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  • BDD Moderators: Keif’ Richards | negrogesic

Delayed effect or none at all?

O

Oakperk

Greenlighter
Joined
May 16, 2016
Messages
4
I have a mildly low tolerance to addies. I maybe take 3 a month and even then only take a half of a 20mg IR. I had a shit ton of classwork, so I popped a full 20mg IR this morning around 9am. It's now 3pm... And it hasn't kicked in. I've actually felt kind of tired and worn down...

Any idea why?
 
Tired, and lazy. I tried to do some school work but was too unmotivated... Really weird.
 
That's all you are liable to get then. Too much dopamine and norepinephrine just spilled out and activated your presynaptic autoreceptors, which regulate neurtransmitter release, telling the presynaptic cell to shut off release, which dramatically dampened outpour off dopamine and norepinphrine.

This can happen sometimes in sensitive individuals, where you feel these effects instead. And postsynaptic D2 receptors are inhibitory as well.
 
"As an example, norepinephrine released from sympathetic neurons may interact with the alpha-2A and alpha-2C adrenoreceptors to inhibit further release of norepinephrine. Similarly, acetylcholine released fromparasympathetic neurons may interact with M2 and M4 receptors to inhibit further release of acetylcholine. An atypical example is given by the β-adrenergic autoreceptor in the sympathetic peripheral nervous system, which acts to increase transmitter release.[1]
The D2sh autoreceptor interacts with the trace amine-assorted receptor 1 (TAAR1), a recently discovered GPCR, to regulate monoaminergic systems in the brain.[3] Active TAAR1 opposes the autoreceptor's activity by inactivating the dopamine transporter (DAT).[4] In their review of TAAR1 in monoaminergic systems, Xie and Miller proposed this schematic: synaptic dopamine binds to the dopamine autoreceptor, which activates the DAT. Dopamine enters the presynaptic cells and binds to TAAR1, which increases adenylyl cyclase activity. This eventually allows for the translation of trace amines in the cytoplasm and activation of cyclic nucleotide-gated ion channels, which further activate TAAR1 and dump dopamine into the synapse. Through a series of phosphorylation events related to PKA and PKC, active TAAR1 inactivates DAT, preventing uptake of dopamine from the synapse.[5] The presence of two presynaptic receptors with opposite abilities to regulate monoamine transporter function allows for regulation of the monoaminergic system.
Autoreceptor activity may also decrease paired-pulse facilitation (PPF).[citation needed] A feedback cell is activated by the (partially) depolarized post-synaptic neuron. The feedback cell releases a neurotransmitter to which the autoreceptor of the presynaptic neuron is receptive. The autoreceptor causes the inhibition of calcium channels (slowing calcium ion influx) and the opening of potassium channels (increasing potassium ion efflux) in the presynaptic membrane. These changes in ion concentration effectively diminish the amount of the original neurotransmitter released by the presynaptic terminal into the synaptic cleft. This causes a final depression on the activity of the postsynaptic neuron. Thus the feedback cycle is complete."
 
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