Nerve membrane, polarization

Classically, it has been held that this neurotransmitter-receptor complex initiates a process that reconverts the chemical message back into an electrical impulse in the second nerve. This is certainly true for rapid-onset neurotransmitters and can explain the initial actions of some slow-onset neurotransmitters as well. However, it is now known that the postsynaptic neuron has a vast repertoire of responses beyond just whether it changes its membrane polarization to make it more or less likely to fire. Indeed, many important biochemical processes are triggered in the postsynaptic neuron by neurotransmitters occupying their receptors. Some of these begin within milliseconds, whereas others can take days to develop (Figs. 1 — 11 to 1 — 13). 

First, the impulse travels down a nerve to the axonal terminal, or presynaptic area, creating an action potential. (This action potential consists of a change in the resting potential of the polarized nerve membrane.) At the prejunctional area, the action potential stimulates the release of the neurotransmitter ACh from storage in synaptic vesicles. The ACh diffuses across the synaptic cleft and combines with specialized areas—the receptor sites— on the postsynaptic membrane to produce a postsynaptic potential, which may be either a de-... 

Association of the hydrophobic tails of membrane lipids leads, as depicted in Fig. 4.47a, to what Watkins [341] has described as polar discontinuities. Transition to the micellar state is considered to be essential to allow cell fusion to occur as the biomolecular leaflet is thermodynamically a stable system which would resist coalescence with similar structures. External influences can, however, induce phospholipid aggregation and can thus alter the permeability of cell membranes to water-soluble and oil-soluble species. Calcium ions, for example, induce inverse micelle formation in phospholipid systems [342]. Other metal ions also result in this transformation (Fig. 4.47b) addition of adenosine triphosphate (ATP) removes the metal and leads to a reversion to the normal micellar pattern. Maas and Coleman [343] have postulated that such transitions may have significance in nerve membrane operation. Metal-ATP-phospholipid complexes... 

When the nerve cell is polarized positive, ions (Q) are on the outside of the cell membrane and the negative ions ( )) are on the inside of the cell membrane. 

The taste bud is a polarized structure with a narrow apical opening, termed the taste pore, and basolateral synapses with afferent nerve fibers. Solutes in the oral cavity make contact with the apical membranes of the TRCs via the taste pore. There is a significant amount of lateral connectedness between taste cells within a bud both electrical synapses between TRCs and chemical synapses between TRCs and Merkel-like basal cells have been demonstrated to occur [39]. Furthermore, there are symmetrical synapses between TRCs and Merkel-like basal cells [39]. In addition, these basal cells synapse with the afferent nerve fiber, suggesting that they may function in effect as interneurons [39]. The extensive lateral interconnections... 

Fig. Id represents the ionic changes and reversal of polarity of the membrane when the nerve is stimulated. Na+ ions enter the membrane ahead of the electrical charge and K+ ions pass out at the peak of the potential reversal.1 Fig. le shows how the ionic interchange is related to the action potential (or magnitude of polarity change). It must be stressed that the actual percentage changes of concentration are very small indeed. The exact nature of the restoration of the original concentration of ions is not completely known. Obviously a source of energy is required, and this is considered to be derived from the metabolism of the cell.

Normal NMJs have a generally polarized nerve terminal with accumulations of40-50 nm small clear vesicles near the presynap-tic membrane and mitochondria located farther away (Fig. 20.8). In mice, the terminal Schwann cell capping the nerve terminal can be difficult to resolve. The postsynaptic membrane has a series of junctional folds invaginating into the muscle fiber. At the mouth (crest) of each fold, the membrane appears electron dense because of the accumulation of AChRs. The synaptic cleft is pronounced and contains a visible basal lamina. 

Fig. 20.8. Neuromuscular junctions analyzed by transmission electron microscopy. (A) In wild-type mice, the motor nerve terminal (MN) is depressed into the muscle fiber surface. The terminal is polarized, with small clear vesicles near the presynaptic membrane and mitochondria in the more proximal portion of the terminal. The postsynaptic membrane has deep convolutions (junctional folds, JF) and the membrane near the tops of these folds is very electron dense because of the high density of acetylcholine receptors (arrowheads). (B) In some myasthenias where the nerve sprouts but remains in contact with the muscle, terminals with mitochondria and vesicles are observed in the absence of any postsynaptic specialization. Presumably these are sprouting terminals that have not established a functional connection. (C) Partial innervation of postsynaptic sites is evident as elaborate junctional folds in the muscle membrane with no overlying nerve terminal. In these examples, the interpretations were aided by light microscopy examination of other samples as described in Fig. 20.8 in parallel with electron microscopy. The mutation shown in (B, C) is an unpublished ENU-induced allele of agrin.

These equations offer an adequate basis for the development of the negative membrane potential of 70 to 90 mV. Excitation as a process characterizing nerve and muscle cells is associated with a transient reduction or abolition of this membrane potential, and in some cases with a temporary "overshoot" or reversal of its polarity. Just as for the membrane potential, these major but transient perturbations in the production of action potentials have been adequately modeled in dynamics of ionic equilibria by Hodgkin and Huxley (2). 

---