Neuroreceptor Distribution

[Deslaar]

Originally posted by Radical Edward

 

that's post synaptic, and I would be interested to know how a binary AP would be translated into the release of different neurotransmitters. dunno about cortisol though.

 

Ooops, I meant neuroreceptor in that last post.

[Deslaar]

Originally posted by fafalone

I'm not wrong. A few cells being exceptions does not imply that all neurons produce a wide variety of neurotransmitters. You are wrong.

 

My original point was that of neuroreceptor distribution. There should be more varieties of neuroreceptors than neurotransmitters due to the effects non-local neuroproteins. eg. Cortisol, adrenenalin, etc.

[DocBill]

Originally posted by Deslaar

I don't think so. The impulse is called an action potential and while it is binary (on/off) it is triggered by an analog mechanism composed of receptors for inhibitors and enhancers. There should in principle, be an array of receptors on dendrites that reflect there function. Having dendrites that respond to only one neurotransmitter would severly reduce brain plasticity and neurological functions and I don't see any reason why evolution should produce such a constrained architecture.

When a neuron is not being stimulated, it is at its resting potential, the charge at which no signal is transmit and the cell is at normally. The cytoplasm's charge is negative, and the surrounding fluid is positive. Average resting potentials in many animals are -70 milivolts (mV), meaning the inside of the cell has a negative charge of 70 milivolts. Resting potentials are maintained by the permiability of the plasma membrane. One way the membrane keeps the potential is to restrict large negativly charged molecules or proteins from leaving the cell. Another method is to utilize protein "pumps" to circulate certain types of molecules through the membrane. A good example of this "pumping" is in the regulation of potassium (K+) and sodium (Na+) ions.

 

 

For an action potential to be generated, the cell's membrane (restricting Na+ ions from coming in, which are heavily concentrated outside of the cell..and K+ ions which are concentrated inside the cell) are allowed to freely diffuse to the outside (via pump transfer or gradient). Thus a buildup of positive charge outside (in the form of Na+), and the diffusion of positive charge from the cytoplasm to the outside (in the form of K+) make a more negative interior. Protein pumps (called sodium-potassium pumps) contribute by pumping controlled quantities of K+ and Na+ in and out of the cytoplasm. The pumps activly transport Na+ out of the cells (increasing the concentration outside) and pump K+ in. They pump more Na+ out than K+ in, thereby making the charge more negative inside. This process is the main method by which the cell's resting potential is maintained. The action potential itself is triggered by stimuli. In the case discussed in the previous post, the simuli may be the actual breaking of the plasma membrane. The plasma membrane immediately opens the Na+ channels, allowing the concentrated sodium to flow into the cell. K+ channels close, trapping the concentrated potassium inside the cell. Thus the charge increases until it reaches threshold potential, in many animals cells -50 mV. The threshold potential is the tripping point for the action potential. The action potential is triggered (the charge continues to increase and it causes more action potentials along the membrane), and the relative charge between the interior and exterior continues to increase. Average membranes reach their maximum charge at about +35 mV. The Na+ channels then close, the K+ channels reopen, and the charge decreases rapidly. It overshoots the resting potential briefly (because the K+ channels close slowly), and then returns to its resting state.

As the action potential travels through the axon (its neuronal fiber beginning at the axon hillock), it comes to the synaptic knobs, the contacts that link axons together. The junction between two synaptic knobs, the synapse, which can be either electrical or chemical. Electrical synapses convey action potentials directly, while chemical synapses release chemicals across the divide between two axons to activate action potentials in the next axon (as the first poster above asked about). Nurotransmitter molecules from the stimulated axon attach to receptor proteins on the connected axon and trigger the opening of ion channels, which activate action potentials in the next axon. This continues in animals, where central nervous systems process the action potentials and respond. These NTM can be a single NT or in many cases, a double NT (as in the case of PNS using Acetacholine and Gabba).

 

Please excuse any spelling errors. It has been a long day, and I have Dyslexia and no spell check.

 

Bill

[Deslaar]

Originally posted by DocBill

When a neuron is not being stimulated, it is at its resting potential, the charge at which no signal is transmit and the cell is at normally. The cytoplasm's charge is negative, and the surrounding fluid is positive. Average resting potentials in many animals are -70 milivolts (mV), meaning the inside of the cell has a negative charge of 70 milivolts. Resting potentials are maintained by the permiability of the plasma membrane. One way the membrane keeps the potential is to restrict large negativly charged molecules or proteins from leaving the cell. Another method is to utilize protein "pumps" to circulate certain types of molecules through the membrane. A good example of this "pumping" is in the regulation of potassium (K+) and sodium (Na+) ions.

