Neural Circuits
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Introduction
All circuits have some sort of input, which is usually a set of axons which originate elsewhere and synapse within the local circuit. Inputs can also be from within. For example, while the thalamus brings sensory information into the cortex, by far the most numerous inputs to the cortex are from the cortex itself.
Interneurons vary widely in structure and function, and can be both excitatory and inhibitory. The cerebellum contains as many as 1011excitatory granule cells, which are interneurons.
Neural Networks
Local neural circuits usually operate in highly interactive, simultaneously interdependent, networks. While cells are arranged in series, within a circuit, there are usually massive numbers of circuits operating in parallel.
Circuits also communicate with each other, showing a tremendous amount of crosstalk.
Reflexes are among the simplest neural circuits.
Central pattern generators create rhythmic activity.
Modulatory systems have diffuse central connections and widespread effects.
Spinal Reflexes
see also: assessing reflexes
Reflexes represent some of the most basic neural circuits. Relatively simple reflexes are responsible for simple behaviors. However, they are also involved in more complex circuits, whereby complex behaviours can be built up from sequences of simple reflexive responses.
Axons descending from multiple sites within the brainstem and cortex synapse on motor interneurons and on some lower motor neurons directly. These descending pathways mediate conscious and unconscious movement but can also alter the strength of both stretch and flexor reflexes. During walking, for example, reflexes of the leg vary dramatically.
- stretch
- golgi tendon
- flexor
- Babinski
Stretch Reflex
When a muscle is stretched, the stretch reflex activates a rapid contraction of the same muscle to increase muscle tension and oppose the stretch. It is particularly strong in muscles that oppose gravity.
Increasing a muscle length stimulates spindle afferents, especially Ia fibres. These terminate in the spinal cord on alpha motor neurons that innervate the same muscle.
Monosynapic conenctions account for the rapid component of the stretch reflex, but at the same time parallel circuits, involving interneurons, inhibit the alpha motor neurons of antagonist muscles. This reciprocal innervation increases the effectiveness of the stretch reflex.
Golgi tendon reflex
Golgi tendon organs are aligned in series in a muscle and are very sensitive to the tension within a tendon. Thus, instead of responding to muscle length, they are activated by the force generated within a muscle and are stimulated most during active contraction.
Ib sensory neurons act through interneurons to inhibit the muscle experiencing stretch while activating the antagonistic muscle, resulting in the opposite effect of the stretch reflex.
Flexor Reflex
The flexor reflex responds to painful stimuli, such as stepping on a sharp stick. The injured limb withdraws while the oppositve leg is extended. It is primarily mediated by Aδ axons.
This bilateral reflex is coordinated within the spinal gray matter.
The flexor reflex is remarkable in that it induces withdrawal away from the stimulus and is realted in its amplitude to the stimulus intensity.
Babinski
The Babinski reflex is used to diagnose problems with upper motor neurons.
A normal test is a downwards curl of the toes, while a positive test is an upper curling of the toes.
Visceral reflexes, which control autonomic outflow, tend to be multisynaptic.
Neural Plasticity
Perhaps the brain's greatest asset is its ability to learn and store experiences and events. Memory is the ability to store and recall learned changes. Short-term synaptic plasicity usually involves presynaptic changes.
Potentiation
Facilitation is a short term increase in strength lasting only milliseconds, while potentiation lasts tens of seconds to several minutes, outlasting the period of high-freqency stimulation. In general, longer-lasting modifications require longer periods of stimulation.
Three potential explanations may be behind potentiation, with the first most often true
- more neurotransmitter may be released, usually due to increased Ca2+ influx
- postsynaptic receptors may become more responsive in number or sensitivity
- both mechanisms may be acting
Long term potentiation
Long term potentiation, or LTP, can be generated by high frequency stimulation. LTPs are easily seen in the CA1 region of the hippocampus, a part of the cortex long associated with memory formation.
LTPs are input specific, meaning only the previously involved pre-synaptic neuron's synapses will induce increased EPSPs. They also require concurrent postsynaptic depolarization for LTP to form.
What this means is LTP is best induced by cooperativity, where enough presynaptic inputs must fire at the same time. In this way, weak synaptic inputs can become associated with each other and remain so thereafter.
Cells in the CA1 region of the hippocampus use glutamate, with both AMPA and NMDA receptors activated. LTP requires increases in postsynaptic Ca2+, mediated by NMDA channels. Ca2+ then goes on to activate protein kinase C and calcium-calmodulin dependent kinase, through from this point on how LTPs remain is obscure.
Habituation
Habituation is a decrease in synaptic strength following a period of increased firing. At least some of the time, habituation results from decreased levels of neurotransmitter being released, again demonstrating the importance of presynaptic changes in synaptic plasticity.
Long term depression
Long term depression can occur in the Purkinje cells in the cerebellum. Purkinje cells use inhibitory GABA as a neurotransmitter and represent the only output from the cerebellar cortex. Each Purkinje cell receives powerful excitatory contact from climbing fibres from the inferior olive and from about 150,000 parallel fibres from tiny granule cells.
Parallel fibre synapses lose strength when they are active in parallel with climbing fibre activation. This happens primarily through reduction of post-synaptic AMPA glutamate channels.
Long term potentiation can also occur in Purkinje cells, through mechanisms involving the presynaptic terminal.
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