Missed Questions from Physiological Psych Exam 2 Study Questions

metabotropic glutamate receptors

mGluRs, at least 8 subtypes and some are autoreceptors

excitatory amino acid transporters (EAAT)

clear glutamate from the synapse in astrocytes, presynaptic neurons, and postsynaptic neurons

glutamine synthase

breaks down glutamate in the cytoplasm (primarily of astrocytes)

GABA production locations

• nucleus accumbens

• frontal cortex

• amygdala

• hippocampus

• cerebellum

• cerebral cortex

• olfactory bulbs

synthesis of GABA

glutamic acid (glutamate) — glutamic acid decarboxylase (GAD)→ GABA

GABA-A receptor

• ionotropic Cl- channel

• benzodiazepines, barbiturates, alcohol

GABA-B receptor

• metabotropic

• activity opens a K+ channel

GABA-C receptor

• ionotropic, Cl- channel

• retina

clearing GABA fro the synapse

• GABA transporters (GAT)

• broken down by GABA aminotransferase

clearing glycine from the synapse

• glycine transporters (GlyT1)

• broken down by glycine cleavage systems

drugs impacting glycine

• bacteria that causes tetanus blocks glycine and GABA release

• strychnine blocks glycine receptors

synthesis of acetylcholine (ACh)

acetyl CoA + choline —-CHAT→ ACh + coenzyme A

breakdown of ACh

ACh —AChE→ choline + acetic acid

ACh pathways in the brain

• pons/midbrain

  • pedunculopontine nucelus and laterodorsal tegmental nucleus (REM sleep)

• basal forbrain

  • nucleus basalis (activation of cortex, facilitation of learning)

  • medial septal nucleus and nucleus of the diagonal band (rhythms of hippocampus, formation of some types of memories)

Types of ACh receptors

• nicotinic (ionotropic)

• muscarinic (metabotropic)

Dopaminergic pathways

• nigrostriatal (mesostriatal)

• mesolimbic (to amygdala, hippocampus, nucleus accumbens) → reinforcement/reward

• mesocortical (to cortex) → especially PFC: working memory, learning, attention planning, strategies for problem-solving

Dopamine receptors

• D₁(most common, excitatory)

• D₂(most common, inhibitory)

• D₃(inhibitory)

• D₄(inhibitory)

• D₅(exctitatory)

removing dopamine from the synapse

• dopamine transporter (DAT)

• broken down by monoamine oxidase (MAO) or COMT

norepinephrine functions

excitatory behavioral effects, increase vigilance, attentiveness to events in the environment; important in sexual behavior and behavior control of appetite

making norephinephrine

released from locus coeruleus in the pons and lateral tegmental system in the midbrain; released on innervated tissue of the symptathetic NS, also as a hormone directly from adrenal medulla

norephinephrine receptors

alpha 1, alpha 2, beta 1, beta 2 (in CNS) beta 3 in periphery

removing norephinephrine from the synapse

• norephinephrine transporter (NET)

• broken down by monoamine oxidase (MAO) in the cytoplasm or COMT

Serotonin (5-HT)

located in the raphe nucleus throughout the medulla, pons, and midbrain

serotonin function

involved in mood, eating, sleep and arousal, regulation of pain, dreaming, nausea and vomiting

serotonin synthesis

tryptophan (from diet) —TH→ 5-HTP— 5-HTP decarboxylase→ 5HT

serotonin receptors

14 types, all metabotropic except for 5-HT₃

Zofran effects on serotonin receptors

blocks depolarization at 5-HT₃ ionotropic receptor

Prozac effects on serotonin receptors

increase activity at all receptor subtypes

Buspar effects on serotonin receptors

targets 5-HT_1A subtype

making neuropeptides

made and packaged in the soma and sent to the terminal in vesicles

removing neuropeptides from the synapse

destroyed by enzymes outside of the axon terminal

functions of neuropeptides

stress response, social bonding, regulation of eating and drinking, response to pleasure and pain

