pyramidal neuron

With regard to the glutamatergic system, studies suggest that ChEIs may stimulate the release of glutamate from pyramidal neurons during normal neuronal activity, while NMDA receptor antagonists are believed to block the abnormal neuronal activity that results from the presence of excess glutamate in the synapse under resting conditions. Thus, ChEIs and NMDA receptor antagonists appear to have complementary effects, as the former enhance the signals received by postsynaptic neurons during normal neurotransmission, and the latter diminish the background 'noise' that is constantly being detected by those same receptors. PubMed:16273023

Pyramidal neurons, which account for ~70% of all neurons in the neocortex, use glutamate as their primary neurotransmitter. Nonetheless, in addition to possessing glutamatergic receptors on their surface, these neurons often also possess cholinergic receptors, which are capable of receiving cholinergic inputs into the neocortex from the basal forebrain. The presence of these cholinergic receptors has been putatively linked to an important finding regarding the interaction between the cholinergic and glutamatergic neurotransmission systems. In particular, rodent studies have revealed that cholinesterase inhibitors (ChEIs) promote the release of glutamate from pyramidal neurons,16 with the proposed explanation being that ChEI administration leads to increased cortical ACh concentrations and, consequently, increased binding of ACh by cholinergic receptors on pyramidal neurons, thereby stimulating neuronal firing (ie, glutamate release). PubMed:16273023

With regard to the glutamatergic system, studies suggest that ChEIs may stimulate the release of glutamate from pyramidal neurons during normal neuronal activity, while NMDA receptor antagonists are believed to block the abnormal neuronal activity that results from the presence of excess glutamate in the synapse under resting conditions. Thus, ChEIs and NMDA receptor antagonists appear to have complementary effects, as the former enhance the signals received by postsynaptic neurons during normal neurotransmission, and the latter diminish the background 'noise' that is constantly being detected by those same receptors. PubMed:16273023

Pyramidal neurons, which account for ~70% of all neurons in the neocortex, use glutamate as their primary neurotransmitter. Nonetheless, in addition to possessing glutamatergic receptors on their surface, these neurons often also possess cholinergic receptors, which are capable of receiving cholinergic inputs into the neocortex from the basal forebrain. The presence of these cholinergic receptors has been putatively linked to an important finding regarding the interaction between the cholinergic and glutamatergic neurotransmission systems. In particular, rodent studies have revealed that cholinesterase inhibitors (ChEIs) promote the release of glutamate from pyramidal neurons,16 with the proposed explanation being that ChEI administration leads to increased cortical ACh concentrations and, consequently, increased binding of ACh by cholinergic receptors on pyramidal neurons, thereby stimulating neuronal firing (ie, glutamate release). PubMed:16273023

Pyramidal neurons, which account for ~70% of all neurons in the neocortex, use glutamate as their primary neurotransmitter. Nonetheless, in addition to possessing glutamatergic receptors on their surface, these neurons often also possess cholinergic receptors, which are capable of receiving cholinergic inputs into the neocortex from the basal forebrain. The presence of these cholinergic receptors has been putatively linked to an important finding regarding the interaction between the cholinergic and glutamatergic neurotransmission systems. In particular, rodent studies have revealed that cholinesterase inhibitors (ChEIs) promote the release of glutamate from pyramidal neurons,16 with the proposed explanation being that ChEI administration leads to increased cortical ACh concentrations and, consequently, increased binding of ACh by cholinergic receptors on pyramidal neurons, thereby stimulating neuronal firing (ie, glutamate release). PubMed:16273023