Synapses can be excitatory or inhibitory, depending on whether they activate or inhibit the postsynaptic neuron
. (4),(5) When a presynaptic neuron releases excitatory neurotransmitters (such as glutamate) into the synaptic cleft, some of them bind to ion channels that open to allow an influx of positively charged ions, which generates an excitatory postsynaptic potential (EPSP) (Fig.
CGP55845 act via decreasing the GABAergic tone in the basal forebrain, most prominently occupying the GABAB receptor on postsynaptic neuron
thus preventing the action of GABA at the synapse (Mayse, 2009).
The [alpha]-function delivers the neurotransmitter from the presynaptic neuron to the postsynaptic neuron
where [[delta].sub.pk] is the error signal of a postsynaptic neuron
k and [W.sub.kj] is the weight of the connection from j-th hidden neuron to the k-th postsynaptic neuron
Both of them increase dopamine signalling by increasing the amount of dopamine in the synapse (so more dopamine ends up binding to the dopamine receptors in the postsynaptic neuron
). The key difference is their action on the dopamine transporter, which generally moves a lot of the dopamine in the synapse back into the presynaptic neuron - which reduces the amount of dopamine in the synapse, and dopamine signalling. Ritalin increases dopamine signalling by effectively blocking the dopamine transporter.
The net effect is a negative charge of the postsynaptic neuron
. The result of this negative hyperpolarization of the cell is that there is no depolarization and no electric impulse generated.
An increase in intracellular [Ca.sup.2+] in presynaptic terminals triggers glutamate exocytosis, followed by postsynaptic neuron
excitation, which induces an increase in intracellular [Ca.sup.2+] in postsynaptic neurons
The appropriate machinery for synthesizing and releasing the retrograde messenger must be located in the postsynaptic neuron
The released neurotransmitter binds to postsynaptic receptors, leading to a response in the postsynaptic neuron
. The coupling between calcium channels and sensors of exocytosis is key in determining the speed, timing and probability of synaptic transmission.
The first part consists of establishing a baseline at which low-frequency electrical stimulations (e.g., one stimulation per second) of the presynaptic neurons cause stable firings of postsynaptic neurons
. The second part is to present a high-frequency electrical stimulation ("tetanus") of presynaptic neurons, generating hundreds of action potentials in a short period of time (e.g., two seconds), and whose final consequence is the increase of the postsynaptic neuron
A third variable modulating dopamine's effect is the number of dopamine receptors on the postsynaptic neuron
. The ability of typical antipsychotics to block nearly all the postsynaptic D2 receptors may lead to MDS (Carvalho et al.