Well “they” named this DRUG correctly. “Neuro-rotten”. Gabapentin marketed under the name Neurontin initially as an anti-seizure medicine and was first approved in 1993.
Serious side-effects DO INCLUDE increased risk of suicide, aggressive behavior reduce mental or cognitive ability including memory. During the onset attempting to gain market share and wide spread acceptance Park-Davis a sub-company of Pfizer used a number of, in my opinion, questionable techniques to encourage doctors to push the drug for disorders not approved for use.
Drug Dealers Of America
Drug dealers bribing Profession Health Care Providers to sell more drugs lead to multiple lawsuits by patience who were harmed and ultimately where settled with multi-million dollar “go away” settlements and millions of dollars in “pay us” fines, before you pay us and let us approve it for first fees.
In 2010 the American Headache Society (AHS) and American Academy of Neurology (AAN) guidelines classify gabapentin as a drug with “insufficient data to support or refute use for migraine prophylaxis.“[1] Furthermore, a 2013 Cochrane review concluded that gabapentin was not useful for the prevention of episodic migraine in adults.*[2].
Gabapentin uses the brains GABA pathways to gain access to the synopitic clef and affect neurotransmission. Please
GABA
GABA is the major inhibitory neurotransmitter in the brain. It is an amino acid derived from glutamate, which is decarboxylated by glutamate decarboxylase. After interaction with its receptors, GABA is actively pumped back into nerve terminals and metabolized. Glycine, which resembles GABA in its action, occurs principally in interneurons (Renshaw cells) of the spinal cord and in circuits that relax antagonist muscles.
GABA receptors are classified as GABAA (activating chloride channels) and GABAB (potentiating cAMP formation). GABAA receptors are the site of action for several neuroactive drugs, including benzodiazepines, barbiturates, picrotoxin, and muscimol. GABAB receptors are activated by baclofen, used to treat muscle spasms (eg, in multiple sclerosis).
Gabapentin has been shown to bind to the α2δ-1 subunit of voltage gated calcium ion channels, which contributes to its pain attenuation effects in diabetic neuropathy and post-herpetic neuralgia.
Other neurophysiological findings indicate that gabapentin also interacts with NMDA receptors, protein kinase C, and inflammatory cytokines.
NMDA N-methyl-D-aspartate receptor is a glutamate receptor and ion channel protein found in nerve cells. It is activated when glutamate and glycine (or D-serine) bind to it, and when activated it allows positively charged ions to flow through the cell membrane. The NMDA receptor is very important for controlling synaptic plasticity and memory function.
Memory is created through ones experience and sensory perception which all work on vibration and energy. Our mind or brain use this electrical energy processing and storing it in memory. Tiny amounts of electrical charge is carried via structures (wiring) in the brain dependent on certian eleocto chemicals such as calcium, magniusim and money amino acids. It is curcial that receptors for which feed the memory portion of the brain function properly and allow the memory to be stored.
When receptors are blocked due to toxicity (booze), Chemicals (drugs) or have be damaged from injury memory will be impaired.
The NMDAR is a specific type of ionotropic glutamate receptor.[4] The NMDA receptor is named this because the agonist molecule N-methyl-D-aspartate (NMDA) binds selectively to it, and not to other glutamate receptors. Activation of NMDA receptors results in the opening of an ion channel that is nonselective to cations, with a reversal potential near 0 mV. While the opening and closing of the ion channel is primarily gated by ligand binding, the current flow through the ion channel is voltage dependent.
Extracellular magnesium (Mg2+) and zinc (Zn2+) ions can bind to specific sites on the receptor, blocking the passage of other cations through the open ion channel. Depolarization of the cell dislodges and repels the Mg2+ and Zn2+ ions from the pore, thus allowing a voltage-dependent flow of sodium (Na+) and small amounts of calcium (Ca2+) ions into the cell and potassium (K+) out of the cell.
Gabapentin using the GABA pathway to inhibit the firing of synopsis will adversely effect memory, cognitive abilities, and mood. Also the brain will react to reduced activity due to blocked receptors and brain die off will begin to occur. Brain die off will reduce plasticity of the brain.
So GABA is the pathway used by Gabapentin but what is the pentin part? The drug. Is it a benzo? Benzodiazepine prohapse? Absolutely. Benzodiazepines are a class of phycoactives drugs which have a carbon ring which is easy to identify.
The subset of GABAA receptors that also bind benzodiazepines are referred to as benzodiazepine receptors (BzR). The GABAA receptor is a heteromer composed of five subunits, the most common ones being two as, two ßs, and one ? (a2ß2?). For each subunit, many subtypes exist (a1–6, ß1–3, and ?1–3). GABAA receptors that are made up of different combinations of subunit subtypes have different properties, different distributions in the brain and different activities relative to pharmacological and clinical effects.[147] Benzodiazepines bind at the interface of the a and ? subunits on the GABAA receptor. Binding also requires that alpha subunits contain a histidine amino acid residue, (i.e., a1, a2, a3, and a5 containing GABAA receptors). For this reason, benzodiazepines show no affinity for GABAA receptors containing a4 and a6 subunits with an arginine instead of a histidine residue.[148] Once bound to the benzodiazepine receptor, the benzodiazepine ligand locks the benzodiazepine receptor into a conformation in which it has a greater affinity for the GABA neurotransmitter. This increases the frequency of the opening of the associated chloride ion channel and hyperpolarizes the membrane of the associated neuron. The inhibitory effect of the available GABA is potentiated, leading to sedatory and anxiolytic effects. For instance, those ligands with high activity at the a1 are associated with stronger hypnotic effects, whereas those with higher affinity for GABAA receptors containing a2 and/or a3 subunits have good anti-anxiety activity.[149]
The benzodiazepine class of drugs also interact with peripheral benzodiazepine receptors. Peripheral benzodiazepine receptors are present in peripheral nervous system tissues, glial cells, and to a lesser extent the central nervous system.[150] These peripheral receptors are not structurally related or coupled to GABAA receptors. They modulate the immune system and are involved in the body response to injury.[151][152] Benzodiazepines also function as weak adenosine reuptake inhibitors. It has been suggested that some of their anticonvulsant, anxiolytic, and muscle relaxant effects may be in part mediated by this action.[153]