Segmentation of the Globus Pallidus Internus Using Probabilistic Diffusion Tractography for Deep Brain Stimulation Targeting in Parkinson Disease
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Basal Ganglia & Cerebellum
1/2/2019 This power point is made available as an educational resource or study aid for your use only. This presentation may not be duplicated for others and should not be redistributed or posted anywhere on the internet or on any personal websites. Your use of this resource is with the acknowledgment and acceptance of those restrictions. Basal Ganglia & Cerebellum – a quick overview MHD-Neuroanatomy – Neuroscience Block Gregory Gruener, MD, MBA, MHPE Vice Dean for Education, SSOM Professor, Department of Neurology LUHS a member of Trinity Health Outcomes you want to accomplish Basal ganglia review Define and identify the major divisions of the basal ganglia List the major basal ganglia functional loops and roles List the components of the basal ganglia functional “circuitry” and associated neurotransmitters Describe the direct and indirect motor pathways and relevance/role of the substantia nigra compacta 1 1/2/2019 Basal Ganglia Terminology Striatum Caudate nucleus Nucleus accumbens Putamen Globus pallidus (pallidum) internal segment (GPi) external segment (GPe) Subthalamic nucleus Substantia nigra compact part (SNc) reticular part (SNr) Basal ganglia “circuitry” • BG have no major outputs to LMNs – Influence LMNs via the cerebral cortex • Input to striatum from cortex is excitatory – Glutamate is the neurotransmitter • Principal output from BG is via GPi + SNr – Output to thalamus, GABA is the neurotransmitter • Thalamocortical projections are excitatory – Concerned with motor “intention” • Balance of excitatory & inhibitory inputs to striatum, determine whether thalamus is suppressed BG circuits are parallel loops • Motor loop – Concerned with learned movements • Cognitive loop – Concerned with motor “intention” • Limbic loop – Emotional aspects of movements • Oculomotor loop – Concerned with voluntary saccades (fast eye-movements) 2 1/2/2019 Basal ganglia “circuitry” Cortex Striatum Thalamus GPi + SNr Nolte. -
Gene Expression of Prohormone and Proprotein Convertases in the Rat CNS: a Comparative in Situ Hybridization Analysis
The Journal of Neuroscience, March 1993. 73(3): 1258-1279 Gene Expression of Prohormone and Proprotein Convertases in the Rat CNS: A Comparative in situ Hybridization Analysis Martin K.-H. Schafer,i-a Robert Day,* William E. Cullinan,’ Michel Chri?tien,3 Nabil G. Seidah,* and Stanley J. Watson’ ‘Mental Health Research Institute, University of Michigan, Ann Arbor, Michigan 48109-0720 and J. A. DeSeve Laboratory of *Biochemical and 3Molecular Neuroendocrinology, Clinical Research Institute of Montreal, Montreal, Quebec, Canada H2W lR7 Posttranslational processing of proproteins and prohor- The participation of neuropeptides in the modulation of a va- mones is an essential step in the formation of bioactive riety of CNS functions is well established. Many neuropeptides peptides, which is of particular importance in the nervous are synthesized as inactive precursor proteins, which undergo system. Following a long search for the enzymes responsible an enzymatic cascade of posttranslational processing and mod- for protein precursor cleavage, a family of Kexin/subtilisin- ification events during their intracellular transport before the like convertases known as PCl, PC2, and furin have recently final bioactive products are secreted and act at either pre- or been characterized in mammalian species. Their presence postsynaptic receptors. Initial endoproteolytic cleavage occurs in endocrine and neuroendocrine tissues has been dem- C-terminal to pairs of basic amino acids such as lysine-arginine onstrated. This study examines the mRNA distribution of (Docherty and Steiner, 1982) and is followed by the removal these convertases in the rat CNS and compares their ex- of the basic residues by exopeptidases. Further modifications pression with the previously characterized processing en- can occur in the form of N-terminal acetylation or C-terminal zymes carboxypeptidase E (CPE) and peptidylglycine a-am- amidation, which is essential for the bioactivity of many neu- idating monooxygenase (PAM) using in situ hybridization ropeptides. -
Imaging of the Confused Patient: Toxic Metabolic Disorders Dara G
