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The ENS is estimated

to contain more than 100 million neurons, including afferent


neurons, interneurons, and efferent postganglionic parasympathetic
neurons. Enteric neurons contain many different
neurotransmitters and neuromodulators. Thus, not only
does the total number of neurons in the enteric division
exceed that of the spinal cord, but the neurochemical complexity
of the ENS also approaches that of the CNS. The
anatomy of the ENS as well as its role in controlling gastrointestinal
function is discussed in Chapter 41.
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Under physiological conditions, the soma of the sensory neurons are generally th
ought not to contribute information to the activity arising at their peripheral
receptor terminals, but simply to monitor the activity as it travels to the cent
ral terminations of the axons in the NTS. It is essential then that the soma mai
ntain a stable, negative resting membrane potential (-50 to -60 mV) to ensure th
at they fire only when sensory information from the peripheral receptor terminal
is received. The underlying basis of this stability is not completely known. At
the resting membrane potential, the hyperpolarization-activated, cyclic-nucleot
ide-gated (HCN) family of ion channels is active, driving the membrane potential
toward the reversal of about -35 mV. This depolarizing drive is offset by undet
ermined potassium current(s) . In this study we sought to identify the potassium
current contributing to the resting membrane potential. A potential candidate w
hich had not previously been identified in these cells was the M-current (IM). T
he M-current is a slowly activating, non-inactivating, voltage-dependent potassi
um (K+) current that activates in the range of the resting membrane potential. I
t acts to maintain the membrane potential below the threshold for sodium current
activation, thereby regulating neuronal firing and excitability These subunits
have a relatively restricted distribution in that they are primarily confined t
o the nervous system. The importance of these channels in maintaining cells at r
esting potential is illustrated by the observation that mutations in KCNQ2 and K
CNQ3 play a role in causing benign familial neonatal convulsions (BFNC), a form
of epilepsy (Jentsch, 2000)
+ informatie din BORON
A well-characterized effect of muscarinic neurotransmission
in autonomic ganglia is inhibition of a specifi c K+
current called the M current. The M current is widely distributed
in visceral end organs, autonomic ganglia, and the
CNS. In the baseline state, the K+ channel that underlies the
M current is active, thereby producing slight hyperpolarization.
In the example shown in Figure 14-9B, with the stabilizing
M current present, electrical stimulation of the neuron
causes only a single spike. If we now add muscarine to the
neuron, activation of the muscarinic receptor turns off the
hyperpolarizing M current and thus leads to a small depolarization.
If we repeat the electrical stimulation in the continued
presence of muscarine (Fig. 14-9C), repetitive spikes
appear because loss of the stabilizing infl uence of the M
current increases the excitability of the neuron. The slow,
modulatory effects of muscarinic responses greatly enhance
the ability of the ANS to control visceral activity beyond
what could be accomplished with only fast nicotinic
EPSPs.

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