204
Chapter 7
muscles and respond both to the absolute magnitude of mus-
cle stretch and to the rate at which the stretch occurs (to be
described in Chapter 10). Vision and the vestibular organs
(the sense organs of balance) also support the senses of pos-
ture and movement. Mechanoreceptors in the joints, tendons,
ligaments, and skin also play a role. The term
kinesthesia
refers to the sense of movement at a joint.
Temperature
Recent experiments have identifi
ed mechanisms by which two
types of thermoreceptors respond to temperature in the skin,
one group detecting cold and the other warmth. Cold-sens-
ing receptors have nonselective cation channels that open in
response to temperatures below body temperature. These chan-
nels are active over a broad range of temperatures ranging from
35°C down to near 0°C, with an infl ux of sodium depolarizing
the associated afferent neurons. The plant compound
menthol
activates these same channels, explaining the perception of cool-
ness experienced when it is applied to the skin. At temperatures
from 30°C up to about 50°C, warmth-sensing thermorecep-
tors are activated. Nonselective cation channels found in those
neurons depolarize the cell in response to warm temperatures.
Interestingly,
capsaicin
(a chemical found in chili peppers) and
ethanol also activate these channels, explaining the burning
sensation caused by eating some spicy foods or drinking a shot
of whiskey. Extremes of temperature that cause tissue damage
activate pain receptors, which are described next.
Pain
A stimulus that causes or is on the verge of causing tissue dam-
age usually elicits a sensation of pain. Receptors for such stimuli
are known as
nociceptors.
They respond to intense mechani-
cal deformation, excessive heat, and many chemicals. Examples
of the latter include neuropeptide transmitters, bradykinin,
histamine, cytokines, and prostaglandins, several of which are
released by damaged cells. Some of these chemicals are secreted
by cells of the immune system (described in Chapter 18) that
have moved into the injured area. These substances act by
binding to specifi c ligand-gated ion channels on the nociceptor
plasma membrane. In contrast to mechanoreceptors, nocicep-
tors are free nerve endings without any form of specialization.
The primary afferents having nociceptor endings synapse
on ascending neurons after entering the central nervous sys-
tem (
Figure 7–17a
). Glutamate and the neuropeptide, sub-
stance P, are among the neurotransmitters released at these
synapses.
Pain stimulus
Afferent pain fiber
Periphery
Periaqueductal
gray matter
Reticular formation
Opiate
neurotransmitter
Exogenous
morphine
Opiate
receptor
Substance P
release blocked
Thalamus
Somatosensory
cortex
Pain stimulus
Thalamus
Somatosensory
cortex
Substance P
+
+
+
(a)
(b)
CNS
Periphery
CNS
Figure 7–17
Cellular pathways of pain transmission and modulation. (a) Painful stimulation releases the neuropeptide substance P from afferent fi bers in the
spinal cord. (b) Substance P release is blocked by a descending analgesic system using axo-axonic synapses on the afferent neuron. Details of
this system not shown include descending neurons releasing norepinephrine and serotonin onto spinal interneurons that, in turn, release opiate
neurotransmitters. Morphine inhibits pain in a similar manner.
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