Nerve and Muscle Physical Work

Neuron Structure and Function

An excitable cell reacts to stimuli by altering its membrane characteristics p. 32). There are two types of excitable cells: nerve cells, which transmit and modify impulses within the nervous system, and muscle cells, which contract either in response to nerve stimuli or autonomously (^ p. 59).

The human nervous system consists of more than 1010 nerve cells or neurons. The neuron is the structural and functional unit of the nervous system. A typical neuron (motor neuron, ^ A1) consists of the soma or cell body and two types of processes: the axon and den-drites. Apart from the usual intracellular organelles (^ p. 8ff.), such as a nucleus and mitochondria (^ A2), the neuron contains neuro-fibrils and neurotubules. The neuron receives afferent signals (excitatory and inhibitory) from a few to sometimes several thousands of other neurons via its dendrites (usually arborescent) and sums the signals along the cell membrane of the soma (summation). The axon arises from the axon hillock of the soma and is responsible for the transmission of efferent neural signals to nearby or distant effectors (muscle and glandular cells) and adjacent neurons. Axons often have branches (collaterals) that further divide and terminate in swellings called synaptic knobs or terminal buttons. If the summed value of potentials at the axon hillock exceeds a certain threshold, an action potential (^ p. 46) is generated and sent down the axon, where it reaches the next synapse via the terminal buttons (^ A1,3) described below.

Vesicles containing materials such as proteins, lipids, sugars, and transmitter substances are conveyed from the Golgi complex of the soma (^ p. 13 F) to the terminal buttons and the tips of the dendrites by rapid axonal transport (40 cm/day). This type of antero-grade transport along the neurotubules is promoted by kinesin, a myosin-like protein, and the energy required for it is supplied by ATP (^ p. 16). Endogenous and exogenous substances such as nerve growth factor (NGF), herpes virus, poliomyelitis virus, and tetanus 42 toxin are conveyed by retrograde transport from the peripheral regions to the soma at a rate of ca. 25 cm/day. Slow axon transport (ca. 1 mm/day) plays a role in the regeneration of severed neurites.

Along the axon, the plasma membrane of the soma continues as the axolemma (^ A1,2). The axolemma is surrounded by oligodendrocytes (^ p. 338) in the central nervous system (CNS), and by Schwann cells in the peripheral nervous system (^ A1,2). A nerve fiber consists of an axon plus its sheath. In some neurons, Schwann cells form multiple concentric double phospholipid layers around an axon, comprising the myelin sheath (^ A1,2) that insulates the axon from ion currents. The sheath is interrupted every 1.5 mm or so at the nodes of Ranvier (^ A1). The conduction velocity of myelinated nerve fibers is much higher than that of unmyelinated nerve fibers and increases with the diameter of the nerve fiber (^ p. 49C).

A synapse (^ A3) is the site where the axon of a neuron communicates with effectors or other neurons (see also p. 50 ff.). With very few exceptions, synaptic transmissions in mammals are mediated by chemicals, not by electrical signals. In response to an electrical signal in the axon, vesicles (^ p. 1.6) on the presynaptic membrane release transmitter substances (neurotransmitters) by exocytosis (^ p.30). The transmitter diffuses across the synaptic cleft (10-40 nm) to the postsynaptic membrane, where it binds to receptors effecting new electrical changes (^ A3). Depending on the type of neurotransmitter and postsynaptic receptor involved, the transmitter will either have an excitatory effect (e.g., acetylcholine in skeletal muscle) or inhibitory effect (e.g., glycine in the CNS) on the postsynaptic membrane. Since the postsynaptic membrane normally does not release neurotransmitters (with only few exceptions), nerve impulses can pass the synapse in one direction only. The synapse therefore acts like a valve that ensures the orderly transmission of signals. Synapses are also the sites at which neuronal signal transmissions can be modified by other (excitatory or inhibitory) neurons.

