Question

2. Long-term Potentiation is a process that strengthens the transmission of a single synapse in a circuit. This is achieved when pre-synaptic cells and post-synaptic cells fire action potentials at the same time. Usually multiple pre-synaptic cells synapse onto one post-synaptic cell, increasing the probability of inducing an action potential in the post- synaptic cell. You may need to refer to your textbooks or online resources for this question, as we do not cover this in explicit detail in class. a. Draw the expected voltage curves if you stimulate one of the pre-synaptic cells and record the voltage from a post-synaptic cell in this circuit: i. before LTP conditioning ii. short after LTP conditioning and ii. several months after LTP conditioning. (Assume the pre-synaptic cell releases glutamate and you are stimulating the pre-synaptic cell with the same intensity for each condition) b. If you were to use an antagonist that selectively blocked NMDA receptors, what would happen to LTP? Draw the voltage response shortly after LTP conditioning. Explain your answer. (Assume the antagonist was present before and during LTP conditioning, but you remove it before performing the experiment) How could use of this antagonist affect C. i. Central sensitization in the spinal cord after tissue injury? ll. Learning and memory?

Answer 1

Long term potentiation is a process that strengthens the transmmison of a single synapse in a circuit.This is achieved when pre-synaptic cells and post synaptic-cells fire action potentials at the same time.Usally multiple presynaptic cells synapse onto one post synaptic cells, increasing the probability of inducing an action potential in the post synaptic cell.

he function of the synapse is to transfer electric activity (information) from one cell to another. The transfer can be from nerve to nerve (neuro-neuro), or nerve to muscle (neuro-myo). The region between the pre- and postsynaptic membrane is very narrow, only 30-50 nm. It is called the synaptic cleft (or synaptic gap). Direct electric communication between pre- and postjunctional cells does not take place; instead, a chemical mediator is utilized. The sequence of events is as follows:

1. An action pulse reaches the terminal endings of the presynaptic cell.
2. A neurotransmitter is released, which diffuses across the synaptic gap to bind to receptors in specialized membranes of the postsynaptic cell.
3. The transmitter acts to open channels of one or several ion species, resulting in a change in the transmembrane potential. If depolarizing, it is an excitatory postsynaptic potential (EPSP); if hyperpolarizing, an inhibitory postsynaptic potential (IPSP).

Figure 5.1 shows the synapse between a nerve and muscle cell, a neuromuscular junction.
In cardiac muscle the intercellular space between abutting cells is spanned by gap junctions, which provide a low-resistance path for the local circuit currents and may be regarded as an electric (myo-myo) synapse. (The gap, however, is not called a synaptic cleft.) This type of junction is discussed in a later chapter.
The presynaptic nerve fiber endings are generally enlarged to form terminal buttons or synaptic knobs. Inside these knobs are the vesicles that contain the chemical transmitters. The arrival of the action pulse opens voltage-gated Ca²⁺ channels that permit an influx of calcium ions. These in turn trigger the release into the synaptic gap, by exocytosis, of a number of the "prepackaged" vesicles containing the neurotransmitter.
On average, each neuron divides into perhaps 1000 synaptic endings. On the other hand, a single spinal motor neuron may have an average of 10,000 synaptic inputs. Based on this data, it is not surprising that the ratio of synapse to neurons in the human forebrain is estimated to be around 4×10⁴. In neuro-neuro synapses, the postjunctional site may be a dendrite or cell body, but the former predominates.

The driver of a car receives visual signals via photoreceptors that initiate coded afferent impulses that ascend nerve fibers and terminate in the visual cortex. Once the brain has processed the information, it sends efferent signals to the muscles in the foot and hands. Thus the car is slowed down and can make a right turn. But if our hand is mistakenly brought to rest on a hot surface, a set of signals to the hand and arm muscles result that are not initiated in the higher centers; cognition comes into play only after the fact. We say that a reflex path is involved in both of these examples. The first is complex and involves higher centers in the central nervous system, whereas the second describes a simpler reflex at a lower level. In fact, a great deal of reflex activity is taking place at all times of which we are unaware. For example, input signals are derived from internal sensors, such as blood pressure, or oxygen saturation in the blood, and so on, leading to an adjustment of heart rate, breathing rate, etc.
The reflex arc, illustrated above, is considered to be the basic unit of integrated neural activity. It consists essentially of a sensory receptor, an afferent neuron, one or more synapses, an efferent neuron, and a muscle or other effector. The connection between afferent and efferent pathways is found, generally, in the spinal cord or the brain. The simplest reflex involves only a single synapse between afferent and efferent neurons (a monosynaptic reflex); an example is the familiar knee jerk reflex.
Homeostasis refers to the various regulatory processes in the body that maintain a normal state in the face of disturbances. The autonomic nervous system is organized to accomplish this automatically with regard to many organs of the body; its activity, like that of the somatic nervous system, is based on the reflex arc. In this case signals, which arise at visceral receptors, are conveyed via afferent neurons to the central nervous system, where integration takes place, resulting in efferent signals to visceral effectors (in particular, smooth muscle) to restore or maintain normal conditions. Integration of signals affecting blood pressure and respiration takes place in the medulla oblongata; those controlling pupillary response to light are integrated in the midbrain, whereas those responding to body temperature are integrated in the hypothalamus - to give only a few examples.

The electric behavior at a synapse can be estimated by examining an equivalent circuit of the postsynaptic membrane, such as that shown in Figure 5.2. Two regions are identified: One represents the membrane associated with receptors sensitive to the transmitter, and the other the normal excitable membrane of the cell. In Figure 5.2 these two regions are represented by discrete elements, but in reality these are distributed along the structure that constitutes the actual cell. This figure depicts a neuromuscular junction, where the release of acetylcholine results in the elevation of sodium and potassium conductance in the target region, which is in turn depicted by the closing of the ACh switch. Upon closure of this switch,

ΔINa = ΔGNa(Vm - VNa)

(5.1)

ΔIK = ΔGK(Vm - VK)

(5.2)

where	INa, IK	=	sodium and potassium ion currents [µA/cm²]
	ΔGNa, ΔGK	=	additional sodium and potassium conductances following activation by ACh (i.e., nearly equal large conductances) [mS/cm²]
	VNa, VK	=	the Nernst voltages corresponding to the sodium and potassium concentrations [mV]
	Vm	=	membrane voltage [mV]