Neuron first-order

As discussed, the first-order neuron is the afferent neuron that transmits impulses from a peripheral receptor toward the CNS. Its cell body is located in the dorsal root ganglion. This neuron synapses with the second-order neuron whose cell body is located in the dorsal horn of the spinal cord or in the medulla of the brainstem. The second-order neuron travels upward and synapses with the third-order neuron, whose cell body is located in the thalamus. Limited processing of sensory information takes place in the thalamus. Finally, the third-order neuron travels upward and terminates in the somatosensory cortex where more complex, cortical processing begins. 

Stimulation of a nociceptor in the periphery of the body elicits action potentials in the first-order neuron, which transmits the signal to the second-order neuron in the dorsal horn of the spinal cord. From the spinal cord, the signal is transmitted to several regions of the brain. The most prominent ascending nociceptive pathway is the spinothalamic tract. Axons of the second-order sensory neurons project to the contralateral (opposite) side of the spinal cord and ascend in the white matter, terminating in the thalamus (see Figure 8.1). The thalamus contributes to the basic sensation or awareness of pain only it cannot determine the source of the painful stimulus. 

Impulse traffic in the neo- and pa-leospinothalamic pathways is subject to modulation by descending projections that originate from the reticular formation and terminate at second-order neurons, at their synapses with first-order neurons, or at spinal segmental interneurons (descending antinociceptive system). This system can inhibit impulse transmission from first- to second-order neurons via release of opio-peptides (enkephalins) or monoamines (norepinephrine, serotonin). 

Figure 8-1 The oculosympathetic pathway. Note its origin in the hypothalamus and its course through the brainstem and cervical spinal cord (central or first-order neuron), the upper thorax and lower neck (pregangUonic or second-order neuron), and upper neck, middle cranial fossa, cavernous sinus, and orbit as it finally reaches Muller s muscle of the lid and the iris dilator muscle (postganglionic or third-order neuron), (a. = artery n. = nerve.) (Reprinted with permission from Glaser JS.The pupils and accommodation. In Duane TD, Jaeger EA, eds. Clinical ophthalmology. Hagerstown, MD Harper Row, 1987.)...

The central (first-order) neuron originates in the hypothalamus, courses through the brainstem and cervical cord, and terminates at the ciliospinal center of Budge atC8-T2. 

Odor molecules that enter the nasal cavities and bind to first-order neurons, olfactory receptor neurons... 

The cell bodies of second-order sensory neurons are found in the dorsal horn. These neurons receive input from afferent neurons (first-order sensory neurons) entering the CNS from the periphery of the body through the dorsal... 

Afferent neurons that transmit sensory information toward the spinal cord are referred to as first-order sensory neurons. The cell bodies of these neurons are found in the dorsal root ganglia. These ganglia form a swelling in each of the dorsal roots just outside the spinal cord. The portion of the axon between the distal receptor and the cell body is referred to as the peripheral axon and the portion of the axon between the cell body and the axon terminal within the CNS is referred to as the central axon. 

Upon entering the spinal cord, the first-order sensory neurons may enter the gray matter and may then synapse with one or more of the following neurons ... 

Synapses between first-order sensory neurons and alpha motor neurons, either directly or by way of intemeurons, result in spinal cord reflexes. Reflexes are discussed in more detail in a subsequent section in this chapter. 

Alternatively, the first-order sensory neurons may initially enter the white matter of the spinal cord. In this case, the axons of these neurons may ascend the cord to the medulla or travel up or down the cord to a different spinal segment. Upon reaching its destination, the axon then enters the gray matter of the spinal cord and synapses with one or more of the neurons discussed previously. 

The mechanism of action of these anesthetics involves the blockade of sodium channels in the membrane of the second-order sensory neuron. The binding site for these anesthetics is on a subunit of the sodium channel located near the internal surface of the cell membrane. Therefore, the agent must enter the neuron in order to block the sodium channel effectively. Without the influx of sodium, neurons cannot depolarize and generate an action potential, so the second-order sensory neuron cannot be stimulated by impulses elicited by pain receptors associated with the first-order sensory neuron. In other words, the pain signal is effectively interrupted at the level of the spinal cord and does not travel any higher in the CNS. In this way, the brain does not perceive pain. 

A reflex is initiated by stimulation of a sensory receptor located at the peripheral ending of an afferent or first-order sensory neuron. This afferent neuron transmits impulses to the spinal cord. Within the gray matter of the spinal cord, the afferent neuron synapses with other neurons. As such, the spinal cord serves as an integrating center for the sensory input. The afferent neuron must ultimately synapse with an efferent or motor neuron. When the afferent neuron synapses directly with the motor neuron, it forms a monosynaptic reflex. An example of this type of reflex is the stretch reflex. When the afferent neuron synapses with an intemeuron that then synapses with the motor neuron, it forms a polysynaptic reflex, e.g., the withdrawal reflex. Most reflexes are polysynaptic. The motor neuron then exits the spinal cord to innervate an effector tissue, which carries out the reflex response. 

Chemical Source Enzyme involved in synthesis Effect on first-order sensory neuron Pharmacological intervention... 

Substance P First order sensory neuron Sensitization Opioid receptor agonists (e.g., morphine)... 

Morphine may be administered orally, intravenously, or epidurally. An advantage of epidural administration is that it provides effective analgesia while minimizing the central depressant effects associated with systemic administration. The mechanism of action with the epidural route of administration involves opioid receptors on the cell bodies of first-order sensory neurons in the dorsal root ganglia as well as their axon terminals in the dorsal hom. Stimulation of these receptors inhibits release of substance P and interrupts transmission of the pain signal to the second-order sensory neuron. 

Axons of male-specific antennal ORCs specialized to detect components of the sex pheromone project exclusively to the MGC (64, 89), and all AL neurons that respond to antennal stimulation with sex pheromone components have arborizations in the MGC (65, 72, 73). The MGC in M. sexta has two major, easily distinguishable divisions a donut-shaped neuropil structure (the "toroid") and a globular structure (the "cumulus") adjacent to the toroid and closer to the entrance of the antennal nerve into the AL (74). AL PNs that respond to antennal stimulation with sex pheromone component A have arborizations in the toroid and PNs responsive to component B, in the cumulus (74). Thus first-order synaptic processing of sensory information about these key components of the sex pheromone apparently is confined to different, distinctive neuropil regions of the MGC. 

Opioids basically exert their analgesic effects by inhibiting synaptic transmission in key pain pathways in the spinal cord and brain. This inhibitory effect is mediated by opioid receptors that are located on both presynaptic and postsynaptic membranes of pain-mediating synapses (Fig. 14—2). In the spinal cord, for example, receptors are located on the presynaptic terminals of primary (first-order) nociceptive afferents, and when bound by opioids, they directly decrease the release of pain-mediating transmitters such as substance P.35,38 Opioid drug-receptor interactions also take place on the postsynaptic membrane of the secondary afferent neuron—that is, the second-order nociceptive afferent neuron in the spinal cord.19,33 When stimulated, these receptors also inhibit pain transmission by hyperpolarizing the postsynaptic neuron.19... 

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