Exam 3 Flashcards
What happens at the synapse when an agonist binds to an opioid receptor (i.e. which ion channel(s) are opened/closed and is the effect inhibitory or excitatory?)
- when an agonist binds to an opioid receptor G-Protein subunits break away, opening K+ ion channels and allowing flow of positively charged K+ ions out of the cell which is inhibitory
- Voltage sensitive Ca2+ channels close and don’t allow ions in the cell which are inhibitory; leaving the cell hyperpolarized
Provide two effects of opioids on the body?
- Nausea and vomiting
- Vasodilation
- Pinpoint pupils
What are two withdrawal symptoms from opioids?
- Cramps, vomiting, diarrhea
- twitching
Describe how activation of mu and kappa opioid receptors alter dopamine release in the “reward” system (i.e. the projection from the ventral tegmental area to the nucleus accumbens)
Mu (µ) – MOR on GABA interneurons in the VTA cause stimulation of dopamine release from the VTA to the nucleus accumbens (inhibition if GABA = excitatory).
Kappa (𝜅) – KOR are dysphoric as they decrease the dopamine transmission to the nucleus accumbens which is found to be more adverse than rewarding.
Name and provide the mechanism of action for one “maintenance” therapy and one “antagonist” therapy for heroin addiction
Maintenance Therapy = Methadone
* Is a partial Mu (µ) receptor agonist that blocks the effects of heroin and withdrawal by binding tightly without producing a strong effect
Antagonist Therapy = Naltrexone
* Is a pure Mu (µ) receptor agonist given to detoxed patients that binds to receptors, not allowing heroin to bind to them and completely blocks the effects of opioids.
List one positive symptom (1 point) and one negative symptom (1 point) of schizophrenia
A positive symptom is hallucinations, and a negative symptom is attention deficits.
How do typical and atypical antipsychotics differ with respect to receptor affinities (2 points) and effects on behavioral or mental performance (e.g. side effect profile) (2 points)?
Typical antipsychotics have a high affinity for dopamine D2 receptors and atypical antipsychotics have a high affinity to D3 and D4 and low affinity to D2 receptors.
Typical antipsychotics produce adverse extrapyramidal signs and symptoms (EPS) and atypical antipsychotic drugs are more effective in treating negative symptoms of schizophrenia and do not produce debilitating extrapyramidal signs and symptoms (EPS)
- Briefly describe procedure used in the neonatal ventral hippocampal lesion model of schizophrenia (2 points) and two brain changes (i.e., neurotransmission) that result later in development (2 points).
In the NVHL model consists of infusion of a high dose of MK-801, an NMDA receptor antagonist into the hippocampus during the first postnatal week.
Two Brain Changes Later in life that Result in Later Development:
* Dysregulated Dopaminergic Transmission
* Enhanced sensitivity to NMDA antagonists
Briefly describe the “diathesis-stress” model of schizophrenia (2 points).
The diathesis-stress model proposes genetic predisposition combined with prenatal or early neonatal insult produces schizophrenia.
- Briefly describe the mechanism of action for tricyclic antidepressants and MAOIs
Tricyclic Antidepressants – prevents the reuptake of a lot of monoamines but have anticholinergic effects, decreasing the effects of cholinergic receptors.
MAOIs – are monoamine agonists that blocks the enzyme that breaks down monoamines so that monoamines are built up in the synapse.
Describe the results of a study that demonstrates a depression-like behavioral change resulting from exposure to chronic stress
This study mimics the types of stressors that are common in everyday people. Tested on rats by tilting their cage, leaving their lights on, taking away water briefly and leaving cage soiled for an extra day inconsistently to ensure they did not have time to adapt or begin coping. In doing this their sucrose levels should come down when they are stressed. Showing that imipramine does work in bringing levels to normal when stressed and decreasing depression.
effect on that behavior of administering a tricyclic antidepressant alone (1 point) or co-administering a tricyclic antidepressant with a dopamine D1 receptor antagonist (1 point).