 

 

For an action potential to be generated, the cell's membrane (restricting Na+ ions from coming in, which are heavily concentrated outside of the cell..and K+ ions which are concentrated inside the cell) are allowed to freely diffuse to the outside (via pump transfer or gradient). Thus a buildup of positive charge outside (in the form of Na+), and the diffusion of positive charge from the cytoplasm to the outside (in the form of K+) make a more negative interior. Protein pumps (called sodium-potassium pumps) contribute by pumping controlled quantities of K+ and Na+ in and out of the cytoplasm. The pumps activly transport Na+ out of the cells (increasing the concentration outside) and pump K+ in. They pump more Na+ out than K+ in, thereby making the charge more negative inside. This process is the main method by which the cell's resting potential is maintained. The action potential itself is triggered by stimuli. In the case discussed in the previous post, the simuli may be the actual breaking of the plasma membrane. The plasma membrane immediately opens the Na+ channels, allowing the concentrated sodium to flow into the cell. K+ channels close, trapping the concentrated potassium inside the cell. Thus the charge increases until it reaches threshold potential, in many animals cells -50 mV. The threshold potential is the tripping point for the action potential. The action potential is triggered (the charge continues to increase and it causes more action potentials along the membrane), and the relative charge between the interior and exterior continues to increase. Average membranes reach their maximum charge at about +35 mV. The Na+ channels then close, the K+ channels reopen, and the charge decreases rapidly. It overshoots the resting potential briefly (because the K+ channels close slowly), and then returns to its resting state.

As the action potential travels through the axon (its neuronal fiber beginning at the axon hillock), it comes to the synaptic knobs, the contacts that link axons together. The junction between two synaptic knobs, the synapse, which can be either electrical or chemical. Electrical synapses convey action potentials directly, while chemical synapses release chemicals across the divide between two axons to activate action potentials in the next axon (as the first poster above asked about). Nurotransmitter molecules from the stimulated axon attach to receptor proteins on the connected axon and trigger the opening of ion channels, which activate action potentials in the next axon. This continues in animals, where central nervous systems process the action potentials and respond. These NTM can be a single NT or in many cases, a double NT (as in the case of PNS using Acetacholine and Gabba).

 

Please excuse any spelling errors. It has been a long day, and I have Dyslexia and no spell check.

 

Bill

 

Thanks for the comprehensive response Bill. Just a couple of points of clarification:

 

1. Do all neurotransmitters that effect AP firing in a post-synaptic neuron originate from the pre-synaptic local axon?

 

2. Has it been established as scientific fact that individual axons release only two neurotransmitters; a classical neutrotransmitter and a neuropeptide? If so, how do they compliment each other?

 

3. How do nitrous oxide and other neuromodulators fit into the picture?

 

I'd appreciate your insights. Thanks.

[DocBill]

Thank you. I will check on Wednesday with Dr. Deb Kreiss at the biology department where I work. Her speciality is brain neurochemistry. I have a good idea, but would want you to get correct information. This is not my line--merely something I have studied off and on for the past 12 years. I am hardly an expert. I can e mail your questions to her, and will post her reply asap.

 

Thanks

 

Bill

[Deslaar]

Originally posted by DocBill

Thank you. I will check on Wednesday with Dr. Deb Kreiss at the biology department where I work. Her speciality is brain neurochemistry. I have a good idea, but would want you to get correct information. This is not my line--merely something I have studied off and on for the past 12 years. I am hardly an expert. I can e mail your questions to her, and will post her reply asap.

 

Thanks

 

Bill

 

Did you get an answer yet DocBill?

[DocBill]

She said that although this was once thought, "we" now know it is untrue: there can be more than one receptor or gated protien at SOME post synaptic sites, so they are activiated by diferent nt or protiens (??).

 

I suspect you understood that? I didn't, but she's the expert. I am just learning this stuff.

 

 

Bill

[fafalone]

At some, but certainly not most.

[DocBill]

Originally posted by fafalone

At some, but certainly not most.

 

I would say that were true..so far as I know (not having many functioning neurons myself).

 

So, like..ok.

 

Bill