REFLEXES AND SPINAL CORD CIRCUITS/RESPONSES
FLEXION AND CROSSED EXTENSION REFLEX RECIPROCAL INHIBITION DIVERGENCE OF Ia AFFERENTS SPINAL REFLEX AND ITS COMPONENTS,
STRETCH REFLEX
1. Stimulation of nociceptors/pain 1. Ia afferent in spinal cord branches into 1.Ia afferent project onto ALL motor neurons
receptors/cutaneous receptors leads to withdrawal collaterals that also synapse onto inhibitory of homonymous muscle =autogenic spinal= automatic, stereotypes motor response
of affected limb interneurons with EPSP excitation to sensory stimulus
- This inc efficiency and speed of - Initiated by stim of peripheral receptors
2. Muscles on ipsilateral side of pain source inc in movement because muscles acting 2. Also divergence to heteronymous muscles, including cutaneous, joint stretch,
excitation of flexor muscles and inhibition of as prime movers don't have to work particularly synergistic —but this reflex is not tendon tap, activation of GTO or
extensor muscles against contraction of antagonists as strong as homonymous multiple AP
- Consists of sensory neurons,
3. While withdrawing limb from painful source, 2. Inhib interneurons release IPSP onto **stim of one muscle group leads to interneurons (most abundant) and
muscles in contralateral limb inc excitation of antagonist muscle (i.e: triceps during flexion) excitation/contraction of all fibers of that motor neurons
extensor muscles and inhibit flexor muscles = allowing flexion to occur same muscle and contraction of another - Can be mono- , di- or polysynaptic
allows maintenance of postural support muscle in that same group
3.simultaneously, Ia afferent has direct Stretch reflex= contraction of muscle evoked by
**is a protective reflex excitatory (EPSP) connection with spinal stretch
- Activates divergent polysnaptic reflex pw motor neurons - Mediated by Ia input from spindles
- One is excitatory other is inhibitory - Powerful reflex, monosynaptic with
response latency ~20-40ms can be
shorter for smaller person
Ib (GTO) INHIBITION, SOURCES Ib GTO FACILATORY/EXCITATORY EFFECT RECURRENT INHIBITION HOFFMAN REFLEX VS TENDON REFLEX
ON ANTAGONIST MN
1.active muscle contraction activates GTO= 1.as MN descend their axons, collaterals H-Reflex: electrically stimulate Ia fibers in peripheral
synapses 1b afferent 1.inhib IN has IPSP that inhibits an inhibitory branch off and with an EPSP synapse onto nerve
MN pool renshaw cell - At low stimulus= Ia afferent turn on first due
to lower thresh than motor axons
2.disynaptic or sometimes trisynaptic connection to
- Inc stim strength = excite motor axons
MN via 1b inhibitory IN 2. Facilitation via inhibiting inhibition - M-wave=direct stim of axons H-wave= travel
(withdrawing inhibition from alpha MN pool of 2. Renshaw cell feeds back to alpha MN with down to SC through synapse and to muscle
3. Leads to autogenic inhibition of muscle GTO antagonist) an IPSP=inhib of MN pool - As stim continually inc, M wave inc but H
resides in - Project to MN that excite them and wave eventually declines because
- Leads to precise spinal control of muscle Ia inhib interneurons antidromic has > effect than orthodromic
force - Also connect to gamma MN, other - M-wave plateaus due to rec all axons
renshaw cells T-reflex: initiated by brief tap on tendon of muscle=
activate muscle spindles= monosynaptic connection to
Receives input from: joint afferents, cutaneous **stabilize firing rate of MN and reg strength
MN
afferents and descending inputs—all converge of inhib of antagonist MN **both test coupling b/w Ia aff and MN, and level of
MN excitability but T-reflex also tests spindle
sensitivity
FLEXION AND CROSSED EXTENSION REFLEX RECIPROCAL INHIBITION DIVERGENCE OF Ia AFFERENTS SPINAL REFLEX AND ITS COMPONENTS,
STRETCH REFLEX
1. Stimulation of nociceptors/pain 1. Ia afferent in spinal cord branches into 1.Ia afferent project onto ALL motor neurons
receptors/cutaneous receptors leads to withdrawal collaterals that also synapse onto inhibitory of homonymous muscle =autogenic spinal= automatic, stereotypes motor response
of affected limb interneurons with EPSP excitation to sensory stimulus
- This inc efficiency and speed of - Initiated by stim of peripheral receptors
2. Muscles on ipsilateral side of pain source inc in movement because muscles acting 2. Also divergence to heteronymous muscles, including cutaneous, joint stretch,
excitation of flexor muscles and inhibition of as prime movers don't have to work particularly synergistic —but this reflex is not tendon tap, activation of GTO or
extensor muscles against contraction of antagonists as strong as homonymous multiple AP
- Consists of sensory neurons,
3. While withdrawing limb from painful source, 2. Inhib interneurons release IPSP onto **stim of one muscle group leads to interneurons (most abundant) and
muscles in contralateral limb inc excitation of antagonist muscle (i.e: triceps during flexion) excitation/contraction of all fibers of that motor neurons
extensor muscles and inhibit flexor muscles = allowing flexion to occur same muscle and contraction of another - Can be mono- , di- or polysynaptic
allows maintenance of postural support muscle in that same group
3.simultaneously, Ia afferent has direct Stretch reflex= contraction of muscle evoked by
**is a protective reflex excitatory (EPSP) connection with spinal stretch
- Activates divergent polysnaptic reflex pw motor neurons - Mediated by Ia input from spindles
- One is excitatory other is inhibitory - Powerful reflex, monosynaptic with
response latency ~20-40ms can be
shorter for smaller person
Ib (GTO) INHIBITION, SOURCES Ib GTO FACILATORY/EXCITATORY EFFECT RECURRENT INHIBITION HOFFMAN REFLEX VS TENDON REFLEX
ON ANTAGONIST MN
1.active muscle contraction activates GTO= 1.as MN descend their axons, collaterals H-Reflex: electrically stimulate Ia fibers in peripheral
synapses 1b afferent 1.inhib IN has IPSP that inhibits an inhibitory branch off and with an EPSP synapse onto nerve
MN pool renshaw cell - At low stimulus= Ia afferent turn on first due
to lower thresh than motor axons
2.disynaptic or sometimes trisynaptic connection to
- Inc stim strength = excite motor axons
MN via 1b inhibitory IN 2. Facilitation via inhibiting inhibition - M-wave=direct stim of axons H-wave= travel
(withdrawing inhibition from alpha MN pool of 2. Renshaw cell feeds back to alpha MN with down to SC through synapse and to muscle
3. Leads to autogenic inhibition of muscle GTO antagonist) an IPSP=inhib of MN pool - As stim continually inc, M wave inc but H
resides in - Project to MN that excite them and wave eventually declines because
- Leads to precise spinal control of muscle Ia inhib interneurons antidromic has > effect than orthodromic
force - Also connect to gamma MN, other - M-wave plateaus due to rec all axons
renshaw cells T-reflex: initiated by brief tap on tendon of muscle=
activate muscle spindles= monosynaptic connection to
Receives input from: joint afferents, cutaneous **stabilize firing rate of MN and reg strength
MN
afferents and descending inputs—all converge of inhib of antagonist MN **both test coupling b/w Ia aff and MN, and level of
MN excitability but T-reflex also tests spindle
sensitivity
