Why does cl entry cause ipsps

When the neuron is at rest, there is a baseline level of ion flow through leak channels. However, the ability of neurons to function properly and communicate with other neurons and cells relies on ion flow through channels other than the non-gated leak channels.

We will cover how these channels open in a later lesson. This chapter will examine ion flow through these channels after a stimulus and how the membrane potential changes in response.

Postsynaptic potentials are changes in membrane potential that move the cell away from its resting state. For our purposes, postsynaptic potentials are measured in the dendrites and cell bodies. Ion channels that are opened by a stimulus allow brief ion flow across the membrane. A stimulus can range from neurotransmitters released by a presynaptic neuron, changes in the extracellular environment like exposure to heat or cold, interactions with sensory stimuli like light or odors, or other chemical or mechanical events.

The change in membrane potential in response to the stimulus will depend on which ion channels are opened by the stimulus. An excitatory postsynaptic potential EPSP occurs when sodium channels open in response to a stimulus. The electrochemical gradient drives sodium to rush into the cell.

At 0 mV, there is no potential or polarization across the membrane, so moving toward 0 would be a decrease in potential. This depolarization increases the likelihood a neuron will be able to fire an action potential, which makes this ion flow excitatory. As potassium is also the ion with the most-negative equilibrium potential, usually the resting potential can be no more negative than the potassium equilibrium potential.

This voltage is called the resting membrane potential and is caused by differences in the concentrations of ions inside and outside the cell. If the membrane were equally permeable to all ions, each type of ion would flow across the membrane and the system would reach equilibrium. Because ions cannot simply cross the membrane at will, there are different concentrations of several ions inside and outside the cell. The negative resting membrane potential is created and maintained by increasing the concentration of cations outside the cell in the extracellular fluid relative to inside the cell in the cytoplasm.

The cell possesses potassium and sodium leakage channels that allow the two cations to diffuse down their concentration gradient. However, the neurons have far more potassium leakage channels than sodium leakage channels. Therefore, potassium diffuses out of the cell at a much faster rate than sodium leaks in.

More cations leaving the cell than entering it causes the interior of the cell to be negatively charged relative to the outside of the cell. The actions of the sodium-potassium pump help to maintain the resting potential, once it is established. As more cations are expelled from the cell than are taken in, the inside of the cell remains negatively charged relative to the extracellular fluid.

Signals are transmitted from neuron to neuron via an action potential, when the axon membrane rapidly depolarizes and repolarizes. A neuron can receive input from other neurons via a chemical called a neurotransmitter. If this input is strong enough, the neuron will pass the signal to downstream neurons. Transmission of a signal within a neuron in one direction only, from dendrite to axon terminal is carried out by the opening and closing of voltage-gated ion channels, which cause a brief reversal of the resting membrane potential to create an action potential.

As an action potential travels down the axon, the polarity changes across the membrane. Once the signal reaches the axon terminal, it stimulates other neurons. Formation of an action potential : The formation of an action potential can be divided into five steps. The hyperpolarized membrane is in a refractory period and cannot fire. At excitatory synapses, positive ions flood the interior of the neuron and depolarize the membrane, decreasing the difference in voltage between the inside and outside of the neuron.

Once the threshold potential is reached, the neuron completely depolarizes. At this point, the sodium channels return to their resting state, ready to open again if the membrane potential again exceeds the threshold potential. For an action potential to communicate information to another neuron, it must travel along the axon and reach the axon terminals where it can initiate neurotransmitter release.

Myelin acts as an insulator that prevents current from leaving the axon, increasing the speed of action potential conduction. Diseases like multiple sclerosis cause degeneration of the myelin, which slows action potential conduction because axon areas are no longer insulated so the current leaks. Action potential travel along a neuronal axon : The action potential is conducted down the axon as the axon membrane depolarizes, then repolarizes.

A node of Ranvier is a natural gap in the myelin sheath along the axon. Nodes of Ranvier also save energy for the neuron since the channels only need to be present at the nodes and not along the entire axon. Nodes of Ranvier : Nodes of Ranvier are gaps in myelin coverage along axons.

