m8ta
You are not authenticated, login.
text: sort by
tags: modified
type: chronology
[0] Elble RJ, Central mechanisms of tremor.J Clin Neurophysiol 13:2, 133-44 (1996 Mar)

[0] Bar-Gad I, Morris G, Bergman H, Information processing, dimensionality reduction and reinforcement learning in the basal ganglia.Prog Neurobiol 71:6, 439-73 (2003 Dec)

{232}
hide / / print
ref: Prescott-2006.01 tags: basal_ganglia action selection motor control robot date: 03-01-2012 17:56 gmt revision:4 [3] [2] [1] [0] [head]

PMID-16153803[0] The robot basal ganglia: action selection by an embedded model of the basal ganglia

  • they implemented a model of the basal ganglia in a robot. The model switches between competing (hypothetical) actions based on input salience. There are only a possible actions in their robot.
  • they reiterate the common conception that the basal ganglia are implicated in action selection: what to do next ( also mentioned are other functions - perception and cognition working memory and many other aspects of motor function. )
  • huh, interesting : cognitive psychologists have discovered that when an observable system has more than three interacting parts, it becomes very difficult for human minds to predict accurately how that system will change over time. (!!!) I dig disclaimers like this.
    • therefore, very limited understanding can be gleaned from informal, box and arrow style models.
      • I think the same is true of many biological analysis - including analysis of the immune and nervous systems - it needs to be at a much higher level of quantification
    • they also say that a model must be validated by placing it within the entire behavioral system.
  • the basal ganglia seem to be suitable for switching between competing channels & providing the required clean selection of a winner.
    • (1) striatal cells have up and down states, and can only switch between them with heavy coincident inputs.
    • (2) selective local inhibition between channels.
    • (3) dopamine innervation D1 = exitation; D2 = inhibition. I never really got how this enters their model; figure 1 seems like it would describe it, but it needs more math :)
    • (4) feedforward off-center, on surround network. they ref some other work..
      • I still don't feel like their explanation is the best (they use kinda wishy-washy terms) - though it is a step in the right direction.
  • people with schizophrenia sometimes switch cognitive focus rapidly; schizo is though to be due to a dopamine imbalance. Same problem with ADD.
    • treatment for ADD: amphetamine (blocks monoamine transporter, increases extracellular concentration of DA), ritalin. Both allow for heightened concentration: once you select a task, you stick with 'it' (the thought / prediction pathway) for longer. Dopamine is definintely involved in action selection, duhh.
    • their model supports this behavior: If the tonic dopamine level is very low, the robot has difficulty initiating actions; if the DA level is high, then it tends to select more than one action at the same time. (wait.. this implies that DA is too high in people with ADD? what? perhaps this is a consequence of the two different types of DA receptors? )
  • (...) basal ganglia - thalamo-cotrical loops my act to provide a positive feedback pathway that can maintain appropriate level of salience to selected behavior.
  • much of the input to the basal ganglia comprises collateral fibers from motor regions that project to the spinal cord and brainstem structures.
    • activity changes in the BG occur slightly after the beginning of EMG activity (good evidence!) Such signals may be important for controlling the maintenance and termination of selected behavior.

My thoughts:

  • what if the STN is involved in controlling the stability of neuronal activity - that is, preventing motor feedback instability by knocking down the gain. (whereas the cerebellum is involved in the balance and coordination interpretations of stability)
    • Normally, the human motor system is very stable, but when you lack dopamine innervation, you both cannot move (become very rigid) & have tremor (an inability to control cyclical oscillations).
      • That is, perhaps oscillation is due to a intrinsic inability to modulate gain.
      • more likely it is a manifestation/symptom of pathological activity in the control loop.

____References____

[0] Prescott TJ, Montes González FM, Gurney K, Humphries MD, Redgrave P, A robot model of the basal ganglia: behavior and intrinsic processing.Neural Netw 19:1, 31-61 (2006 Jan)

{169}
hide / / print
ref: Hamani-2004.01 tags: STN subthalamic nucleus movement disorders PD parkinsons basal_ganglia globus_pallidus anatomy DBS date: 02-22-2012 15:03 gmt revision:8 [7] [6] [5] [4] [3] [2] [head]

