Nervous control (15/10/13 lecture)

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Nervous control

(15/10/13 lecture)

Nervous control is primarily involved in rapid movement, but also in

collecting, processing and responding to information from the environment. The

brain is also an integrating centre for homeostasis, allowing it to be a part

of longer term control too.

The ‘information’ propagated through the nervous system can take

several forms: action potentials, neurotransmitter release, and graded

potentials. Many variations may occur in a reflex arc, which allows for control

of these signals. Ion channels are important

in the nervous system as they allow for the generation of action potentials

(depolarisation) when a change in the resting membrane potential or

neurotransmitter binding occurs. There are also mechanically gated ion channels

activated by pressure/distortion of membrane.

Nervous system divisions: The main divisions are the central and

peripheral nervous systems. The CNS is divided into the brain and spinal cord.

The PNS is divided into motor neurons and sensory neurons. The motor neurons

are divided into the somatic and autonomic nervous systems (though the ANS has

sensory neurons too). The ANS is divided into the sympathetic (fight or flight)

and parasympathetic (maintenance).

Somatic motor neurons are monosynaptic, heavily myelinated

cholinergic neurons; their long axons extend from the CNS to the effector with

no ganglia (alpha-motorneurons) for fast propagation.

Autonomic motor pathways consist of two neurons: the

pre-ganglionic, heavily myelinated cholinergic neuron which is short and

extends from the CNS to a peripheral ganglion; and the post-ganglionic

unmyelinated, adrenergic, longer neuron which extends to an effector organ from

the ganglion.

Somatic efferent pathway: Sensory information arrives through dorsal

root (where cell bodies of sensory neurons are) to dorsal horn of spinal cord →

Information travels through an interneuron → An α-motoneuron is stimulated in

the ventral horn and the action potential is propagated through the ventral

root to the effector organ e.g. skeletal muscle.

Autonomic efferent pathway: Sensory information arrives through dorsal

root ganglion to dorsal horn of spinal cord → Information travels through an

interneuron → A pre-ganglionic neuron extends from the CNS to the white ramus →This

synapses with the unmyelinated grey ramus in a peripheral ganglion using ACh and

a nicotinic receptor → The post-ganglionic neuron extends to the effector organ

and stimulates it.

The peripheral

sympathetic chain ganglia are connected, which allows for communication and the

possibility for the generation of a systemic/widespread effect.

At the

target tissue:

Sympathetic cAMP signal

transduction: adrenaline/noradrenaline binds

to α2 or β-adrenoceptor → binding causes conformational change which

separates G protein complex (α separates from βγ) (α2-adrenoceptor

linked with G-inhibitory protein complex; β-adrenoceptor linked with

G-stimulatory complex) → The α subunit migrates through the membrane and binds

to adenylate cyclase → Giα downregulates conversion of ATP to cAMP

whereas Gsα upregulates it → cAMP phosphorylates protein kinase A →protein

kinase A phosphorylates another protein e.g. myosin light chain phosphatase →cellular

response e.g. dephosphorylation of myosin light chains and smooth muscle

relaxation.

Sympathetic

phospholipase C signal transduction: adrenaline/noradrenaline

binds to α1-adrenoceptor → the Gs complex is separated

into its α and βγ subunits → the α subunit migrates through the membrane and

binds to amplifier enzyme phospholipase C, activating it → phospholipase C

converts membrane proteins (phosphatidylinositol bisphosphate – PIP2)

into diacylglycerol (DAG) and inositol triphosphate (IP3), secondary

messengers → DAG activates protein kinase C which phosphorylates proteins to

generate a response and propagate the signal → IP3 migrates from the

membrane to the endoplasmic/sarcoplasmic reticulum and binds to a Ca2+

channel, opening it → in smooth muscle, the response is that Ca2+

binds to calmodulin which activates myosin light chain kinase, phosphorylating

myosin light chains, and causing smooth muscle cell contraction.

Nicotinic ACh

receptor: Na+ channel. Muscarinic ACh receptor: G-protein

associated/K+ channel.

