Neuro of Drug Addiction Test 2

Name the amino acid Neurotransmitters

Glutamate, GABA, glycine

Name the monoamine neurotransmitters

dopamine, norepinephrine, epinephrine, serotonin, histamine

Name purine neurotransmitters

ATP, Adenosine

What are some properties of gaseous neurotransmitters

First, the gasotransmitter molecules are produced in cellular locations other than the axon terminals, especially the dendrites, and molecules of gasotransmitters are not held in or released from vesicles; the substance simply diffuses out of the neuron as soon as it is produced.

Second, the released transmitter doesn't interact with membrane-bound receptors on the surface of the target cell, but rather it diffuses into the target cell and affects the production of second messengers.

Co-release and Co-transmission are distinct modes of release; describe them

(a)With co-release, both neurotransmitters (mixed red and blue) are packaged into the same set of synaptic vesicles. Upon an action potential invading the presynaptic terminal, vesicles containing both neurotransmitters are released into the synaptic cleft.

(b)In contrast, co-transmission requires neurotransmitters be sequestered into distinct populations of synaptic vesicles with differential release mediated by differential Ca2+ sensitivities (left panel). For example, a single action potential might release one set of vesicles (red), but multiple action potentials might be required to release both sets of vesicles (red and blue). Alternatively, co- transmission can rely on spatial segregation of vesicle populations to different boutons (right panel) in which case, unique information is transmitted to different postsynaptic targets.

Do allosteric modulators have effect on their own? T/F

F

Allosteric modulators can bind to such sites, and by themselves have no effect, but can modify the action of an agonist

Drugs of abuse, despite diverse initial actions, produce some common effects on the VTA and NAc T/F

True

Stimulants directly increase dopaminergic transmission in the NAc. Opiates do the same indirectly: they inhibit γ-aminobutyric acid (GABA) interneurons in the VTA, which disinhibits VTA dopamine neurons. Opiates also directly act on opioid receptors on NAc neurons, and opioid receptors, like dopamine (DA) D2 receptors, signal via Gi proteins. Hence, the two mechanisms converge within some NAc neurons. The actions of the other drugs remain more conjectural. Nicotine seems to activate VTA dopamine neurons directly by stimulating nicotinic cholinergic receptors on those neurons and indirectly by stimulating its receptors on glutamatergic nerve terminals that innervate dopamine cells. Alcohol, by promoting GABAA receptor function, may inhibit GABAergic terminals in the VTA and hence disinhibit VTA dopamine neurons. It may similarly inhibit glutamatergic terminals that innervate NAc neurons. Many additional mechanisms (not shown) are proposed for alcohol. Cannabinoid mechanisms seem complex, and they involve the activation of cannabinoid CB1 receptors (which, like D2 and opioid receptors, are Gi-linked) on glutamatergic and GABAergic nerve terminals in the NAc and on NAc neurons themselves. Phencyclidine (PCP) may act by inhibiting postsynaptic NMDA glutamate receptors in the NAc. Finally, there is some evidence that nicotine and alcohol may activate endogenous opioid pathways and that these and other drugs of abuse (such as opiates) may activate endogenous cannabinoid pathways

Name the precursors and postcursor of dopamine

Tyrosine to DOPA through Tyrosine Hydroxylase, DOPA to Dopamine through Aromatic amino acid decarboxylase, and Dopamine to Norepinephrine through Dopamine beta-hydroxylase

dopaminergic fibers possess

intermittent swellings that are filled with synaptic vesicles

and that serve as the sites of DA release T/F

True

Name the catecholamines

dopamine, norepinephrine, epinephrine

To main mechanisms for DA of cocaine

enchancing DA transmission and increasing frequency of transient DA release events

Cocaines actions on SERT:

blunt the rewarding and reinforcing effects

At relatively high concentrations, cocaine can:

inhibit voltage-gated Na+ channels in axons and sensory neurons, acting as a topical/local application