https://deepblue.lib.umich.edu/bitstream/2027.42/28186/1/0000638.pdf

The functional anatomy of basal ganglia disorders.

The sections in this article are:


1
Essence of Prefrontal Function: Regulation of Behavior by Representational Knowledge
11
Subdivisions of Prefrontal Cortex

12
Global Nature of Prefrontal Syndrome in Humans

13
Animal Model for Prefrontal Function in Humans

14
Delayed-Response Tests and Varying Interpretations of Their Functional Significance

15
Distractability and Perseveration: Secondary Consequences of Basic Defect in Representational Memory

16
Representational Memory in Wisconsin Card Sort and Other Diagnostic Tests of Prefrontal Function in Humans

17
Localization of Delayed-Response Function: Principal Sulcus

18
Circuit Basis of Visuospatial Functions




2
Accessing and “On-Line” Processing of Representations in Visuospatial Domain: Parietal-Prefrontal Connections
21
Visuospatial Representational Memory in Humans

22
Spatial-Mnemonic Nature of Delayed-Response Deficit: Domain-Specific Memory Loss

23
Topography of Representational Memory in Prefrontal Cortex

24
Electrophysiological Evidence of Spatial-Mnemonic Processes in Principal Sulcus

25
Parietal-Prefrontal Connectivity

26
Columnar and Laminar Framework for Feedforward and Feedback Mechanisms

27
Functional Significance of Parietal-Prefrontal Collaboration




3
Long-Term Memory and “Off-Line” Processing: Prefrontal-Limbic Connections
31
Role of Hippocampus in Spatial Memory

32
Multiple Connections Between Principal Sulcus and Hippocampal Formation

33
Quadripartite Neural Network: Parietal-Temporal-Cingulate-Prefrontal Circuit

34
Limbic Contribution to Spatial Memory




4
Response Initiation and Inhibition: Projections to Striatum, Tectum, Thalamus, and Premotor Cortex
41
Motor-Control Functions of Prefrontal Cortex

42
Cortical-Striatal Pathway and Related Feedback Loops

43
Cortical-Tectal Pathway

44
Thalamic-Cortical Systems

45
Prefrontal-Premotor Connections: Anterior Supplementary Motor Cortex Relays

46
Functional Speculations




5
Modulatory Mechanisms: Brain Stem Catecholamine Projections
51
Activation of Cognitive Machinery

52
Concentration and Synthesis of Catecholamines in Primate Cortex

53
Brain Stem Innervation of Prefrontal Cortex

54
Delayed-Response Deficits and Recovery Produced by Catecholamine Loss and Replacement in Prefrontal Cortex

55
Circuit Basis for Neuromodulation in Principal Sulcus




6
Multiple Subsystems of Prefrontal Cortex: Unity or Diversity of Function
61
Unity or Diversity of Prefrontal Function

62
Frontal Eye Fields

63
Inferior Convexity

64
Orbital Prefrontal Cortices

65
Problem of Integration




7
Diseases Affecting Prefrontal Cortex
71
Schizophrenia: Loss of Corticocortical Processing and Regulation of Behavior by Representational Knowledge

72
Wernicke-Korsakoff Syndrome: Loss of Thalamocortical and Brain Stem Modulatory Mechanisms

73
Huntington's Chorea and Parkinson's Disease: Loss of Prefrontal-Striatal Mechanisms and Initiation or Inhibition of Motor Response

74
Overview of Neurobiology of Disease




8
Summary

Circuitry of Primate Prefrontal Cortex and Regulation of Behavior by Representational Memory

Objective: To model in vivo the dynamic interrelations of head size, gray matter, white matter, and cerebrospinal fluid (CSF) volumes from infancy to old age using magnetic resonance imaging (MRI). Design: Cross-sectional, between-subjects using an age-regression model. Setting: A Veterans Affairs medical center and community hospitals. Participants: There were 88 male and female subjects aged 3 months to 30 years whose clinical MRI film had been read as normal and 73 healthy male volunteers aged 21 to 70 years who had an MRI performed specifically for this study. Main Outcome Measures: These MRI data were quantified using a semiautomated computer technique for segmenting images into gray matter, white matter, and CSF compartments. The cortex was defined geometrically as the outer 45% on each analyzed slice, and the volumes of cortical white matter, gray matter, and CSF were computed. Subcortical (ventricular) CSF volume was computed for the inner 55% of each analyzed slice. Results: In the younger sample, intracranial volume increased by about 300 mL from 3 months to 10 years. The same patterns of change in volume of each compartment across the age range were seen in both sexes: cortical gray matter volume peaked around age 4 years and decreased thereafter; cortical white matter volume increased steadily until about age 20 years; cortical and ventricular CSF volumes remained constant. In the older sample, brain volumes were statistically adjusted for normal variation in head size through a regression procedure and revealed the following pattern: cortical gray matter volume decreased curvilinearly, showing an average volume loss of 0.7 mL/y, while cortical white matter volume remained constant during the five decades; complementary to the cortical gray matter decrease, cortical CSF volume increased by 0.6 mL/y and ventricular volumes increased by 0.3 mL/y. Conclusions: These patterns of growth and change seen in vivo with MRI are largely consistent with neuropathological studies, as well as animal models of development, and may reflect neuronal progressive and regressive processes, including cell growth, myelination, cell death, and atrophy.

