I do not have a simple answer for you, but I can look into it. Let's look at one way to approach this:
which further has something to do with the mandibular motor nerve 5
You are referring to the 5th cranial nerve (aka the trigeminal nerve or nervus trigeminus), usually identified by roman numbers, V in this case. While these nerves belong to the peripheral part of the nervous system (except for cranial nerve II which innervates the eye), they do not run through your spinal cord which explains their name.
Now the N. trigeminus innervates the face. It originates from four neuronal clusters ('nuclei'), 3 of which are sensory while the remaining fourth nucleus is motoric. The nerve has 3 branches, the largest being the mandibular nerve which innervates the lower portion of the face (the mandibula is the lower jaw).
Now while the sensory fibers are running through all 3 trigeminal branches, most of the motoric fibers are found in the lowest branch, the mandibular nerve. Now this is where the magic happens. If you are talking about bruxism, the mandibular is the bad boy causing it.
So naturally, you want to find out what makes the mandibular nerve tick. This is where things become very complex. :D In other words: I am pretty clueless as to what exactly causes bruxism, but I will look into it!
So it looks like serotonin activity alone can cause this side effect, as can dopamine activity on its own.
There is no such thing, is there? :D
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3081266/ said:
Etiology [of bruxism]
Bruxism is considered to have multifactorial etiology. SB and grinding have been associated with peripheral factors such as tooth interference in dental occlusion, psychosocial influences such as stress or anxiety and central or pathophysiological causes involving brain neurotransmitters or basal ganglia [3].
Central or Pathophysiological Factors
More and more pathophysiological factors are suggested to be involved in the precipitation of bruxism. As the bruxism often occurs during sleep, the physiology of sleep has been studied extensively especially the ‘arousal response’ in search of possible causes of disorder. Arousal response is a sudden change in the depth of the sleep during which the individual either arrives in the lighter sleep stage or actually wakes up. Such a response is accompanied by gross body movements, increased heart rate, respiratory changes and increased muscle activity. Macaluso et al. [10] in their study showed 86% of bruxism episodes were associated with arousal response along with involuntary leg movements. This shows that bruxism is a part of arousal response indeed.
Recently it is derived that disturbances in central neurotransmitter system may be involved in the etiology of the bruxism [11, 12]. It is hypothesized that the direct and indirect pathways of the basal ganglion, a group of five subcortical nuclei that are involved in the coordination of movements is disturbed in bruxer. The direct output pathway goes directly from the stratum to the thalamus from where afferent signals project to the cerebral cortex. The indirect pathway on the other hand passes by several other nuclei before reaching it to the thalamus [13]. If there is imbalance between both the pathways, movement disorder results like Parkinson’s disease. The imbalance occurs with the disturbances in the dopamine mediated transmission of action potential. In case of bruxism there may be an imbalance in both the pathways. Acute use of dopamine precursors like L-dopa inhibits bruxism activity [11] and chronic long term use of l-dopa results in increased bruxism activity [11]. SSRTs (serotonin reuptake inhibitors) which exert an indirect influence on the dopaminergic system [14] may cause bruxism after long term use. Amphetamine [11] which increases the dopamine concentration by facilitating its release has been observed to increase bruxism. Nicotine stimulates central dopaminergic activities which might explain the finding that cigarette smokers report bruxism two times more than the non smokers [15].
3
Sleep bruxism; an overview of an oromandibular sleep movement disorder
10
Sleep bruxism is an disorder related to periodic arousals of sleep
11
The effect of catecholamine precursor L-dopa on sleep bruxism: a controlled clinical trial.
12
Striatal D2 receptor binding in sleep bruxism: a controlled study with iodine-123-iodobenzamide, single photon emission computed tomography
13
Bruxism is mainly regulated centrally and not peripherally
14
Reports of SSRI-associated bruxism in the family physician office
15
Recognition of amphetamine addicts
So in short, and we really could've figured this out, the mandibular nerve's action potential is reached through dopaminergic activity (as to how exactly, ask someone who's better at this shit than I am. I have next to no clue about all the crazy-ass brain circuitry). However serotonergic activity can cause dopaminergic activity (this really is infinitely more complex than I make it sound).
So let's break it down again:
Bruxism
↑ ↑ ↑ ↑
Mandibular nerve
(branch of trigeminal nerve)
↑ ↑ ↑ ↑
Motor nucleus of the trigeminal nerve
↑ ↑ ↑ ↑
Dopaminergic activation
↑ ↑ ↑ ↑
Increased serotonergic activity