Action potentials travel down the axon by jumping from one node to the next. Synaptic transmission is a chemical event which is involved in the transmission of the impulse via release, diffusion, receptor binding of neurotransmitter molecules and unidirectional communication between neurons. In a chemical synapse, the pre and post synaptic membranes are separated by a synaptic cleft, a fluid filled space.

The chemical event is involved in the transmission of the impulse via release, diffusion, receptor binding of neurotransmitter molecules and unidirectional communication between neurons. Neurotransmission at a chemical synapse begins with the arrival of an action potential at the presynaptic axon terminal. Calcium ions entering the cell initiate a signaling cascade. The synaptic vesicles fuse with the presynaptic axon terminal membrane and empty their contents by exocytosis into the synaptic cleft.

The cell possesses potassium and sodium leakage channels that allow the two cations to diffuse down their concentration gradient. However, the neurons have far more potassium leakage channels than sodium leakage channels. Therefore, potassium diffuses out of the cell at a much faster rate than sodium leaks in. Because more cations are leaving the cell than are entering, this causes the interior of the cell to be negatively charged relative to the outside of the cell.

The actions of the sodium potassium pump help to maintain the resting potential, once established. As more cations are expelled from the cell than taken in, the inside of the cell remains negatively charged relative to the extracellular fluid. It should be noted that calcium ions Cl — tend to accumulate outside of the cell because they are repelled by negatively-charged proteins within the cytoplasm. A neuron can receive input from other neurons and, if this input is strong enough, send the signal to downstream neurons.

Transmission of a signal between neurons is generally carried by a chemical called a neurotransmitter. Transmission of a signal within a neuron from dendrite to axon terminal is carried by a brief reversal of the resting membrane potential called an action potential.

At excitatory synapses, this opening allows positive ions to enter the neuron and results in depolarization of the membrane—a decrease in the difference in voltage between the inside and outside of the neuron. A stimulus from a sensory cell or another neuron depolarizes the target neuron to its threshold potential mV. At this point, the sodium channels will return to their resting state, meaning they are ready to open again if the membrane potential again exceeds the threshold potential.

Which part of the action potential would you expect potassium channels to affect? This video presents an overview of action potential. For an action potential to communicate information to another neuron, it must travel along the axon and reach the axon terminals where it can initiate neurotransmitter release. Myelin acts as an insulator that prevents current from leaving the axon; this increases the speed of action potential conduction.

In demyelinating diseases like multiple sclerosis, action potential conduction slows because current leaks from previously insulated axon areas. The nodes of Ranvier, illustrated in Figure Nodes of Ranvier also save energy for the neuron since the channels only need to be present at the nodes and not along the entire axon.

Synapses usually form between axon terminals and dendritic spines, but this is not universally true. There are also axon-to-axon, dendrite-to-dendrite, and axon-to-cell body synapses.

The neuron transmitting the signal is called the presynaptic neuron, and the neuron receiving the signal is called the postsynaptic neuron. Note that these designations are relative to a particular synapse—most neurons are both presynaptic and postsynaptic.

There are two types of synapses: chemical and electrical. Calcium ions entering the cell initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles , containing neurotransmitter molecules to fuse with the presynaptic membrane. Synaptic vesicles are shown in Figure This can be accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be degraded by enzymes in the synaptic cleft, or it can be recycled sometimes called reuptake by the presynaptic neuron.

Several drugs act at this step of neurotransmission. This inhibition of the enzyme essentially increases neurotransmission at synapses that release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and unbind to postsynaptic receptors. While electrical synapses are fewer in number than chemical synapses, they are found in all nervous systems and play important and unique roles. The mode of neurotransmission in electrical synapses is quite different from that in chemical synapses.

In an electrical synapse, the presynaptic and postsynaptic membranes are very close together and are actually physically connected by channel proteins forming gap junctions. Gap junctions allow current to pass directly from one cell to the next.

In addition to the ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction pores. There are key differences between chemical and electrical synapses. Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels.

