Class Notes (1,100,000)
CA (630,000)
UTSC (30,000)
Lecture 6

NROC69H3 Lecture Notes - Lecture 6: Striatum, Nucleus Accumbens, Pars Reticulata


Department
Neuroscience
Course Code
NROC69H3
Professor
Rutsuko Ito
Lecture
6

This preview shows pages 1-3. to view the full 10 pages of the document.
Abrreviations:
R. - receptor
N - neuron, Ns
Esp - especially
Synap - synaptic
b/c - because
DA - dopamine
PD = parkinson's disease
W = with
Nac = nucleus accumbens
Bhv = behaviour
Anatomy & function of BG
BG composed of many nuclei
oStriatum: input structure of BG, receive input from thalamus, cortex, DAergic
input
Caudate
Putamen
NAc (nucleus accumbens)
oGlobus pallidus
Internal (Gpi) - output structure of BG
External (GPe)
oSubthalamic nucleus (STN)
oSubstantia nigra (SN)
Pars compacta (SNc)- region where DA ergic inputs originate
Pars reticulata (SNr)
High cross species homology - all have defined striatum and BG
Function of BG?
oMovement control

Only pages 1-3 are available for preview. Some parts have been intentionally blurred.

Gating functions -> motor, selecting and inhibiting some inputs over
others
oAction selection
oProcedural learning - skills ex. Playing piano
Esp dorsal part of striatum
oExecutive function (e.g. working memory, behavioral flexibility)
oSensorimotor integration
oLimbic-motor integration (associative influences)
oReward learning
oImportant in integrating info to influence bhv output
Output is more motor/bhv
Select most important plan based on info received
oMultifaceted functions
Competing input selection
Select & sequence internally generated motor programs for posture &
voluntary movements
Limbic-motor interface (NAc)
Select a goal / actions to achieve, & movement to achieve actions
On basis of limbic info travelling to striatum
Learning
Associating cues with actions & outcomes to optimize responses to
changes in envt
Cognition
Bhv flexibility, working memory
oFunctional cortico-striatal-thalamic loops
BG is intimately linked to sensory, motor, cognitive & motivational
apparatus of the brain
Motor, spatial, visual and affective loops
Somatotopic organization in the motor circuit
oSpatial arrangement preserved across diff regions of the loops
Thalamo-cortical-striatal circuit
o1 way to make selection
oThink that cortex and thalamus act together to generate action plan, BG can
inhibit some of those action plans while activating selected
oGABA ergic mechanisms, allow some motor plans to be executed
Detailed connectivity
oSNr/GPI - output of BG
oSNc sends DA ergic N's into striatum
oOutput: SNr/Gpi connected to brainstem & thalamus
Afferent input to striatal principal N's
Medium spiny Ns (MSN) Have many spines; 90% of principal Ns of striatum
oCortical (glutamatergic) input terminates on dendrites of MSN's

Only pages 1-3 are available for preview. Some parts have been intentionally blurred.

oEach receive convergent input from many cortical Ns originating in functionally
related (& interconnected) areas
oGABA ergic (unlike other principal Ns) w 2 types of peptide expression
Substance P/Dynorphin in D1 N's
Enkephalin in D2 N's (indirect pathway of BG)
oHas ~25-30 dendritic terminal branches radiating from cell body
Spines 1st appear at ~20 µm from soma, peak in density at 80 µm, and
taper off in density at distal
There's some indication that changes in spine density & #'s could
be correlated with improved motor performance (esp dorsal striatum)
Repeated administration of drugs of abuse can
density of spines
(on striatal MSN) at distal dendritic sites
But what does change in density mean for bhv output?
oDistribution of synap inputs to MSN
Every one receives ~11000 synap contacts from cortex & thalamus
>90% inputs terminate on distal parts of the dendritic tree
Local inputs (other MSNs, interneurons) terminate on proximal parts of
dendritic shaft / soma
Influencing cortical inputs that MSN might get -> maybe has to do
with drugs of abuse
Intrinsic properties of MSN & interneurons
oIntrinsic memb properties of MSN
Quiet at rest: RMP close to Ek -> high permeability/conduction to K+ ions
High K+ conductance mediated by Kir voltage-sensitive inward
rectifying channels that are permeable to K at hyperpolarized potentials,
but blocked by intracellular polyamines (e.g. spermine) & Mg2+ at
depolarized potentials
IV profile
Very polarized potentials (control shows high inward K+
conductance / K inward current, cell remains hyperpolarized)
Voltages higher than RMP, begin to see slight outward K+
ion
b/c channels are inward rectifying, channels blocked by
polyamines & Mg2+ depolarizing potentials, this channel
preferentially allows inward flow of conductance (more easily in than
out)
Cs+ will un-rectify the channels -> abolish the strong
inward K+ current
Kir channels important in maintaining strong K+
inward current at hyperpolarizing potentials
oMSN excitability
Usually quiescent (silent) due to high K+ conductance
Require high convergent & simultaneous input from cortex
i.e. coactivation of many cortical Ns and lots of EPSPs to
depolarize
oRamp-like depolarising response - depo by convergent cortical input (or
current injection) induces a long lasting plateau potential
Underlying currents
INA - slow activation of a non-inactivating (persistent) Na+ channel
You're Reading a Preview

Unlock to view full version