Could your current but unknown infection increase the glutamate in your brain? That glutamate happens to be an excitatory toxin associated with anxiety, panic, phobias, insomnia, and even pain. Is some type of infection, maybe even a 'dead' tooth in your mouth where the nerve has died or a leaky seal on a root canal (inflammation at the bottom of the root) causing the issue? Or perhaps it's an undiagnosed fungal, bacterial, or viral infection somewhere in your body.
Instead of getting at the root cause of the problem, doctors usually prescribe sedatives or tranquilizers to calm your neurotransmitters. But the root cause of why your immune system is being activated could be an underlying infection or inflammation. Seems a lot of doctors might not be looking for the cause of the inflammation in your body causing your anxiety, fear, nervousness, phobias, or panic, but instead they keep prescribing tranquilizers or other calming drugs. So the infection continues increasing the glutamate in your brain, which in turn, is an exitatory toxin, that's a toxin that excites and arouses your nervousness or phobias.
If you check out the May 31, 2006 news release, "Striking the right balance between excitation and inhibition," researchers in La Jolla, California at the Salk Institute found that neurons in the brain and spinal cord come in two flavors, excitatory neurons that transmit and amplify signals, and inhibitory neurons that inhibit and refine those signals.
Salk Institute researchers uncover a pathway about how cells become excitatory or inhibitory
Although investigators have long appreciated that these two classes of neurons exist in the central nervous system, little is known about how cells decide to become inhibitory or excitatory during embryonic development. Researchers at the Salk Institute for Biological Studies have now uncovered a pathway that plays a central role in regulating this choice.
That path is described in a study from Martyn Goulding, PhD., an associate professor in the Molecular Neurobiology Laboratory. Goulding, along with co-lead authors, postdoctoral fellow Rumiko Mizuguchi, PhD., and Sonja Kriks, a graduate student at Georg-August University in Goettingen, Germany, analyzed the origins of a group of spinal cord "interneurons," neurons that bridge communications between other neurons.
Many interneurons emerging in the dorsal part of the spinal cord arise from a common progenitor cell
Since mature neurons can be either excitatory or inhibitory, the researchers asked how a single parental progenitor cell could produce both excitatory and inhibitory daughter cells, and how approximately equal numbers of each daughter cell are produced.
In a study published in the June 2006 edition of Nature Neuroscience (available online), the team found that a receptor protein known as Notch, which was already known to regulate maturation of neurons from neural stem cells, has a reciprocal function in precursors of inhibitory and excitatory neurons: cells with high levels of activated Notch became excitatory neurons, while cells with low levels of Notch became inhibitory.
Interestingly, the researchers found that one way Notch combats an inhibitory fate is to turn off another a factor known as Ptf1a, which promotes that fate. Describing the role of Notch as an arbitrator of the choice between excitation and inhibition, Goulding says, according to the news release, "The degree of Notch expression on one neuron tells the sibling cell that it cannot be the same thing. If it is up-regulated in one cell, Notch will be down-regulated in its sibling.
"There are thousands of different kinds of neurons in our incredibly complex nervous system, and we don't understand how this diversity comes about," Goulding explains in the news release. Referring to the multiple roles of Notch, not only in controlling the differentiation of neurons but in determining their excitatory/inhibitory activity, he adds, in the news release, "Given that we now have a detailed description of how Notch signaling provides a switch that controls the choice between two different neuronal fates, we can now look and see if it is used in similar ways elsewhere to make different kinds of neurons."
The neurons in the dorsal spinal cord analyzed by the Goulding lab form a relay station receiving and interpreting sensory signals from the environment and then sending them to the brain. In doing so these neurons evaluate the strength of sensations.
"An example of how the system works is illustrated by what happens when you cut your finger," Goulding explains in the news release. "Initially it hurts a lot, but the pain then eases. One of the reasons that this happens is because inhibitory interneurons in the dorsal spinal cord dampen down their excitatory counterparts, thus dialing down the pain."
Since interneurons play such critical roles in transmitting pain signals, it is thought that some chronic forms of pain are due to an imbalance in excitatory and inhibitory signals carried by interneurons. As such, the findings by the Goulding group are likely to be important for devising animal models to study these pain pathways.
Other authors who contributed to this work include Ralf Cordes and Achim Gossler, from the Institute for Molecular Biology at the Medizinische Hochschule Hannover, and Qiufu Ma, from the Dana Farber Cancer Institute. Also you may wish to take a look at the abstract of another study, "More neurons may not make you smarter."
How botulinum toxin could affect you
Also check out the April 1, 2008 news release, "News tips from the Journal of Neuroscience." The section titled, "Could Botulinum Toxin Be Bad for You?" by Flavia Antonucci, Chiara Rossi, Laura Gianfranceschi, Ornella Rossetto, and Matteo Caleo, explains that botulinum toxins (BoNTs) are used increasingly to treat maladies from spasms and migraines to obesity and wrinkles.
It has been assumed that the toxin remains localized at the injection site, where it cleaves proteins involved in vesicle fusion, thereby blocking neurotransmitter release. But now, according to the news release, Antonucci et al. demonstrate that BoNT/A is retrogradely transported along microtubules, transcytosed, and taken up by afferent terminals.
When BoNT/A was injected into one hippocampus in rats, it cleaved its target [synaptosomal-associated protein of 25 kDa (SNAP-25)] in the contralateral hippocampus, resulting in reduced neuronal activity. Similarly, when BoNT/A was injected into the superior colliculus or whisker pads, SNAP-25 was cleaved in the retina and facial nucleus, respectively. In the retina, BoNT/A remained active for at least 25 d after injection. Although cleaved SNAP-25 was detected only in afferents that projected directly to the injection site, it is not clear whether further transcytosis would occur over time.
Find out what the root causes of your symptoms are
The point of the these news tips from various scientific journals is that when you and your doctor discuss your symptoms, find out whether the root of the causes of the symptoms is being researched or explored by you and your health care team working together to help you fix what started the problem in the first place instead of prescribing a drug to calm the excitation or anxiety, phobia or panic without first looking to see what is causing the symptoms.
Could it be an infection or inflammation caused by something that won't go away by itself? Could it be caused by an infection that's increasing the neuortoxins in your brain, such as an excitatory toxin associated with anxiety? You don't even have to be eating excess glutamate added to your foods or protein powders. Your brain might be manufacturing the glutamate in response to an infection or inflammation somewhere going unnoticed, like the dead nerve in a tooth that hasn't started to pain you yet.
Perhaps your body is trying to get rid of the infection, and you're not aware of what's happening. That's why if you are having chronic anxiety, find out whether it's due to sudden hormonal changes or an infection that your brain is responding to by increasing the glutamate in your brain? Also you may wish to see, "Curbing C. difficile's toxin production," and "'Nanosponge vaccine' fights MRSA toxins."