A reflex is an automated patterned response to sensory stimuli:

stimulus → sensory receptor → sensory afferent neuron → CNS integration →

efferent motor neuron → effector → response → feedback effect on stimulus. Although a monosynaptic neural reflex

may appear to have minimal modulation, there are 2-3000 other synapses attached

to the α-motoneuron which are stimulatory/inhibitory and dictate whether it

fires – here is modulation.

Ways of classifying neural reflexes:

Effector division

Integration site

Neurons in pathway

Origin

Somatic (movement in

external world)

Autonomic (motor activity in

internal world)

Spinal (‘low’ level,

relatively simple)

Brain (‘high’ level, more

complex)

Mono-synaptic

Poly-synaptic (all autonomic

reflexes)

Innate (knee-jerk reflex,

pupillary reflex)

Learned (Pavlovian,

walking)

Reflexes

Autonomic/visceral reflexes are usually involved in regulating internal

organs (e.g. moving or limiting movement of products in hollow organs) and are

integrated in the spinal cord and lower (subconscious) brain. However, they can

be modulated by higher (conscious) levels. Typically:

Stimulus → sensory receptor in viscera → impulse in visceral

(sensory) fibre →travels to dorsal root ganglion then to dorsal horn →

integrated in the spinal cord, perhaps by the preganglionic neuron → impulse

travels out of ventral horn along a preganglionic axon → it reaches an

autonomic ganglion and synapses with a ganglionic neuron → these exist as chain

ganglia so there can be divergence of response → impulse travels along the

postganglionic axon to the visceral effector →a response occurs → there is

feedback to the CNS as to the status of the stimulus.

The pupillary light

reflex: constriction is

parasympathetic, relaxation is sympathetic. Light hits the

photoreceptors in the retina in one or both eyes → The

pupillary reflex is activated and signals travel through the optic nerve to the

thalamus, then to the midbrain → Signals then continue to travel through the efferent, parasympathetic

neurons (if too much light, sympathetic if too little) running through cranial

nerve III (the oculomotor nerve) to constrict the pupils in both

eyes via circular pupillary muscles in the iris or dilate the pupils in both eyes via contraction of radial muscles lying

perpendicular to the circular muscles → Less

light hits the retina in both eyes (the consensual reflex) or more light hits

it → Signals return to the thalamus that the light level is

appropriate → Contraction of the pupillary muscles in the iris stops at the

optimal diameter for the pupils and dilatory signals are inhibited, or

contraction of the radial muscles stops at the optimal diameter for the pupils

and constrictive signals are inhibited.

The baroreceptor reflex: baroreceptors in the

aortic arch and the internal carotid arteries are sensitive to stretch. The

receptors are active during normal pressure and sending constant impulses to

the medulla regarding the level of stretch, the heart rate, and the rate of

change in pressure.

When arterial pressure changes, arterial

walls are subjected to more or less stretch, and the sensory nerves coming from the carotid

sinus (sinus nerve) and from the aortic arch (depressor nerve) become more or less active

and send more or fewer impulses. Upon receiving more or fewer impulses

from the baroreceptors, the cardiovascular centres respond by exciting sympathetic and inhibiting parasympathetic

nerves (if BP has dropped) or exciting parasympathetic and inhibiting

sympathetic nerves (if BP has risen). This

either results in increased cardiac output, increased constriction of arterioles,

and increased constriction of veins (if BP has dropped), or a decrease in these factors (if BP has risen).

The

hypothalamus is the main integration centre of ANS activity, but at the

conscious level there can be limbic lobe and cerebral cortex (frontal lobe)

control, and control from the lower levels of the reticular formation of the

brain stem, and from the spinal cord.

Somatic reflexes involve the skeletal muscles as effectors, but sensors

can classically be muscle spindles (in stretch reflex), Golgi tendon organs (in

autogenic inhibition), or ‘pain’ receptors (in flexion).

Proprioceptors include muscle spindles (which sense stretch), Golgi

tendon organs (which sense force) and joint receptors (which sense pressure,

interpreted as position).

Muscle spindles are made up of small muscle fibres, the centre

portions of which have no contractile proteins as there are nerve endings there.