Imaging of the Confused Patient: Toxic Metabolic Disorders Dara G. Jamieson, M.D. Weill Cornell Medicine, New York, NY The patient who presents with either acute or subacute confusion, in the absence of a clearly defined speech disorder and focality on neurological examination that would indicate an underlying mass lesion, needs to be evaluated for a multitude of neurological conditions. Many of the conditions that produce the recent onset of alteration in mental status, that ranges from mild confusion to florid delirium, may be due to infectious or inflammatory conditions that warrant acute intervention such as antimicrobial drugs, steroids or plasma exchange. However, some patients with recent onset of confusion have an underlying toxic-metabolic disorders indicating a specific diagnosis with need for appropriate treatment. The clinical presentations of some patients may indicate the diagnosis (e.g. hypoglycemia, chronic alcoholism) while the imaging patterns must be recognized to make the diagnosis in other patients. Toxic-metabolic disorders constitute a group of diseases and syndromes with diverse causes and clinical presentations. Many toxic-metabolic disorders have no specific neuroimaging correlates, either at early clinical stages or when florid symptoms develop. However, some toxic-metabolic disorders have characteristic abnormalities on neuroimaging, as certain areas of the central nervous system appear particularly vulnerable to specific toxins and metabolic perturbations. Areas of particular vulnerability in the brain include: 1) areas of high-oxygen demand (e.g. basal ganglia, cerebellum, hippocampus), 2) the cerebral white matter and 3) the mid-brain. Brain areas of high-oxygen demand are particularly vulnerable to toxins that interfere with cellular respiratory metabolism. -
Neuron Numbers Increase in the Human Amygdala from Birth to Adulthood, but Not in Autism
Neuron numbers increase in the human amygdala from birth to adulthood, but not in autism Thomas A. Avinoa, Nicole Bargera, Martha V. Vargasa, Erin L. Carlsona, David G. Amarala,b,c, Melissa D. Baumana,b, and Cynthia M. Schumanna,1 aDepartment of Psychiatry and Behavioral Sciences, UC Davis MIND Institute, School of Medicine, University of California, Davis, Sacramento, CA 95817; bCalifornia National Primate Research Center, University of California, Davis, CA 95616; and cCenter for Neuroscience, University of California, Davis, CA 95618 Edited by Joseph E. LeDoux, New York University, New York, NY, and approved March 1, 2018 (received for review February 12, 2018) Remarkably little is known about the postnatal cellular develop- process, however, may also make the amygdala more susceptible ment of the human amygdala. It plays a central role in mediating to developmental or environmental insults. emotional behavior and has an unusually protracted development ASD is characterized by impairments in social communication well into adulthood, increasing in size by 40% from youth to combined with restricted interests and behaviors. Alterations in adulthood. Variation from this typical neurodevelopmental trajec- amygdala growth can be detected as early as 2 y of age (23–26) tory could have profound implications on normal emotional devel- and persist into late childhood (5, 27). The severity of the indi- vidual’s social and communicative symptoms positively correlates opment. We report the results of a stereological analysis of the – number of neurons in amygdala nuclei of 52 human brains ranging with amygdala enlargement, suggesting a potential structure from 2 to 48 years of age [24 neurotypical and 28 autism spectrum function relationship (23). -
Characterization of Substantia Nigra
Mourtzi et al. Stem Cell Research & Therapy (2021) 12:335 https://doi.org/10.1186/s13287-021-02398-3 RESEARCH Open Access Characterization of substantia nigra neurogenesis in homeostasis and dopaminergic degeneration: beneficial effects of the microneurotrophin BNN-20 Theodora Mourtzi1,2*, Dimitrios Dimitrakopoulos2†, Dimitrios Kakogiannis2†, Charalampos Salodimitris2, Konstantinos Botsakis1, Danai Kassandra Meri2, Maria Anesti2,3, Aggeliki Dimopoulou1, Ioannis Charalampopoulos4,5, Achilleas Gravanis4,5, Nikolaos Matsokis3, Fevronia Angelatou1† and Ilias Kazanis2*† Abstract Background: Loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) underlines much of the pathology of Parkinson’s disease (PD), but the existence of an endogenous neurogenic system that could be targeted as a therapeutic strategy has been controversial. BNN-20 is a synthetic, BDNF-mimicking, microneurotrophin that we previously showed to exhibit a pleiotropic neuroprotective effect on the dopaminergic neurons of the SNpc in the “weaver” mouse model of PD. Here, we assessed its potential effects on neurogenesis. Methods: We quantified total numbers of dopaminergic neurons in the SNpc of wild-type and “weaver” mice, with or without administration of BNN-20, and we employed BrdU labelling and intracerebroventricular injections of DiI to evaluate the existence of dopaminergic neurogenesis in the SNpc and to assess the origin of newborn dopaminergic neurons. The in vivo experiments were complemented by in vitro proliferation/differentiation assays of adult neural stem cells (NSCs) isolated from the substantia nigra and the subependymal zone (SEZ) stem cell niche to further characterize the effects of BNN-20. * Correspondence: [email protected]; [email protected]; [email protected] †Dimitrios Dimitrakopoulos and Dimitrios Kakogiannis contributed equally to this work. -
