Carol Barrett2 said:@Rebecca Rivera3 I get what you're saying—I really do—but honestly, I just get lost in my own head and forget everything else. I’m going to try to make it happen, though... either getting on permanent disability or securing some kind of long-term social assistance with those caregiver benefits.
If I can actually pull that off, I’d look into going back to school—you know, trying to retrain for something else. Something where I could maybe put in just four or five hours a day. Maybe something like running a stall at a local farmers market or something similar. Right now, it’s just not feasible because I don't have the startup capital for a market stand, nor the funds for retraining.
Back in the day, when I was younger and actually had some health left in me, I used to do a bit of side hustling—under the table stuff, mostly reselling things. Kind of like how the Trotters used to do it. I’d show up looking like that tall guy, the brother of that guy Dale.
@Kimberly Cooper, dealing with a serious illness is tricky, and it’s highly specific—from what I understand about schizophrenia, it hits everyone differently. For me, it’s like I’m constantly living in my own little world. My mind is elsewhere, no matter what I’m physically doing.
It’s hard to put into words, really. When I’m online, I’m lost in my own world; watching TV, it’s the same thing. Listening to the radio? Same deal. Even if I turn everything off, it doesn't stop—actually, it gets worse once the noise stops and I'm just left with myself while I'm trying to do something.
The ideas and thoughts just swarm in—it’s like a hive. They multiply, and it feels like my brain is racing at a hundred miles an hour or more. I can't slow them down. I end up feeling trapped inside those thoughts, just drifting away into them.
I don't know if I explained that very well. I sort of drifted off mid-sentence myself.
Blocking dopamine isn't just some niche biohack—it's a total system reset. Researchers think certain psychotic experiences are actually caused by...
Overproduction is a mess. It’s all about dopamine levels in the brain. That's why people say...
Most antipsychotics work by blocking dopamine receptors in the brain. This slows down that rapid-fire messaging that happens way too often during psychotic episodes.Dopamine receptors aren't just about feeling good. They drive motivation, memory, learning, fine motor skills, and even how our brain signals hormones. It’s a massive web of neurological processes.
Neurotransmission.
A neuron fires an action potential down its axon, then hits the synapse by releasing neurotransmitters. This triggers a response in the target cell—think muscle cells or various endocrine glands. Depending on the specific neurotransmitters and receptors involved, that signal will either kickstart or shut down the target cell. 207. NEUROTRANSMISSION
An impulse can jump from one neuron to another via an axon to a cell body, an axon to a dendrite, cell body to cell body, or even dendrite to dendrite. A single neuron is constantly bombarded by various excitatory and inhibitory signals at once, which it then integrates into specific firing patterns.
Signal propagation: It’s all about electricity. An action potential travels down the axon driven by shifts in sodium and potassium ions across the membrane. Every single time a neuron gets triggered, it fires an identical signal at a constant speed. That speed depends on how thick the axon is and whether it’s myelinated—we're talking anywhere from 1 m/s in thin, unmyelinated fibers up to a blistering 75 m/s in the big, myelinated ones. Myelination makes things much faster because those gaps, known as Nodes of Ranvier, allow the electrical impulse to jump from one spot to the next rather than crawling along the whole length. This is exactly why conditions like Multiple Sclerosis are so devastating; when that myelin sheath gets damaged, the signal breaks down, leading to all those neurological issues.
Action potential transfer happens when neurotransmitters jump from axon terminals via a chemical reaction. These chemicals diffuse across the synaptic gap and latch onto receptors on the next neuron or target cell. Depending on the receptor involved, the result is either excitatory or inhibitory.
Electrical synapses don't bother with neurotransmitters. Instead, ion channels link the cytoplasm of the pre- and post-synaptic neurons directly. It's the fastest way to send an action potential. Period.
The nerve cell body pumps out enzymes that build most neurotransmitters. These get packed into vesicles right at the nerve endings. A single vesicle holds a specific amount—called a quantum—usually involving thousands of molecules. Once an action potential hits the axon terminal, calcium channels swing open. That influx of calcium forces the vesicles to fuse with the axon membrane, dumping the neurotransmitters into the synaptic cleft through exocytosis. Simple mechanics.
Neurotransmission basics: An action potential triggers those axonal calcium channels to open. That calcium influx kicks off the release of neurotransmitters from their storage vesicles. These molecules flood the synaptic cleft, some hitting postsynaptic receptors to trigger a response, while the rest either get reabsorbed back into the axon for storage or just diffuse into the surrounding tissue. Simple enough.
