine in the brain- increasing the concentration
can be given as treatment for parkinson’s as dopamine itself cannot cross the blood-brain barrier
increase conc of dopamine controls symptoms of the disease
L-dopa is main therapy used in parkinson’s
dopamine agonists
drugs that activate the dopamine receptor directly
given in form of combined pill
mimic the role of dopamine in the brain- bind to dopamine receptors at synapses- triggering action potentials
useful in treatment of Parkinson’s
strengths of dopamine agonist
avoid higher than normal levels of dopamine in the brain
abnormally high dopamine levels can have negative ffects
gene therapy
genes for proteins that increase dopamine production, and that promote the growth and survival of nerve cells are inserted into the brain
cell therapy in which the proteins themselves are injected in to the brain are also being trialled
deep brain stimulation
type of surgery used to treat symptoms of the disease
means the person may be able to reduce their medication- so any side effects will be reduced
excess dopamine
believed to be a major cause of schizophrenia
treatment of excess dopamine
rugs that block the binding of dopamine to its postsynaptic receptor sites
drugs usually similar to dopamine in structure but unable to stimulate receptors
side effect is to induce the symptoms of parkinson’s disease
serotonin
neurotransmitter which plays an important part in determining a person’s mood
neurones that secrete serotonin are in the brain stem
their axons extend into the cortec, cerebellum and spinal cord
lack of serotonin
linked to depression
depression symptoms
associated with feelings of sadness, anxiety and hopelessness, loss of interest in pleasurable activities and reduced levels of energy
insomnia, restlessness and thoughts of death
causes of depression
not completely understood
probably multifactorial
may be a genetic element
neurotransmitters may play a role in it: including dopamine and noradrenaline
reduced serotonin levels most commonly involved
multifactorial condition
several genes may be involved in condition
probably confer a susceptibility to the condition- environmental factors also contribute
5-HTT
gene known to influence susceptibility to depression
codes for a transporter protein that controls serotonin re-uptake into presynaptic neurones
people with ‘short’ version of gene are more likely to develop depression after a stressful life event
effect of depression on nerves
fewer nerve impulses are transmitted around the brain when someone is depressed
pathways involving serotonin have a number of abnormalities in people with depression
molecules needed for serotonin synthesis often present in low concentrations
serotonin binding sites are more numerous than normal
MAOIs
monoamine oxidase inhibitors used to treat symptoms of depression
break down neurotransmitters- including serotonin
- rarely used due to large range of adverse side effects
SSRI
selective serotonin re-uptake inhibitor
used to treat depression
inhibits the re-uptake of serotonin from synaptic clefts
prozac
SSRI
maintains a higher level of serotonin and increases the rate of nerve impulses in serotonin pathways
has the effect of reducing some of the symptoms of depression
how drugs affect synaptic transmission
chemical with similar molecular structure to a particular NT is likely to bind to the same receptor sites and perhaps stimulate the postsynaptic neurone
other chemicals may prevent the release of a neurotransmitter, block or open ion channels or inhibit a breakdown enzyme (such as acetylcholinesterase or monoamine oxidase)
5 stages in synaptic transmission that can be affected by drugs
neurotransmitter synthesis and storage
neurotransmitter release
neurotransmitter-receptor binding
neurotransmitter re-uptake
neurotransmitter break down