endogenous opiod receptors

Mu, Kappa, and delta are the receptors for endorphins, dynorphins, and enkaphalins respectively

nitric oxide functions

plays a role in synaptic plasticity, vasodilation, and a retrograde neurotransmitter. It’s a neuromodulator

making nitric oxide

made on demand and can’t be stored in vesicles

functions of carbon monoxide

blood flow, inflammation, synaptic plasticity, circadian rhythms, neuroprotectors, retrograde transmitter

dose response curve (DRC)

a graph of the relationship between a drug dose and effect (usually its a log scale)

effective dose (ED₅₀)

dose when a drug shows half its maximal effect

therapeutic index

the ratio of effective dose (ED₅₀) to the toxic dose (TD₅₀) or lethal dose (LD₅₀)

bioavailable

free to act on the target (some drugs are more so because its easier to cross the blood brain barrier)

tolerance

a decrease in the effectiveness of a drug that is administered repeatedly

sensitization

an increase in the effectiveness of a drug that is administered repeatedly

metabolic tolerance

organ systems get more effective at eliminating the drug

functional tolerance

target tissue may show altered sensitivity to the drug

withdrawal

unpleasant symptoms that occur when someone stops using a drug that has established tolerance

compensatory mechanisms lead to tolerance, now there’s a lot of compensation without the drug

How drugs can alter presynaptic events

effects on transmitter production, transmitter release, or transmitter clearance

production

drugs can inhibit or increase enzymes used in transmitter synthesis, block axonal transportm or prevent or enhance storage of transmitter

release

drugs can block or facilitate Na+ or Ca²⁺ channels, prevent or directly trigger release of specific transmitters (various mechanisms), or alter autoreceptor signals to slow or increase release of NT

clearance

block or enhance transporters involved in reuptake; inhibit or activate enzymes that degrade transmitters

autoreceptors

help to “monitor” how much transmitter has been released in a kind of feedback loop

Designer receptors exclusively activated by designer drugs (DREADDs)

• receptors expressed only by neurons of interest

• drugs are designed to selectively activate or inhibit only the targeted cells

• used in research to determine the function of the targeted neurons

primary mechanism of 1st/2nd generation antipsychotics

D₂ antagonists and 5-HT_2A antagonists

categories of antidepressants

• monoamine oxidase inhibitors (MAOIs)

• tricyclic antidepressants (TCAs)

• selective serotonin reuptake inhibitors (SSRIs)

• selective norepinephrine reuptake inhibitors (SNRIs)

monoamine oxidase inhibitors

prevent breakdown of monoamines increasing availability (5-HT, DA, NE) (Parnate, Nardil)

tricyclic antidepressants

increase NE and 5-HT at synapses by blocking their reuptake, but act at many other receptors also (Tofranil, Pamelor, Norpramin)

selective serotonin reuptake inhibitors

selectively block SERT to allow serotonin to accumulate in synapses, with fewer side effects than tricyclics (Prozac, Zoloft, Lexapro, Paxil, Celexa)

serotonin-norephinephrine reuptake inhibitors

inhibit reuptake of serotonin and norepinephrine (Effexor, Cymbalta, Pristiq)

anxiolytics

CNS depressants, they reduce nervous system activity by working at GABA receptors, which have several binding sites that enhance or inhibit GABAs effects

Barbiturates vs Benzodiazepenes

both work on GABA receptors, but benzodiazepenes are more dangerous because they depress the central nervous system much more

allopregnalone

a neurosteroid that acts at a different GABA_A receptor and produces calming effects

it is naturally elevated in the body during pregnancy and the menstrual cycle

Analgesics in opium

morphine, codine

Fentanyl vs morhpine

50x stronger

opioid effects

opioid drugs have widespread effects throughout the brain and body because there are numerous mu opiod receptors

periaqueductal gray (PAG)

pain control (in spinal cord, too)

withdrawal: aches, cramps, hyperalgesia

locus coeruleus (LC)

decreases stress response and memory (blocks NE)

withdrawal: anxiety, sweating, insomnia, hyperarousal

medulla

decreases breathing and heart rate

withdrawal: hyperventilation, racing heart, elevated blood pressure

agonists at the mu opioid receptor

heroin, morphine, fentanyl, methadone, etc.