Neurotransmitter levels in nerve endings don't really care how active the nerve itself is. They stay pretty much constant by just swapping out precursor intake or tweaking the enzymes involved in synthesis.
Stimulating presynaptic receptors can actually cut down neurotransmitter synthesis, while blocking them tends to ramp it up.
Neurotransmitter interaction with receptors has to be lightning-fast so those receptors can reset and fire again immediately. It’s a high-speed cycle: the neurotransmitter gets pumped back into the presynaptic terminal via an ATP-dependent process, or it's broken down by enzymes nearby. Once it's back inside the cell, it just gets repackaged into vesicles for the next round. When this system glitches—whether it's production, release, binding, or cleanup—you get neurological and psychological issues. Drugs that tweak this transmission can actually help manage or fix conditions like Parkinson’s or depression.
Receptors: Think of these as complex proteins spanning the cell membrane. Their specific type dictates whether a neurotransmitter triggers an excitatory or inhibitory response. When receptors are constantly bombarded by neurotransmitters, they go numb through negative feedback. Conversely, if they aren't being stimulated—or if drugs are constantly blocking them—they become hypersensitive via positive feedback. This loop is exactly why tolerance and physical addiction happen. It’s also critical in tissue and organ transplants, where denervation cuts off the neurotransmitter supply to those receptors. You can explain withdrawal symptoms, at least partially, as a direct result of these shifts in receptor affinity and density.
Most neurotransmitters hit those postsynaptic receptors, but some actually sit on the presynaptic neurons to regulate how much gets released.
Some receptor families—think NMDA, kainate, nicotinic acetylcholine, glycine, and GABA—have neurotransmitter binding sites tied directly to ion channels, which triggers an instant response. Other groups, like serotonin, adrenergic, and dopamine receptors, rely on a "second messenger" to pass the signal along. Usually, that messenger is an enzyme that kicks off a chain reaction, leading to protein phosphorylation or calcium mobilization. These second-messenger responses are slower. Bottom line: there are way more neurotransmitters out there than there are specific second messengers.
The main neurotransmitters and receptors:
There are at least twenty different substances that function as neurotransmitters, but eighteen of them are absolutely critical. A handful of those show up in slightly different forms.
Glutamate and aspartate are the heavy hitters when it comes to excitatory neurotransmitters in the central nervous system. You'll find them in the cortex, cerebellum, and spinal cord. Glutamate basically signals neurons to ramp up nitric oxide synthesis. If you have too much glutamate, it spikes intracellular calcium, free radicals, and protease activity—which can get toxic fast. These neurotransmitters can also drive opioid tolerance and play a role in hyperalgesia.
Glutamate receptors fall into two categories: NMDA and non-NMDA. Both PCP—that "angel dust" stuff—and Memantine, which is used for Alzheimer's, bind directly to those NMDA receptors.
GABA: This is the brain's primary inhibitory neurotransmitter. It's an amino acid produced via the decarboxylation of glutamic acid, facilitated by glutamate decarboxylase. Once it hits the receptors, GABA is transported back into the nerve endings through active transport to be metabolized. Glycine, which functions similarly to GABA, shows up mainly in spinal cord interneurons (Renshaw cells) and circuits that relax antagonist muscles.
GABA receptors are categorized into two types: GABA-A (which activate chloride channels) and GABA-B (which boost cAMP production). GABA-A receptors are the target sites for several neuroactive drugs, including benzodiazepines, newer anticonvulsants like lamotrigine, barbiturates, picrotoxin, and muscimol. Baclofen activates GABA-B receptors and is used to treat muscle spasms.
Serotonin: Serotonin (5-hydroxytryptamine or 5-HT) is synthesized in the raphe nuclei as well as neurons in the pons and upper brainstem. Tryptophan is hydroxylated by tryptophan hydroxylase into 5-hydroxytryptophan, which is then decarboxylated into serotonin. Serotonin levels are regulated by tryptophan intake and intracellular monoamine oxidase (MAO).
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Ugh, when I start talking nonsense in this heat, I clearly haven't lost my mind yet—I need to actually study this stuff. Personally? Start tracking what you eat. You might actually find something interesting. See how your neurotransmitters react to certain triggers. Note down when you hit the salt, sugar, or just binge. Or try cutting back on food and see what happens. Even pro bodybuilders track every single thing they shove in their mouths every two hours alongside their workouts. And if you're on medication too... man, this is only day one for me and I can already tell
what on earth was I thinking 😁