Is caffiene a dopamine antagonist?

[sands of time]

Is caffiene a dopamine antagonist like other stimulents?

i think but slightly... like only in certain people... it effects me... but it wont bring me out of a bad mood... but it will help me if i am already... so i think its only slightly... i dont know a whole lot tho so...anyone else?

[ShadyMilkman]

No, its an agonist.

[rit_guy]

Not an agonist at all, tho it releases small amounts of dopamine and noradreline by antagonizing adenosine (the hormone that stopts dopamine/adrenaline release and makes you sleepy).

[Micklemouse]

In that case wouldn't it be a partial-agonist? Anyhoo, here's a load of stuff about caffeine from those lovely people at Wikipedia!

[Nitrate]

RG said it right - it does not directly produce dopamine. This
can be "proven?" with a simple experiment. Go take as many
wakeups as you dare say 5? (500mg of caffine) with nothing else.
You will be perky, nausous, and paranoid but not high. Caffine is
essentialy non-euphoric. It can be a pickup but not much
more.



It works by blocking the effects of adenosine which is produced by
cells exhausting there ATP supply (a fairly universal energy token used
by almost all living cells). ATP (adenosine triphosphate) is
converted to ADP (di-phos.) then AMP (mono-phos.) then finaly
adenosine. Typicaly high adenosine levels are a sign of
exaustion, poor blood flow, lack of O2, etc. all signs you should slow
down and get some rest. Since this system influences other
systems but does
not
controll any vital life function itself, caffine is a relitivly safe
drug with
fairly forgiving overdoeses and withdrawls (as compared to drugs that
directly perturb
the dopamine system). Your body also adapts to it quickly as
well, 3 days being all that is required to be rid of physical withdrawl
symtomes (or develop a 10 cup of joe a day habit)


Edited by: Nitrate

[McDiggy]

From Gold Standard Media's Clinical Pharmacolgy:

Mechanism of action:



Caffeine is a mild, direct stimulant at all levels of the CNS and also
stimulates the heart and cardiovascular system. The related xanthine,
theophylline, shares these properties and is widely used in the
treatment of pulmonary disease. Both caffeine and theophylline are CNS
stimulants, with theophylline exerting more dramatic effects than
caffeine at higher concentrations. Caffeine also stimulates the
medullary respiratory center and relaxes bronchial smooth muscle.
Caffeine stimulates voluntary muscle and gastric acid secretion,
increases renal blood flow, and is a mild diuretic.



While the
clinical responses to caffeine are well known, the cellular mechanism
of action is uncertain. Several theories have been proposed. At high
concentrations, caffeine interferes with the uptake and storage of
calcium by sarcoplasmic reticulum of striated muscle. While this action
would explain the effects of caffeine on cardiac and skeletal muscle,
it does not appear to occur at clinically achievable concentrations.
Inhibition of phosphodiesterases (and subsequent accumulation of cyclic
nucleotides) also does not appear to occur at clinically achievable
concentrations.



Currently, it is believed that xanthines act
as adenosine-receptor antagonists. Adenosine acts as an autocoid, and
virtually every cell contains adenosine receptors within the plasma
membrane. Adenosine exerts complex actions. It inhibits the release of
neurotransmitters from presynaptic sites but works in concert with
norepinephrine or angiotensin to augment their actions. Antagonism of
adenosine receptors by caffeine would appear to promote
neurotransmitter release, thus explaining the stimulatory effects of
caffeine. Recently, a distinct syndrome has been associated with
caffeine withdrawal. It is possible that the manifestations of caffeine
withdrawal may be secondary to catecholamine or neurotransmitter
depletion.



The following mechanisms of action are hypothesized
for caffeine's action in apnea of prematurity: 1) stimulation of the
respiratory center, 2) increased minute ventilation, 3) decreased
threshold to hypercapnia, 4) increased response to hypercapnia, 5)
increased skeletal muscle tone, 6) decreased diaphragmatic fatigue, 7)
increased metabolic rate, and 8) increased oxygen consumption. All of
these actions are thought to be related to adenosine receptor
antagonism.

Reputation Comments on this post:

good info