Download Anatomy of the Basal Ganglia

Anatomy of the Basal Ganglia
The striatum (caudaute/putamen) and subthalamic nucleus (STN) receive
excitatory input from the cerebral cortex. Dopamine-releasing neurons in the substantia
nigra pars compacta (SNpc) connect to neurons in the striatum and modulate the inputs
from the cortex. There is an inhibitory connection from the striatum to the globus
pallidus internal segment (GPi) and the substantia nigra pars reticulara (SNpr), as
well as an excitatory projection from STN to GPi that is divergent (one STN neuron
contacts many Gpi neurons). This pathway is called the “direct” pathway. Another,
“indirect” pathway of inhibitory connections extends from the striatum to the globus
pallidus external segment (Gpe) to the STN to the GPi. The GPi and SNpr send
inhibitory output via collaterals to the thalamus and brain stem. The SNpr is involved in
eye movements.
Types of Neurons in the Striatum
Medium spiny neurons—make up 95% of the total. Use GABA as a transmitter.
Are the output neurons of the striatum.
Large aspiny neurons—interneurons that use ACh as a transmitter.
Medium aspiny cells—interneurons that use somatostatin as a neurotransmitter.
Small aspiny cells—interneurons that use GABA.
Neuron Firing in the Basal Ganglia
Neurons in the putamen and throughout the basal ganglia fire after those in the
motor cortex, implying that the striatum is not involved primarily in the initiation of
movement.
The firing of SNpc neurons increases in response to behaviorally significant
events such as reward or the presentation of instructional cues. These neurons can also
“learn” to respond to a cue that predicts a reward.
Consequences of Damage to the Basal Ganglia
Inactivating the putamen leads to slowed movement of the contralateral limb.
Huntington’s Disease, which causes involuntary movements, is linked to the death of
neurons that project from the putamen to the GPe.
Damage to the STN causes large involuntary movements of the limbs.
Lesions to the GPi cause slowness of movement, linked to a tendency of the limbs
to assume an abnormally flexed posture—that is, an inability to turn off muscle activity.
Damage to the SNpc causes symptoms of Parkinson’s disease—tremor and
slowed movement.
Model of Basal Ganglia Function
One hypothesis suggests that the basal ganglia automatically execute learned
movement sequences. This theory is supported by the fact that patients with PD have
difficulty coordinating complex movements of several body parts in sequence, such as
when writing.
Another suggests that the basal ganglia form two opposing motor pathways, the
“direct” and “indirect” pathways described above. Increased activity in the “direct”
pathway causes excessive movement, while activity in the “indirect” pathway inhibits
movement.
A third suggests that the basal ganglia act as a “brake” on motor movement. The
theory suggests that STN neurons excite the GPi widely, inhibiting motor output. At the
same time, signals sent from the cortex to the striatum to the GPi inhibit a small part of
the GPi, selecting a certain motor pattern to be disinhibited and suppressing surrounding
patterns.
Anatomy of the Cerebellum
The cerebellar cortex is divided into three lobes: anterior, posterior, and
flocculonodular. Each lobe consists of thin folds called folia. This sheet is laid over four
cerebellar nuclei (CN) on each side. Three cerebellar peduncles on each side connect the
cerebellum to the brain stem.
The cortex consists of three layers. The granular cell layer, on the bottom,
contains an enormous number of granule cells. The Purkinje cell layer contains cell
bodies of PCs, and the molecular layer contains only dendrites and axons.
Incoming information from all over the brain sends information via mossy fibers
(MFs) to the granule cells. These cells relay the information to the molecular layer via
parallel fibers (PFs), which make contact with the dendrites of PCs. In addition, error
correction signals are sent from the inferior olive to PCs via climbing fibers (CFs). Each
PC is only contacted by one CF.
The PCs send inhibitory signals to the CN. These nuclei are linked reciprocally to
populations of neurons in other parts of the brain, forming attractor networks.
Long-term Depression (LTD) Takes Place Between the Synapses of PFs and PCs
Unlike LTP, LTD requires the presence of three factors in order to take place:
1) Depolarization of the dendrite
2) Activation of glutamate receptors on a particular spine on the dendrite
3) The firing of a CF (training signal) hundreds of milliseconds later
This process marks synapses causing movements that result in error and causes
them to be less effective. Plasticity in the cerebellum is thought to be involved only in
adjusting motor responses, not in forming a link between a conditioned and
unconditioned stimulus.