Auditory and Vestibular Systems Objective • to Learn the Functional
Auditory and Vestibular Systems Objective • To learn the functional organization of the auditory and vestibular systems • To understand how one can use changes in auditory function following injury to localize the site of a lesion • To begin to learn the vestibular pathways, as a prelude to studying motor pathways controlling balance in a later lab. Ch 7 Key Figs: 7-1; 7-2; 7-4; 7-5 Clinical Case #2 Hearing loss and dizziness; CC4-1 Self evaluation • Be able to identify all structures listed in key terms and describe briefly their principal functions • Use neuroanatomy on the web to test your understanding ************************************************************************************** List of media F-5 Vestibular efferent connections The first order neurons of the vestibular system are bipolar cells whose cell bodies are located in the vestibular ganglion in the internal ear (NTA Fig. 7-3). The distal processes of these cells contact the receptor hair cells located within the ampulae of the semicircular canals and the utricle and saccule. The central processes of the bipolar cells constitute the vestibular portion of the vestibulocochlear (VIIIth cranial) nerve. Most of these primary vestibular afferents enter the ipsilateral brain stem inferior to the inferior cerebellar peduncle to terminate in the vestibular nuclear complex, which is located in the medulla and caudal pons. The vestibular nuclear complex (NTA Figs, 7-2, 7-3), which lies in the floor of the fourth ventricle, contains four nuclei: 1) the superior vestibular nucleus; 2) the inferior vestibular nucleus; 3) the lateral vestibular nucleus; and 4) the medial vestibular nucleus. Vestibular nuclei give rise to secondary fibers that project to the cerebellum, certain motor cranial nerve nuclei, the reticular formation, all spinal levels, and the thalamus. -
Digital Neuroanatomy
DIGITAL NEUROANATOMY LM NEUROHISTOLOGY George R. Leichnetz, Ph.D. Professor, Department of Anatomy & Neurobiology Virginia Commonwealth University 2004 Press the Å and Æ keys on your keyboard to navigate through this lecture There are three morphological types of neurons in the nervous system: unipolar, bipolar, and multipolar. While all three types can be found in the PNS, the CNS only contains multipolar neurons. CNS multipolar neurons vary greatly in morphology: eg. spinal cord motor neurons, pyramidal cells of cerebral cortex, Purkinje cells of cerebellar cortex. The supportive cells of the CNS are neuroglia: astrocytes, oligodendrocytes, and microglia. Oligodendrocytes myelinate CNS axons, while Schwann cells myelinate PNS axons. Protoplasmic astrocytes predominate in CNS gray matter, while fibrous astrocytes predominate in CNS white matter. The ventral horn of the spinal cord Lumbar Spinal Cord contains multipolar motor neurons. Dorsal White Horn Matter Gray Matter Ventral Kluver- Horn Barrera Stain (LFB & CV) Cell bodies of motor neurons Dendrite Gray Matter Dendrite Perineuronal H & E oligodendrocyte Stain Nucleus, nucleolus Abundant Nissl substance Dorsal root Dorsal root ganglion Ventral root Gray Matter: contains White Matter: cell bodies of neurons contains x-sections of myelinated axons Multipolar motor neurons Silver Stain of the ventral horn Large multipolar motor neurons of the spinal cord ventral horn: see nucleus, nucleolus, abundant Nissl substance, multiple tapering processes (dendrites). The axon hillock (origin of axon from cell body) lacks Nissl. Nucleus Axon hillock dendrites Nucleolus Nissl substance (RER) Kluver-Barrera Stain (Luxol Fast Blue and Cresyl Violet) Thoracic Spinal Cord The nucleus dorsalis of Clarke, located in the base of the dorsal horn of the thoracic spinal cord, contains multipolar neurons whose nucleus is eccentric and Nissl around the periphery of the cell body (as if it were chromatolytic). -
Neural Plasticity in the Brain During Neuropathic Pain