PMID-14607789[0] The subthalamic nucleus in the context of movement disorders

  • this is a good anatomy article, very descriptive -- almost too much information to grapple with.
  • STN = important structure for the modulation of activity of basal ganglia structures
  • STN is anterior-adjacent to the red nucleus
  • The average number of neurons in each STN nucleus varies from species to species and has been estimated to be ~25 000 in rats, 35 000 in marmosets, 155 000 in macaques, 230 000 in baboons and 560 000 in humans
  • The volume of the STN is ~0.8 mm3 in rats, 2.7 mm3 in marmosets, 34 mm3 in macaques, 50 mm3 in baboons and 240 mm3 in humans.
    • Number of neurons does not scale with volume, uncertain why not.
  • STN is divided into three functional units: motor, associative, and limbic cortical regions innervate, respectively motor, associative, and limbic regions of the striatum, pallidium SNr.
    • they give a complete list of these 3 in 'intrinsic organization of the STN'
    • STN is divided into 2 rostral thirds and one cauldal third.
      • medial rostral = limbic and associative
      • lateral rostral = associative
      • dorsal = motor circuits. (the largest part, see figure 2)
        • hence, the anterodorsal is thought to be the most effective target for DBS.
  • STN is populated primarily by projection neurons
  • the dendritic field of a single STN neurons can cover up to one-half of the nucleus of rodents
  • efferent projections (per neuron, branched axons)
    • GPe, GPi, SNr 21.3%
    • GPe and SNr 2.7%
      • in both segments of the pallidum, projections are uniformly arborized & affect an extensive number of cells.
    • GPe and GPi 48%
    • GPe only 10.7%
    • 17.3% remaining toward the striatum
  • most of the cortical afferents to the STN arise from the primary motor cortex, supplementary motor area, pre-SMA, and PMd and PMv; these target the dorsal aspects of the STN.
    • afferents consist of collaterals from the pyramidal tract (layer 5) & cortical fibers that also innervate the striatum (latter more prevalent). afferents are glutamergic.
  • ventromedial STN recieves afferents from the FEF (area 8) and suppl.FEF (9)
  • GPe projects extensively to STN with GABA. see figure 3 [1]
    • almost every cell in the STN resonds to pallidal GABAergic stimulation.
    • 13.2% of GPe neurons project to GPi, STN, and SNr
    • 18.4% to GPI and STN,
    • 52.6% to only the STN and SNr
    • 15.8% remaining to the striatum.
  • DA afferents from the SNc
  • ACh from the tegmentum
  • Glutamergic afferents from the centromedian thalamus (CM)
  • Serotonin from the raphe nucleus
  • fibers from the tegmentum, SNc, motor cortex, VM.pf of the thalamus, and dorsal raphe synapse on distal dendrites
    • pallidal inhibitory fibers innervate mostly proximal dendrites and soma.
firing properties:
  • about half of STN neurons fire irregularly, 15-25% regularly, 15-50% burst.
    • bursting is related to a hyperpolarization of the cell.
  • movement-related neurons are in the dorsal portion of STN and are activated by either/both active/passive movements of single contralateral joints
  • there is a somatotopic organizaton, but it is loose.
  • many units are responsive to eye fixation, saccadic movements, or visual stim. these are in the ventral portion.
    • activation of the STN drives SNr activity, which inhibits the superior colliculus, allowing maintainance of eye position on an object of interest.
  • ahh fuck: if high currents are delivered to STN or high concentrations of GABAergic antagonists are applied abnormal movements such as dyskinesias can be elicited
    • low concentrationns of GABA antagonists induces postural asymmetry and abnormal movements, but no excessive locomotion.
  • dyskinesias result from high-frequency or high-current stimulation to the STN! low frequency stimulation induces no behavioral effects. [2]
  • small (<4% !!) lesions cause focal dystonias
  • in parkinsonian patients, activity in the STN is characterized by increased synchrony and loss of specificity in receptive fields + mildly increased mean firing rate.
    • 55% of STN units in PD patients respond to passive movements, and 24% to ipsilateral movements (really?) - indicative of the increase in receptive field size caused by the disease.

____References____

[0] Hamani C, Saint-Cyr JA, Fraser J, Kaplitt M, Lozano AM, The subthalamic nucleus in the context of movement disorders.Brain 127:Pt 1, 4-20 (2004 Jan)
[1] Sato F, Lavallée P, Lévesque M, Parent A, Single-axon tracing study of neurons of the external segment of the globus pallidus in primate.J Comp Neurol 417:1, 17-31 (2000 Jan 31)
[2] Beurrier C, Bezard E, Bioulac B, Gross C, Subthalamic stimulation elicits hemiballismus in normal monkey.Neuroreport 8:7, 1625-9 (1997 May 6)

{172}
hide / / print
ref: Foffani-2004.07 tags: STN motor preparation human 2003 basal_ganglia DBS SMA date: 01-26-2012 17:23 gmt revision:3 [2] [1] [0] [head]

PMID-15249649 Involvement of the human subthalamic nucleus in movement preparation

