Admittedly I can't point to any research studies that conclusively prove the neuro-protective properties of Glutamate neurotransmitter and receptor inhibition, as I don't believe any such research papers exist to this day. I believe the reason for this is mostly down to duration. Such a research program would have to span several decades, as in most cases, it takes a number of decades for neuro-degenerative diseases to manifest themselves to a degree that symptoms become more obvious and generally when researches are conducted, they are very limited in their duration, likely due to funding and participant drop outs.
What I do know however is that in most instances of neuro-degenerative diseases, the Glutamatergic system appears to be implicated in some way. People with conditions such as Alzheimer's and Dementia for example show unusually high levels of Glutamatergic activity and lower levels of GABAergic activity, leading to excess NMDA, AMPA and Kainate receptor activation, which subsequently leads to higher Calcium Ion activity in the post-synaptic neurons, leading to increased neuron death over time. This is why these diseases are generally treated using a combination of L-Glutamate receptor antagonists and GABA receptor agonists.
In terms of the mechanism of action involved in stimulating the release of the amine neurotransmitter groups. Higher Glutamatergic activity is directly involved, as it's the influx of Calcium Ions released from the Voltage Dependant Calcium Channels that instruct the pre-synaptic vesicles containing the amine's to bind to the pre-synaptic membrane, allowing the amine's to be released into the Synaptic Cleft.
When you antagonise receptors such as the NMDA receptors, this reduces the Calcium Ion influx and subsequently slows down the release of the amine neurotransmitter's, even under the influence of stimulants. An example of this is the combination of L-Theanine and Caffeine. L-Theanine is structurally very similar to L-Glutamine. This allows it to bypass the Blood Brain Barrier and directly access the Astrocyte's. It then works by plugging the transportation route of L-Glutamine into the Glutamatergic neurons, thus reducing the amount of Glutamate available in the Glutamatergic neurons that can bind to the NMDA, AMPA and Kainate receptors. It doesn't however block the transportation of L-Glutamine into the GABAergic neurons. As a result, the excess Glutamine that can't get into the Glutamatergic neurons is sent back through the Astrocyte and into the GABAergic neurons, where it is then converted into GABA through the GAD (Glutamic Acid Decarboxylase) process. The end result is decreased Glutamatergic activity and an increase in GABAergic activity, resulting in decreased Calcium Ion activity, but an increase in Chloride Ion activity which has the opposing effect of slowing down amine activity. Ultimately, people who consume Caffeine and L-Theanine together find that Caffeine feels less "harsh", lasts longer and doesn't have the usual sudden crash that is commonly associated with it.
GABA receptor agonists can also be useful in reducing undesirable effects from stimulants, again by increasing the influx of Chloride Ion activity. Which is why Taurine is commonly used in Energy Drinks. Although L-Theanine may be a better alternative. It's also a reason why long term stimulant users may start abusing Benzodiazepine's, as they find it helps to "smoothen things out". Although I wouldn't recommend the use of Benzo's in the long run, as they have much more powerful agonist effects compared to an amino acid such as Taurine, which ultimately leads to subunits on the GABA-A receptor uncoupling, causing the receptor to down-regulate and not be able to respond normally to the GABA neurotransmitter without the consistent aid of Benzodiazepine's. Sudden withdrawals from Benzodiazepine's have been linked to 'excitotoxicity', where by the GABAergic system isn't functioning normally, but the Glutamatergic system is. Which leads to an imbalance between Chloride Ion release and Calcium Ion release. The result of this is chronic over-stimulation and a spike in amine activity (because of the Calcium/Chloride imbalance), leading to the Benzo withdrawal symptoms such as increased Anxiety, Panic Attacks and Insomnia as well as more severe symptoms such as Psychosis and Grand Mal Seizures. Symptoms that closely resemble that of Alzheimer's and Dementia.
I realize I've rambled on a bit here and haven't provided a single link for any of this. But all of this information comes from reading a multitude of research papers over the years and to be quite honest, it would be a real headache trying to dig them all back up again. But if there's anything I've said here that you feel unsure about, give it a google and you'll likely find a research paper associated with it.