A quantitative magnetic resonance imaging study of changes in brain morphology from infancy to late adulthood.

The sections in this article are:


1
Biomechanical and Electromyographical Information
1.1
Single Limb During Locomotion

1.2
Interlimb Coordination

1.3
Treadmill Versus Overground Locomotion

1.4
Trunk Movements During Locomotion

1.5
Pathological Gaits

1.6
Summary




2
Neural Generation of “Basic Locomotor Synergy”
2.1
Central Versus Peripheral

2.2
Parts of CNS of Primary Importance for Neural Control of Basic Locomotor Synergy

2.3
Spinal Centers for Locomotion—Behavioral Results

2.4
Reflex Control of Basic Locomotor Synergy

2.5
Activity in Certain Spinal, Cerebellar, and Brain Stem Neurons and in Certain Reflex Pathways During Locomotion

2.6
Cerebellum and Locomotion

2.7
Initiation of Locomotion—Brain Stem Circuitry

2.8
Central Organization of Spinal Pattern Generation

2.9
Possible Rhythm-Generating Mechanisms and Models—Facts and Fiction

2.10
Developmental Aspects

2.11
Summary




3
Adapting Basic Locomotor Synergy to Animal's Needs
3.1
Changing Speed

3.2
Goal-Directed Locomotion—Turning and Walking Along Curvatures

3.3
Modifications of “Locomotor Posture”

3.4
Positioning of Limb in Each Step

3.5
Reflex Adaptation of Step

3.6
Summary




4
Concluding Remarks

Control of Locomotion in Bipeds, Tetrapods, and Fish

Principles and Practice of Sleep Medicine

Cats were subjected to complete lower brainstem transection, and were then tested for learning ability according to a classical conditioning paradigm. An auditory stimulus was systematically paired with a brief shock to the eyelid. Within a few weeks after the operation, the decerebrate cats could learn the conditioned response with a tone frequency discrimination and then a discrimination reversal. Our results support the notion that the brainstem reticular formation can support a conditioned response which isbehaviorally similar to that obtained in the intact animal.

Classical conditioning with auditory discrimination of the eye blink in decerebrate cats

The electrocorticogram in the chronic cerveau isolé cat.

Effects of caudate nuclei or frontal cortical ablations in cats. I. Neurology and gross behavior.

The neurological development of the kitten was studied from birth to 120 days of age. Three motor features present at birth disappeared within the 1st 45 days of life. The labyrinthine head and body righting reactions were present at birth; the latter matured only by 25 days of age when the air righting reaction (mature by 35 days) started to appear. Limb placing reactions developed progressively with proprioceptive components being present at birth whereas tactile components evolved slowly from early contact lifting to forepaws contact placing (60 days) and narrow plank walking (75 days). Standing and walking were well developed by 45 days. Eye opening occurred at 9.5 days and several eyeblink reactions (including blink to light) were present at birth. Adequate binocular coordination was seen by 47 days. Vision progressed parallel to the clearing of the ocular media which were fairly transparent by 32 days. Visually guided paw placing and the visuopalpebral blink reflex matured later (by 37 and 59 days, respectively). The external auditory canal and pinna were fully developed by 12 and 31 days, respectively; spontaneous and tactile pinna movements were present at birth; orienting to animal and nonanimal sounds was well developed by 6.5 and 18 days, respectively; spatial sound localization was developed by 16 days and differential responding to animal sounds matured by 24.5 days. Somatic responses and olfaction were present at birth but matured further thereafter. Playful interactions between kittens started by 10--15 days and well developed play behavior was seen by 36--40 days. In brief, all neurological functions mature progressively during the 1st 3 postnatal months.

Jaime R. Villablanca

Papers

Classical conditioning with auditory discrimination of the eye blink in decerebrate cats

The electrocorticogram in the chronic cerveau isolé cat.

Effects of caudate nuclei or frontal cortical ablations in cats. I. Neurology and gross behavior.

Neurological development of kittens

Behavioral and polygraphic study of "sleep" and "wakefulness" in chronic decerebrate cats.