  • STN receives large afferent from SMA, so it should be involved in movement planning.
  • the STN and nearby structures are active before self-paced movements in humans.
  • normal patients show a negative EEG movement-related potential (MRP) starting 1-2 seconds before the onset of self-paced movements.
  • STN also shows premovement negative MRP.
    • REquire very sensitive methods to record this MRP -- it's on the order of 1 uv.
  • the amplitude of the scalp MRP is reduced in parkinson's patients.
    • impairment of movement preparation in PD may be related to deficits in the SMA and M1, e.g. underactivity.
    • the MRP is normalized with the administration of levodopa.
  • MPTP monkeys have increased activity in the STN
  • examined the role of the STN in movement preparation and inhibition via MRP recorded from DBS electrodes in the STN + simultaneously recorded scalp electrodes.
  • their procedure has the leads externalized during the first week after surgery.

{188}
hide / / print
ref: neuro notes-0 tags: STN globus_pallidus striatum diagram basal_ganglia date: 01-26-2012 17:16 gmt revision:1 [0] [head]

http://www.gpnotebook.co.uk/cache/-1248198589.htm (bitrotted)

  • note that the loop around both preserves sign, more or less, provided you take into account the D2 receptor along the 'indirect' pathway
  • this has some glaring flaws: the globus pallius external projects to the globus pallidus internal, cortex projects to STN, thalamus projects to striatum, etc.

http://www.portfolio.mvm.ed.ac.uk/studentwebs/session1/group71/john.htm

  • has a good diagram of the neurotransmitters involved in the motor selection pathway. need to understand the kinetics of the dopamine receptor family

{165}
hide / / print
ref: Lehericy-2005.08 tags: fMRI motor_learning basal_ganglia STN subthalamic date: 01-25-2012 00:20 gmt revision:2 [1] [0] [head]

PMID-16107540[0] Distinct basal ganglia territories are engaged in early and advanced motor sequence learning

  • generally a broad, well-referenced study.
  • they used a really high-field magnet (3T) during tapping-learning task over the course of a month.
  • STN was activated early in motor learning, but not afterward, specifically the sequence learning
  • during the course of learning (an as the task became progressively more automatic) associative striatal activation shifted to motor activity.
    • STN could act by inhibiting competing motor outputs, thus building a temporally ordered sequence of movements.
  • SN was active throughout the course of the experiment.
  • during the 'fast learning' stage, there was transient activation of the ACC
  • also during the beginning portion of motor learning lobules V and VI of the cerebellum were activated.
  • rostral premotor and prefrontal cortical areas are connected to the associative territory of the striatum, which projects back to the frontal cortex the VA/VL nuclei of the thalamus.

____References____

[0] Lehéricy S, Benali H, Van de Moortele PF, Pélégrini-Issac M, Waechter T, Ugurbil K, Doyon J, Distinct basal ganglia territories are engaged in early and advanced motor sequence learning.Proc Natl Acad Sci U S A 102:35, 12566-71 (2005 Aug 30)

{12}
hide / / print
ref: Breit-2006.1 tags: parkinsons basal_ganglia palladium substantia_nigra motor_control striate date: 01-24-2012 22:10 gmt revision:1 [0] [head]

I wish i could remember where i got these notes from, so as to verify the somewhat controversial statements. I found them written on the back of a piece of scrap paper.

  • neurophysiological recordings in animals show that over half of basal ganglia neurons fire in response to motor activity but none are triggered by passive limb movement.
  • in parkinson's disease (PD), the substantia nigra actually becomes pale to the eye.
  • stimulation of the striatum does not result in low-threshold movements like stimulation of the cortex does.
  • palladium does not seem linked to motor planning. (just execution?)
  • stimulation of the caudate causes movement, i.e. head turning, while stimulation of the ventromedial caudate produces arrest and crouching movements. (Delgado etc)
  • large bilateral striatal leasions cause inattention.
  • striatal units appear to signal movement, not generate/compute it (really?)
  • in parkinson's disease, motor learning appears normal - it is the initial slowness that is abnormal :: PD relates to the quality of movement, not the quality of the motor commands. Thus, perhaps PD is a disease of gating/attention?
  • in PD, all reflexes except the Hoffman-reflex appear normal.
    • The primary difference between the H-reflex and the spinal stretch reflex is that the H-reflex bypasses the muscle spindle and, therefore, is a valuable tool in assessing modulation of monosynaptic reflex activity in the spinal cord. The H-reflex is an estimate of alpha motoneuron ( alphaalpha MN) excitability when presynaptic inhibition and intrinsic excitability of the alphaalpha MNs remain constant.
  • A lesion of the PPN (pedunculo pontine nucleus) was shown to restore decreased activity levels in the SNr and STN of a rat model of parkinson's (lesion of the SNc) PMID-17042796

{239}
hide / / print
ref: Elble-1996.03 tags: tremor STN VIM thalamus basal_ganglia Elble Parkinson's ET dyskinesia thalamus VIM DBS date: 01-24-2012 21:19 gmt revision:7 [6] [5] [4] [3] [2] [1] [head]

PMID-8849968[] Central Mechanisms of Tremor -- available through Duke's Ovid system. also in email.

