Exam 2 Flashcards
Name 3 receptors that are directly targeted by alcohol
- GABAA Receptors
- GABAB Receptors
- NMDA Receptors
How does alcohol contribute at GABAA to an increase or decrease in neural activity?
alcohol is a positive allosteric modulator at GABAA receptors. It enhances the ability of GABA to open the ion channel and lead to an inhibitory effect on neural activity
How does alcohol act as an increase or decrease in neural activity in GABAB?
Alcohol alters the function o some subtypes of GABAB receptors (particularly dopamine synapses) it stimulate the release of dopamine which can have excitatory effects
how does alcohol affect an increase or decrease in neural activity with the NMDA receptors?
alcohol blocks the ion channel controlled by glutamate at NDMA receptors. This results in decrease in neural activity which is an inhibitory effect
Describe three factors that facilitate the absorption of alcohol
- Concentration (higher alcohol concentrations lead to faster absorption rates into the bloodstream)
- empty stomach (alcohol is absorbed faster on an empty stomach as it allows for quicker passage into the bloodstream
- carbonation (carbonated beverages like champagne can facilitate the passage of alcohol through stomach, aiding in absorption
what is grey out?
partial memory loss or impairment of events due to alcohol or drug use
what is en bloc blackout
complete loss of memory for events that occurred during a specific period, typically due to alcohol or drug use
how do benzodiazepines and alcohol differ with respect to their effects on memory?
Benzodiazepines create deficits in explicit memory, not implicit. Trouble recalling info explicitly but can use info acquired implicit.
Alcohol can lead to grey outs or en bloc blackouts, essentially partial or complete memory loss for events
Describe the mechanism through which an en bloc blackout is produced?
brain structure - en bloc blackouts are produced by affecting the hippocampus, a brain region crucial for memory formation
receptor mechanism - alcohol and benzodiazepines act on GABA receptors in the brain, inhibiting neuronal activity and disrupting memory formation in the hippocampus which leads to en bloc blackout
what receptor is the primary target for benzodiazepines, barbiturates, and z drugs?
GABAA receptor
what is the ion associated with the receptor that is primary target for benzodiazepines, barbiturates, z drugs
chloride (cl-)
will an agonist at the receptor will produce inhibitory or excitatory effect?
an agonist at the GABAA receptor will produce an inhibitory effect by hyperpolarizing the cell membrane
describe three differences between the psychological effects of benzodiazepines, barbiturates, and Z drugs
- benzodiazepines
known for anxiolytic effects, muscle relaxation, and anticonvulsant properties
-barbituates, produce sedation, hypnosis, and anesthesia effects, with potential for respiratory depression
z drugs - primarily used for treating insomnia (focus on inducing sleep rather than anxiolytic effects), with less potential for respiratory depression compared to barbitautes
describe three neurotransmission systems through which nicotine increases or decreases dopamine release from the ventral segmental area
- glutamatergic system
- nicotine increases the activity of glutamatergic neurons, boosting glutamate release through presynaptic receptors and increasing depolarization of postsynaptic neurons. This leads to increased dopamine release from the ventral segmental area and nucleas accumbent - nicotinic acetylcholine receptors (nAChRs)
- nicotine acts on nachrs on dopaminergic neurons projecting from the ventral tenemental area to the nucleus accumbent. Activation of these receptors by nicotine influences dopamine release
3.mesolimbic dopamine system
- nicotine affects the mesolimbic dopamine system, leading to increased dopamine release in the nucleus accumbens/ The system plays a crucial role in reward and reinforcement processes
evidence of glutamatergic system with nicotine affect on dopamine release from ventral segmental area
activation of glutamatergic neurons by nicotine leads to increased dopamine activity in the nucleus accumbent when the ventral segmental area is stimulated