antagonists at the mu opioid receptor

used to stop oversode (naloxone/Narcan), or diminish pleasure from other drugs (naltrexone)

main components of cannabis

• THC: produces the psychoactive effect

• CBD: more anxiolytic and medicinal actions

endocannabinoids direction of release

retrograde

nicotine

general effect is stimulation

cocaine

purified extract from the coca shrub; blocks monoamine transporters, especially for DA, inhibiting reuptake

repeated use of cocaine

sensitization in the nucleus accumbens

crack cocaine

acts more rapidly because its smoked and enters the brain

dual dependence

addiction to the effects of the interaction of two drugs (ex. cocaethylene)

mechanisms of amphetamine that amplify catecholamine effects

• induce the release of neurotransmitters even in the absence of action potential

• potentiate neurotransmitter release in the presence of action potentials

• block reuptake

• inhibit breakdown of the transmitters

short-term effects of amphetamines

alterness, euphoria, and stamina

long-term effects of amphetamines

sleeplessness, weight loss, and general deterioration of mental and physical condition; prolonged use may lead to symptoms that resemble schizophrenia

why stimulants have a calming effect on people with ADHD

stimulants increase catecholamines in prefrontal regions that are usually underactive in them

Stimulant medications

• Ritalin

• Concerta

both of the medications block DA and NE reuptake

• Adderall: amphetamine salts that increase DA and NE through multiple mechanisms

• Vyvanse: amphetamine prodrug (after ingestion, enzymes convert to dextroamphetamine)

biphasic

an initial stimulant phase, followed by a depression stage

Korsakoff’s syndrome

a thiamine deficiency in a lot of alcoholics due to a bad diet

neurochemical changes due to alcohol addiction

damages to nerve cells, particularly in the frontal lobe

dissociative drugs

produce feelings of depersonalization and detachment from reality in moderate doses

MDMA (ecstasy)

hallucinogenic amphetamine derivative; it reverses monoamine transporters (DAT, NET, SERT) to increase the levels of those transmitters

addiction according to DSM-5

substance use disorder

moral model

abuse is due to failure of moral character or lack of self control

disease model

addiction is a disease that requires medical treatment

physical dependence model

abusers continue to use drugs to avoid withdrawal symptoms

positive reward model

drug abuse and addiction are due to powerful reinforcement; addiction can occur without physical dependence or withdrawal

biological factos affecting vulnerability

• sex

• genetic predisposition

personal factors affecting vulnerability

• family situation

• personal characteristics

• environmental factors

strategies and medicines to treat drug abuse

• lessen the discomfort of withdrawal and drug craving

• provide alternatives to the addictive drug

• block action of the addictive drug

• alter metabolism of the drug

• block brain’s reward system

• vaccines may be effective in reducing drug’s reward and preventing addiction

control mechanisms of the hypothalamus

• neural/homeostatic mechanisms: rapid, targeted control (hunger, thirst, and temperature)

• neuroendocrine/hormonal mechanisms: systemic, longer-lasting control (growth, reproduction, stress)

types of chemical communication

• endocrine

• neurocrine

• autocrine

• paracrine

• pheromone

• allomone

endocrine

hormone is release into the bloodstream to act on target tissues

neurocrine (synaptic)

chemical release and diffusion across a synapse

autocrine

released chemical acts on the releasing cell

paracrine

released chemical diffuses to nearby target cells

pheromone communication

used to communicate between individuals of the same species