When GABA is released into the synapse, it binds to a population of the available receptors, but typically not all of them Figure If benzodiazepines are present, the effectiveness of GABA binding to its receptor is increased significantly Figure Inhibition is produced by increasing the amount of Cl - that flows into the neuron Figure Recognize that benzodiazepines themselves do not open the receptor but simply enhance GABA binding.

Barbiturates also produce their sedative effects by increasing the effectiveness of GABA binding to its receptor. The naturally occurring toxin called picrotoxin is a potent inhibitor of the GABA A receptor and works by preventing Cl - flow through the receptor Figure The glycine receptor, like the GABA A receptor also permits the influx of Cl - into neurons and displays a reversal potential near mV.

This Cl - -permeable glycine receptor can be blocked by the rat poison strychnine. The mature glycine receptor is constructed from mixtures of at least two subunits each of which has four membrane spanning domains. Glutamate GPCRs are members of a large family of receptors that couple with G proteins to produce their effects.

These receptors like those for serotonin, norepinephrine, epinephrine, muscarinic ACh, and dopamine, produce the large majority of their effects through alterations in the activity of metabolic enzymes and not by directly opening ion channels in the membranes.

All of these receptors are single polypeptides that span the membrane seven times See Fig. The glutamate GPCR's best known effects are the activation of phospholipase C which generates inositol-trisphosphate IP 3 and diacylglycerol DAG from the precursor lipid phosphatidylinositol bisphosphate See Figure The GABA B receptor, like the glutamate GPCR, produces its effects not by directly opening ion channels, but by coupling to G-proteins and enzymes that influence metabolites within the neuron.

Some of the ion channel effects detected are due to the components of the activated G-protein binding directly to ion channels, influencing their properties See Figure 6. Two basic mechanisms, diffusion and high affinity uptake , terminate the response to amino acid transmitters. The high affinity uptake mechanism is the most predominant. The proteins involved in transmitter uptake are related and each contains 12 membrane-spanning domains.

Transporters use energy derived either from the hydrolysis of ATP or electrochemical ion gradients established across the membrane to pump the transmitters into neurons and glia.

The energy-dependent nature of these receptors means that in times of metabolic stress, such as during an ischemic episode, the pumps fail and toxic levels of these transmitters build up. The neurotransmitter glutamate is highly toxic to neurons when present for extended periods. One of the best understood clinical conditions involving glutamate is neuronal injury following stroke or trauma.

Both events produce massive release of glutamate in the brain that over-stimulates glutamate receptors. The absence of energy prevents the pumps from removing glutamate from the synapse. The key to minimizing damage following stroke is well-controlled reestablishment of blood flow so that ATP production is supported and homeostasis is reestablished. Clot breaking agents such as tissue plasminogen activator tPA are now used commonly to reestablish blood flow. Because glutamate is the major excitatory transmitter in the human brain, derangements in glutamate metabolism or receptor activation have been implicated in a wide variety of pathologic conditions.

These include diseases such as Alzheimer's and Huntington's chorea. One explanation for the establishment of focal epilepsy is decreased local GABA-mediated inhibition. Many facets of epilepsy can be elicited experimentally by blocking GABA receptors with the toxin picrotoxin previously described.

The decrease in GABA inhibition permits cells to fire synchronously, thus producing massive local excitation and initiation of a seizure.

Clinically, seizures can often be terminated by inducing a barbiturate coma. High dose barbiturates presumably potentiate GABA's inhibitory effects, preventing local hyperexcitation by hyperpolarizing the cell membranes.

Mood disorders generalized anxiety disorder can also be controlled by drugs which potentiate GABA's inhibitory activity. Some of the most widely prescribed drugs-benzodiazepines Librium and Valium -produce their pharmacological effects by increasing GABA's ability to hyperpolarize neuronal membranes, thereby quieting the system.

This finding suggests that some initial imbalance in the GABAergic system may underlie aspects of this disorder. Glutamate is recovered into a usable pool for neurons through it's metabolism in glial cells. Results in its metabolism into glutamine by glutamine synthase. Results in its metabolism into GABA by glutamic acid decarboxylase. Glutamate is removed from the extracellular space by high-affinity up-take transporters in the plasma membranes of neurons and glia.