  • focuses at first on the nonlinear aspect of all control: the systems are hard to understand because of the complexities of their interactions.
    • nonlinear systems are capable of complex interactions that are not predicted by the sum of their individual behaviors.
  • in general, there are two different types of tremor:
    • mechanical reflex oscillations (depend on sensorimotor loops), permit damped oscillations in response to pulsate perturbations.
      • is effected by the stifness and inertia of the segment involved.
    • central oscillations
      • frequencies independent of limb mechanics/segment length.
      • still subject to modulation by sensorimotor feedback.
      • if the tremor is at the same frequency as the mechanical resonance, the tremor will be worse!
  • physiologic tremor has both components of mechanical oscillations (3-5Hz) and central oscillations (8-12hz), which are usually attenuated by the low-pass property of the musculoskeletal system.
    • associated spindle and tendon organ discharge are not sufficient to produce 8 - 12 Hz oscillation - hence, this is most likely from a central source, eg. the cortex, inferior olive, and thalamus.
  • Essential tremor is also centrally generated, though it appears to be affected by somatosensory driving.
    • essential tremor frequency is strongly correlated with patient age (where the frequency decreases with increasing age).
    • the origin of ET is unknown: postmortem examinations reveal no deficits in M1/S1, thalamus, inferior olive, raphe nucleus, and reticular nuclei, globus pallidus, and spinal cord...
    • but, the inferior olive seems to be the most likely culprit:
      • tremor induced by harmaline increased inhibition-rebound properties of neurons, and this induces intention-related tremor in monkeys
      • harmaline induced olivary oscillation is similar to ET in terms of frequency, EMG, and drug-response.
      • olivary hypothesis is supported by PET scans, which show increased glucose consumption there in ET patients.
      • the ventrolateral (VL) thalamus and Ventralis intermedius (VIM) receives input from the contralateral cerebellar nuclei.
        • this is why VIM is such a good target for treatment of ET.
  • parkinsons tremor:
    • VOP is a better target for treating bradykinesia and other symptoms of PD, while VIM is the best for treating tremor
    • neurons in the globus pallidus and STN become entrained to tremor. STN lesion / HFS is effective in treating dyskinesia and other PD symptoms.
    • in MPTP monkeys, STN/ GPi neurons are also entrained to the tremor frequency.
  • other tremor:
    • neuropathic/tumorogenic tremor usually takes weeks to appear, suggesting that CNS reorganization is a cause of tremor, not intrinsic sensorimotor deafferentation
      • local lesions in the striatum, thalamus, & globus pallidus often cause dystonias, not tremor.
  • Cerebellar tremor
    • seems to be caused by an inability to properly compensate/ brake with antagonist muscles during voluntary and postural movements. movement control becomes heavily dependent on sensory feedback, which is often too slow for adequate compensation.
  • neuroleptic drugs can often cause tremor (or tardive dyskinesia). Neurolepric - calming, tranquilizer, antipsychotic.
    • lithium can cause permanent tremor due to cerebellar gliosis!
  • VOP projects to the supplementary motor area (SMA) and dorsolateral prefrontal cortex (DLPFC) PMID-21629131 ; VIM projects to M1 & contralateral cerebellum, as mentioned above.

____References____

{255}
hide / / print
ref: BarGad-2003.12 tags: information dimensionality reduction reinforcement learning basal_ganglia RDDR SNR globus pallidus date: 01-16-2012 19:18 gmt revision:3 [2] [1] [0] [head]

PMID-15013228[] Information processing, dimensionality reduction, and reinforcement learning in the basal ganglia (2003)