,— A. Nerve cell structure and function-

1 Neuron and1 2 Myelinated and unmyelinated nerve fibers

Unmyelinated fibers

Collaterals

Nerve Cell

Collaterals

Resting Membrane Potential

An electrical potential difference, or membrane potential (Em), can be recorded across the plasma membrane of living cells. The potential of unstimulated muscle and nerve cells, or resting potential, amounts to - 50 to -100 mV (cell interior is negative). A resting potential is caused by a slightly unbalanced p distribution of ions between the intracellular 5 fluid (ICF) and extracellular fluid (ECF) (^ B). ¡3 The following factors are involved in establish-£ ing the membrane potential (see also p.32ff.). £ ♦ Maintenance of an unequal distribution of <u ions: The Na+-K+-ATPase (^ p. 26) continu-^ ously "pumps" Na+ out of the cell and K+ into it (^ A2). As a result, the intracellular K+ concen--o tration is around 35 times higher and the intran cellular Na+ concentration is roughly 20 times g lower than the extracellular concentration ¡D (^ B). As in any active transport, this process z requires energy, which is supplied by ATP. Lack ™ of energy or inhibition of the Na+-K+-ATPase results in flattening of the ion gradient and breakdown of the membrane potential.

Because anionic proteins and phosphates present in high concentrations in the cytosol are virtually unable to leave the cell, purely passive mechanisms (Gibbs-Donnan distribution) could, to a slight extent, contribute to the unequal distribution of diffusable ions (^A1). For reasons of electroneutrality, [K++Na+]icF > [K++Na+]ECF and [CI ]icf < [CI ]ecf. However, this has practically no effect on the development of resting potentials.

♦ Low resting Na+ and Ca2+ conductance, gNa, gca: The membrane of a resting cell is only very slightly permeable to Na+ and Ca2+, and the resting gNa comprises only a small percentage of the total conductance (^ p.32ff.). Hence, the Na+ concentration difference (^ A3-A5) cannot be eliminated by immediate passive diffusion of Na+ back into the cell.

♦ High K+conductance, gi<: It is relatively easy for K+ ions to diffuse across the cell membrane (gK ~ 90% of total conductance; ^ p.32ff.). Because of the steep concentration gradient (^ point 1), K+ ions diffuse from the ICF to the ECF (^ A3). Because of their positive charge, the diffusion of even small amounts of K+ ions

44 leads to an electrical potential (diffusionpotential) across the membrane. This (inside nega tive) diffusion potential drives K+ back into the cell and rises until large enough to almost completely compensate for the K+ concentration gradient driving the IC-ions out of the cell (^ A4). As a result, the membrane potential, Em, is approximately equal to the K+ equilibrium potential EK (^ p. 32).

♦ Cl- distribution: Since the cell membrane is also conductive to Cl- (gCl greater in muscle cells than in nerve cells), the membrane potential (electrical driving "force") expels Cl- ions from the cell (^ A4) until the Cl- concentration gradient (chemical driving "force") drives them back into the cell at the same rate. The intracellular Cl- concentration, [Cl-]i, then continues to rise until the Cl- equilibrium potential equals Em (^ A5). [Cl-] can be calculated using the Nernst equation (^ p. 32, Eq. 1.18). Such a "passive" distribution of Cl- between the intra- and extracellular spaces exists only as long as there is no active Cl- uptake into the cell (^ p. 34).

♦ Why is Em less negative than E<? Although the conductances of Na+ and Ca2+ are very low in resting cells, a few Na+ and Ca2+ ions constantly enter the cell (^ A4,5). This occurs because the equilibrium potential for both types of ions extends far into the positive range, resulting in a high outside-to-inside electrical and chemical driving "force" for these ions (^ B; ^ p. 32f.). This cation influx depolarizes the cell, thereby driving K+ ions out of the cell (1 K+ for each positive charge that enters). If Na+-K+-ATPase did not restore these gradients continuously (Ca2+ indirectly via the 3 Na+/Ca2+ exchanger; ^ p. 36), the intracellular Na+ and Ca2+ concentrations would increase continuously, whereas [K+]i would decrease, and EK and Em would become less negative.

All living cells have a (resting) membrane potential, but only excitable cells such as nerve and muscle cells are able to greatly change the ion conductance of their membrane in response to a stimulus, as in an action potential (^ p. 46).

- A. Causes and effects of resting membrane potentials

1 Passive ion distribution i 2 Active Na+-K+-pump

ECF ICF ECF

3 K+ diffusion potential

3 K+ diffusion potential

Cell Wall Membrane Dividing Icf From Ecf

4 Potential drives CI from ICF to ECF

5 End state: Resting membrane potential

4 Potential drives CI from ICF to ECF

5 End state: Resting membrane potential

Difference Between Icf And Ecf

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