When the ATP converts to ADP, the ATPis said to be .
Note that ATP is an and a fuel.
Adenosine could be an important modulator in triggering a vasovagal response in susceptible patients during examination for syncope.AB - Objectives: This study examined the hypothesis that adenosine could provoke a vasovagal response in susceptible patients.
Charging ADP to form ATP in the mitochondria is called .
Recent findings support the “ADK hypothesis of epileptogenesis”: (i) Mouse models of epileptogenesis suggest a sequence of events leading from initial downregulation of ADK and elevation of ambient adenosine as an acute protective response, to changes in astrocytic adenosine receptor expression, to astrocyte proliferation and hypertrophy (i.e.
ATP is an abbreviation for adenosine ..
They contain over 5,000 different kinds of moleculesand can use sunlight, organic compounds such as carbohydrates,and inorganic compounds as sources of energy to manufacture ATP.
Energy and ATP - Virginia Department of Education
No means of producing ATP existsthat is intermediate between these four basic methods and no transitionalforms have ever been found that bridge the gap between these fourdifferent forms of ATP production.
HYPOTHESIS ON CELLULAR ATP DEPLETION AND ADENOSINE …
All life produces ATP by three basic chemical methods only:oxidative phosphorylation, photophosphorylation, and substrate-levelphosphorylation (Lim, 1998, p.
Our hypothesis is that adenosine accumulates in the …
In contrast to A1 receptors, A2A receptors are coupled to stimulatory Gs or Golf proteins () and both inhibitory as well as excitatory responses mediated via A2A receptors have been described in discrete brain areas (). Inhibitors of the A2AR have profound neuroprotective functions () and the capability to prevent apoptosis (). In addition to regulating neuronal vulnerability, these receptors play a key role in modulating the action of other neurotransmitters and neuromodulators (). In contrast to the global action of inhibitory A1 receptors the activity of A2A receptors appears to be locally restricted to active synapses (). Thus, stimulated nerve terminals can synaptically release ATP. This occurs preferentially at high frequency stimulation (), and extracellular degradation of synaptically released ATP to adenosine is not associated with the activation of inhibitory A1, but with activation of facilitatory A2A receptors (). Synaptic activation of A2A receptors can subsequently downregulate A1 receptors or its responses (; ). Thus, synaptic stimulation of A2A receptors under high frequency conditions in epileptic circuits could lead to downregulation of A1 receptors, a finding confirmed in chronic epilepsy (; ; ). An additional layer of complexity in adenosine receptor function is created by heteromerization with each other (e.g. A1/A2A heteromers) and with other neurotransmitter receptors (e.g. A2A/D2 heteromers) (). In summary, a shift in the A1 / A2A receptor ratio in chronic epilepsy, may reinforce the epileptic state and limit the therapeutic efficacy of adenosine-augmenting therapies. Nevertheless, augmentation of adenosine with an ADK inhibitor is very effective in preventing pharmacoresistant seizures in a mouse model of chronic MTLE (). These powerful therapeutic effects may be due to a global increase in adenosine, which is not restricted to the synapse, but able to exert predominantly inhibitory effects by activation of extra-synaptic A1Rs. Eventually, the combination of adenosine-augmentation with A2AR antagonism might be a preferable strategy for therapeutic intervention. In this regard, it needs to be mentioned that a safe A2AR antagonist KW-6002 is available and already in phase III clinical trials in patients with advanced Parkinson’s disease (; ).