  • long paper! looks like they used latex.
  • they focus on a 'new model' for the basal ganglia: reinforcement driven dimensionality reduction (RDDR)
  • in order to make sense of the system - according to them - any model must ingore huge ammounts of information about the studied areas.
  • ventral striatum = nucelus accumbens!
  • striatum is broken into two, rough, parts: ventral and dorsal
    • dorsal striatum: the caudate and putamen are a part of the
    • ventral striatum: the nucelus accumbens, medial and ventral portions of the caudate and putamen, and striatal cells of the olifactory tubercle (!) and anterior perforated substance.
  • ~90 of neurons in the striatum are medium spiny neurons
    • dendrites fill 0.5mm^3
    • cells have up and down states.
      • the states are controlled by intrinsic connections
      • project to GPe GPi & SNr (primarily), using GABA.
  • 1-2% of neurons in the striatum are tonically active neurons (TANs)
    • use acetylcholine (among others)
    • fewer spines
    • more sensitive to input
    • TANs encode information relevant to reinforcement or incentive behavior

____References____

{154}
hide / / print
ref: OReilly-2006.02 tags: computational model prefrontal_cortex basal_ganglia date: 12-07-2011 04:11 gmt revision:1 [0] [head]

PMID-16378516[0] Making Working Memory Work: A Computational Model of Learning in the Prefrontal Cortex and Basal Ganglia

found via: http://www.citeulike.org/tag/basal-ganglia

____References____

[0] O'Reilly RC, Frank MJ, Making working memory work: a computational model of learning in the prefrontal cortex and basal ganglia.Neural Comput 18:2, 283-328 (2006 Feb)

{234}
hide / / print
ref: Grabli-2004.09 tags: basal_ganglia gobus_pallidus pathology GPe date: 03-11-2007 04:22 gmt revision:0 [head]

PMID-15292053 Behavioural disorders induced by external globus pallidus dysfunction in primates: I. Behavioural study.

  • there is a functional map within the basal ganglia according to its cortical projections.
  • reversible and focal dysfunction induced by microinjections if bicuculline in the sensorimotor territory of the external globus pallidus can generate abnormal movements. They wanted to test this in the other parts.
  • We found that bicuculline microinjections induced stereotypy when performed in the limbic part of the GPe, and attention deficit and/or hyperactivity when performed in the associative part
  • the behavioural effects shared similar features with symptoms observed in Tourette's syndrome, attention deficit/hyperactivity and compulsive disorders

{153}
hide / / print
ref: Stefani-1995.09 tags: electrophysiology dopamine basal_ganglia motor learning date: 0-0-2007 0:0 revision:0 [head]

PMID-8539419 Electrophysiology of dopamine D-1 receptors in the basal ganglia: old facts and new perspectives.

  • D1 is inhibitory (modulatory) on striatal neurons.
  • D1 cloned in 1990
  • D1 stimulates adenyl cyclase. (cAMP)
  • D1 activity shown to be necessary, but not sufficient, to generate long-term depression in striatal slices.
  • SKF 38393 was designed as a selective D1 receptor agonist; it has been available since the late 70's; it has nanomolar affinity for D1-R. SKF 38393 inhibits action potential discharge in striatal neurons as measued through response to intracellular current depolarizations.
  • striatal cells project to the substantia nigra.
  • alternate hypothesis: D1 activation on the striatonigral afferents to the ventral tegmental area (VTA) promotes GABA release.
    • recall that the VTA projects to the frontal/prefrontal cortex (PFC) via the mesocortical dopiminergic pathway. http://grad.uchc.edu/phdfaculty/antic.html There, DA synapese on spines of distal dendrites in juxtaposition with glutamergic synapses. this guy posits that these DA synapses are involved in the pathology of schizophrenia, and he uses optical techniques to measure the DA/Glu synapses.
    • VTA is just below the red nucleus in rats.
  • some people report that SKF 38393 potentiated depolarizing membrane responses to exogenous NMDA (agonist, excitotoxin).
  • they prefer the magnesium-dependent LTD pathway.
    • D1 receptor antagonist SCH 23390 prevented the generation of LTD in striatum. (Calabresi et al 1992).
    • in DA-depleted slices, LTD could be restored by the co-administration of D1 and D2 agonists.

{155}
hide / / print
ref: Wannier-2002.01 tags: globus_pallidus electrophysiology caudate putamen basal_ganglia date: 0-0-2007 0:0 revision:0 [head]

PMID-11924876 Neuronal activity in primate striatum and pallidum related to bimanual motor actions

  • monkeys had to pull on a spring-loaded drawer and grab food with other hand.
  • half the recorded neurons were responsive to this task.
  • targeted: 20.1 to 14.v mm anterior to the interaural plane of the rhesus monkey brain.
    • 19.2 mm looks good for GPe
    • 17.4 for putamen and caudate (right below area 24 in the cortex - Ventral cingulate cortex)
    • 15.6 for putamen, GPe, and GPi.
  • can these be modulated by imagined movement? e.g. in a BMI?