Golgi tendon organs

consist of sensory nerve endings interwoven among collagen fibres, and link the

muscle and the tendon.

In muscle spindle innervation, there is α-γ co-activation. This allows

for greater control over movements. The muscle spindles may send efferent

impulses via sensory nerves to the spinal cord in accordance with skeletal

muscle movement, which stimulates γ-neurons, resulting in the contraction of

the intrafusal muscle fibres of the spindle. This contraction lengthens the

non-contractile spindle, resulting in γ-neuron activity. This is again integrated

in the spinal cord, and impulses may now be sent along α-motoneurons, which

cause skeletal muscle contraction. An example of this may be in being handed a

heavy tray.

A myotactic unit

consists of all pathways controlling a joint (all nerves, receptors, and

muscles).

Renshaw

cells are interneurons that synapse with recurrent branches (those that synapse

in the CNS) of α-motoneurons. They receive excitatory inputs, and make

inhibitory synapses upon the same motor neurons which can limit motor neuron

firing to dampen/reduce reflexes and prevent them becoming too aggressive.

Synergist muscles may also be excited by spindle afferents making excitatory

monosynaptic connections, and antagonist muscles are inhibited with inhibitory

synapses on motor neurons in reciprocal inhibition.

The Golgi tendon reflex prevents

tendons from becoming overstretched. When the tendon is stretched by muscle

contraction, the 1b sensory nerve is are compressed by the collagen in the

Golgi tendon organ and afferent neurons integrate via an inhibitory interneuron

and inhibit further motor neuron excitation, inhibiting contraction and

preventing damage.

The Golgi tendon

organ also makes an excitatory synapse on another interneuron to make an

inhibitory synapse on synergist muscle motor neurons. Further, it makes an excitatory synapse

on an interneuron which makes an excitatory synapse on motor neurons to

antagonist muscles, causing them to contract so that the original muscle is not

only relaxed but stretched out.

The flexor reflex: a painful stimulus

activates nociceptors → the primary sensory neuron enters the spinal cord and

diverges → one collateral activates ascending pathways for sensation (pain) and

postural adjustment → this results in a withdrawal reflex pulling the limb away

from the painful stimulus → the other activates a crossed extensor reflex which

supports the body as the weight shifts away from the painful stimulus (e.g.

stand on a pin, and the opposite leg’s extensors (posterior quadriceps)

contract).

In reflexive movement, there is predominately spinal

integration, and some input to the brain (e.g. you can resist dropping

something important when you stand on something sharp). However, in postural

reflexes, there is cerebellum integration to maintain balance, and input to the

cortex, which is where movement can be consciously influenced.

In postural

reflexes, there is feedforward stimulation, typically in expectation of a

threat. As the brain initiates movement, there is feedforward activity which

adjusts the posture before or as the body moves. There is also feedback after

unanticipated postural disturbance, so that posture can be appropriately

adjusted once more.

Rhythmic movements are learned, for

example walking and driving. These are initiated in the cortex, at a conscious

level. However, after this the control becomes subconscious and there are ‘central

pattern generators’ in the spine which maintain motion. These combine both

voluntary and reflexive movements. The corticospinal tract consists of the

cortex (e.g. primary motor cortex), the medulla oblongata, and the spinal cord,

so that movements may be initiated and then maintained.

The cortex is ‘at the top’ of several CNS integration sites.

This is generally considered voluntary as it is ‘conscious’, but parts can

become involuntary – muscle memory, for example walking and driving. So is this

voluntary, or a complicated reflex?

Voluntary movement: sensory input from the sensory and motor

cortices is received by the prefrontal cortex nd motor association areas →

these impulses are transmitted through the basal nuclei and the thalamus and

back to the prefrontal cortex and motor association areas (‘planning and

decision making’) →impulses travel back to the motor cortex and then to the

cerebellum for coordination and timing → impulses travel to the brain stem for

execution via the spinal cord and somatic motor nerves – influence on posture,

balance and gait → sensory receptors transmit impulses to the spinal cord,

cerebellum and sensory cortex as continuous feedback.

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