Administering tricyclic antidepressants alone leads to and increased monoamine levels in stressed animals indicating of their pharmacological action. Co-administering of a dopamine D1 receptor antagonist would likely lead to alterations in the balance of neurotransmitter systems in the brain that are involved in various cognitive and emotional processes, and their antagonism can affect dopamine neurotransmission.
- Describe the monoamine theory of depression
Theory states that mood is controlled by the level of monoamine activity in the brain. The monoamine fibers of the midbrain and brainstem project to limbic and cortical regions. Decreased levels of monoamines lead to decreased brain activity in which mood is controlled. If monoamines are boosted, then the depression alleviates because depression is decreased cortical functions due to lack of monoamines.
How does prolonged use of SSRI’s alter neural development
Prolonged use of SSRIs can alter neuroplasticity, altering the formation and strength of synaptic connections. It can also alter neural development during pregnancy causing an increased risk of major fetal malformation, cardiac defects, and pulmonary hypertension in newborns.
List one withdrawal symptom of SSRIs and one withdrawal symptom of tricyclic antidepressants
Withdrawal Symptoms:
* SSRIs = fatigue and anxiety
* Tricyclic Antidepressants = restlessness and anxiety
- Describe the phenomena of depolarization-induced suppression of inhibition as it pertains to cannabinoids (2 points).
Depolarization-induced suppression of inhibition represents an important mechanism by which cannabinoids regulate synaptic transmission and neuronal excitability in the brain. Low-frequency stimulation of GABAergic terminals synapsing onto pyramidal cells producing an eIPSC until depolarization is applied to the pyramidal cell and suppressing of presynaptic terminals by voltage -gated calcium channels. By modulating inhibitory neurotransmission, cannabinoids can influence a wide range of physiological and behavioral processes, including pain perception, mood regulation, and motor control.
). List two harmful effects of cannabis
Harmful Effects:
* Mental Disturbance (marijuana psychosis)
* Freak Outs (panic, hallucinations, perceptual distortions)
two withdrawal symptoms of cannabis
Withdrawal Symptoms:
* Anxiety and Irritability
* Decreased food intake
- Briefly describe three medically useful effects of cannabidiol or cannabis
Glaucoma – reduces pressure of fluid in the eyeball but also reduces blood pressure which can compromise blood flow to the optic nerve.
Antiemetic – useful in chemotherapy patients to stop nausea and vomiting.
Antiepileptic/Anticonvulsant – CBD works to reduce seizures without psychoactive side effects.
- Describe the pharmacodynamic mechanisms of action for LSD, MDMA, and ketamine
LSD – Primarily act on 5-HT2A serotonin receptors in the frontal cortex and limbic system to increase receptor activity and is a receptor partial agonist at post-synaptic receptors.
MDMA – Increased serotonin transmission by blocking the serotonin transporter (SERT) and increasing release from terminal buttons and increased dopamine transmission by blocking the dopamine transporter (DAT)
Ketamine – NMDA receptor agonists. NMDA blockade turns down the inhibitory system more than the activating system causing a net increase in dopamine release.
- Name and define three sensory or emotional phenomena that are produced by hallucinogens (1 point for each name, 1 point for each description).
Phantasticants – feelings of emotional significance; induce vivid perceptual experiences.
Psychedelics – Mind manifester that cause surreal sensory experiences.
Psychomimetics – Simulants of psychosis causing delusions and hallucinations.
what is an opiate?
a drug derived from opium
what is an opioid?
drugs with a mechanism of action and affects similar to opiates
what is a narcotic?
abbreviation of narcotic analgesic, causes narcosis (sleep or drowsiness)
what is the source of opiates and opioids?
opium poppy
what are the natural active ingredients in opioids and opiates?
- morphine (10%)
- codeine (0.5 %)
what is an example of a semi-synthetic opioid?
- diacetyl morphine (heroine diamorphine)
- modification of morphine
what are examples of synthetic opioids?
- meperidine or pethidine (demerol)
- methadone
- oxycodone (Percocet (if it is mixed with acetaminophen) oxycontin (high dose, slow release form))
-naltrexone, naloxone (competitive antagonists) - nalorphine (partial agonists)
- mixed (cyclazocine)
Why was heroin created?
attempt to make morphine safer
