Re-uptake involves the reabsorption of neurotransmitters by any of the neurotransmitter receptors or transporters. The transporters involved are usually of pre-synaptic neurons. Re-uptake occurs after the neurotransmitter has transmitted a neural impulse. Re-uptake is very crucial in order for the normal functioning of synapses to take place. This is because it allows the neurotransmitters to be recycled, thereby regulating their levels in the synapse. This in turn dictates the length of time it takes for a signal - generated by neurotransmitter release - to last. Neurotransmitters are usually large hydrophilic molecules that cannot pass through the neuronal membranes. For this reason, certain transport proteins take the responsibility of reabsorbing these neurotransmitters (Carlson, 2007). It is now widely accepted that all receptors are protein molecules that tend to be embedded in the synaptic membranes. These proteins have been found to contain specific areas of action known as active sites that are capable of binding to and with specific neurotransmitters present on the extracellular matrix (ECM). The active site is usually found on the outer side of the protein molecule within the post-synaptic membrane, always facing the synaptic gap.
Many therapeutic drugs are also protein molecules that tend to associate with these receptor molecules. They are able to bind with a receptor molecule and consequently trigger response of an effector complex that allows for the opening and/or closing of ionic channels in the membrane. These effector complexes are part of the post-synaptic mediation channel that responds to neurotransmitter binding. Once a neurotransmitter binds to a specific receptor, the effector complexes are triggered resulting in the formation of a receptor-effector complex. However, the sites where the neurotransmitters bind are very distinct from those sites where the effectors bind to the receptor. Thus, a single neurotransmitter may have dissimilar physiological effects at separate receptor complexes. For this reason, a neurotransmitter may carry stimulatory effects at one point while cause inhibition at another site. This is the same case with therapeutic drugs. Once these drugs bind to a receptor and trigger an effector molecule, they are often referred to as agonists. One good example of such an agonist is heroin. Heroin acts as an agonist of endorphin, a brain neurotransmitter. Some therapeutic drugs, however, lead to the reduction or total elimination of a response of the receptor to any neurotransmitter or their agonists. In this case, they lead to inhibition of receptor-effector complexes that produce specific physiological effects or behavior (Carlson, 2007). One important channel that agonists use is the total occupation of receptor sites, with no signals sent to trigger the effector molecules. In such a manner, the neurotransmitter action is disrupted.
The receptive field of any neuron involved in the visual system is that part of the field of vision that a single neuron focuses on. This means that it is that place where a visual stimulus occurs in order to generate a response in that particular neuron. In fact, the location of a specific neuronal receptive field depends on where its photoreceptors are located. These photoreceptors are important in that they provide the neuron with visual information that enables it to focus. If, for instance, a particular neuron has received visual information from the photoreceptors situated at the fovea, then its field of reception will be located at the fixation site, which is the point where the eye is focusing. If the particular neuron receives its visual information from those photoreceptors in the retinal periphery, then the field of reception will be situated at one side. At the retinal periphery, numerous receptors group together on a ganglion cell to form a wide area of retinal vision and consequently a large visual field. On the other hand, the fovea has almost equal numbers of cones as well as ganglion cells. In this regard, the foveal or central vision tends to be very acute compared to the periphery vision which tends to be less precise.
Kuffler (1952, 1953) discovered that a cat’s receptive field in the retinal ganglion cells contained circular centers that were surrounded by a ring. When this center or its surrounding fields were stimulated, contrary effects were observed. Cells which indicated ON for the circular centers were activated by light which fell on the central field, but were inhibited by the same light falling on the surrounding field. On the other hand, the OFF cells responded to the same stimulus in an opposite manner. Both ON and OFF ganglion cells were stimulated, for a moment, when the light was switched on or off.
Carlson, N.R. (2007). Physiology of Behavior (9th Ed.). Upper Saddle River, NJ: Pearson Ed.