biomedicines Review Neural Plasticity in the Brain during Neuropathic Pain Myeong Seong Bak 1, Haney Park 1 and Sun Kwang Kim 1,2,* 1 Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Korea; [email protected] (M.S.B.); [email protected] (H.P.) 2 Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea * Correspondence: [email protected]; Tel.: +82-2-961-0491 Abstract: Neuropathic pain is an intractable chronic pain, caused by damage to the somatosensory nervous system. To date, treatment for neuropathic pain has limited effects. For the development of efficient therapeutic methods, it is essential to fully understand the pathological mechanisms of neuropathic pain. Besides abnormal sensitization in the periphery and spinal cord, accumulating evidence suggests that neural plasticity in the brain is also critical for the development and mainte- nance of this pain. Recent technological advances in the measurement and manipulation of neuronal activity allow us to understand maladaptive plastic changes in the brain during neuropathic pain more precisely and modulate brain activity to reverse pain states at the preclinical and clinical levels. In this review paper, we discuss the current understanding of pathological neural plasticity in the four pain-related brain areas: the primary somatosensory cortex, the anterior cingulate cortex, the periaqueductal gray, and the basal ganglia. We also discuss potential treatments for neuropathic pain based on the modulation of neural plasticity in these brain areas. Keywords: neuropathic pain; neural plasticity; primary somatosensory cortex; anterior cingulate cortex; periaqueductal grey; basal ganglia Citation: Bak, M.S.; Park, H.; Kim, S.K. -
Dopaminergic Microtransplants Into the Substantia Nigra of Neonatal Rats with Bilateral 6-OHDA Lesions
The Journal of Neuroscience, May 1995, 15(5): 3548-3561 Dopaminergic Microtransplants into the Substantia Nigra of Neonatal Rats with Bilateral 6-OHDA Lesions. I. Evidence for Anatomical Reconstruction of the Nigrostriatal Pathway Guido Nikkhah,1,2 Miles G. Cunningham,3 Maria A. Cenci,’ Ronald D. McKay,4 and Anders Bj6rklund’ ‘Department of Medical Cell Research, University of Lund, S-223 62 Lund, Sweden, *Neurosurgical Clinic, Nordstadt Hospital, D-301 67 Hannover, Germany, 3Harvard Medical School, Boston, Massachusetts 02115, and 4 Laboratory of Molecular Biology, NINDS NIH, Bethesda, Maryland 20892 Reconstruction of the nigrostriatal pathway by long axon [Key words: target reinnervation, axon growth, neural growth derived from dopamine-rich ventral mesencephalic transplantation, tyrosine hydroxylase immunohistochem- (VM) transplants grafted into the substantia nigra may en- istry, Fos protein, Fluoro-Gold] hance their functional integration as compared to VM grafts implanted ectopically into the striatum. Here we report on In the lesioned brain of adult recipients dopamine-rich grafts a novel approach by which fetal VM grafts are implanted from fetal ventral mesencephalon (VM) are unable to reinner- unilaterally into the substantia nigra (SN) of 6-hydroxydo- vate the caudate-putamen unless they are placed close to, or pamine (SOHDA)-lesioned neonatal pups at postnatal day within, the denervated target structure (BjGrklund et al., 1983b; 3 (P3) using a microtransplantation technique. The results Nikkhah et al., 1994b). The failure of regenerating dopaminergic demonstrate that homotopically placed dopaminergic neu- axons to reinnervate the striatum from more distant implantation rons survive and integrate well into the previously sites, including their normal site of origin, the substantia nigra 6-OHDA-lesioned neonatal SN region. -
Neural Circuit and Clinical Insights from Intraoperative Recordings During Deep Brain Stimulation Surgery
brain sciences Perspective Neural Circuit and Clinical Insights from Intraoperative Recordings During Deep Brain Stimulation Surgery Anand Tekriwal 1,2,3 , Neema Moin Afshar 2, Juan Santiago-Moreno 3, Fiene Marie Kuijper 4, Drew S. Kern 1,5, Casey H. Halpern 4, Gidon Felsen 2 and John A. Thompson 1,5,* 1 Department of Neurosurgery, University of Colorado School of Medicine, Aurora, CO 80203, USA 2 Department of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, CO 80203, USA 3 Medical Scientist Training Program, University of Colorado School of Medicine, Aurora, CO 80203, USA 4 Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA 94305, USA 5 Department of Neurology, University of Colorado School of Medicine, Aurora, CO 80203, USA * Correspondence: [email protected] Received: 28 June 2019; Accepted: 18 July 2019; Published: 20 July 2019 Abstract: Observations using invasive neural recordings from patient populations undergoing neurosurgical interventions have led to critical breakthroughs in our understanding of human neural circuit function and malfunction. The opportunity to interact with patients during neurophysiological mapping allowed for early insights in functional localization to improve surgical outcomes, but has since expanded into exploring fundamental aspects of human cognition including reward processing, language, the storage and retrieval of memory, decision-making, as well as sensory and motor processing. The increasing use of chronic neuromodulation, via deep brain stimulation, for a spectrum of neurological and psychiatric conditions has in tandem led to increased opportunity for linking theories of cognitive processing and neural circuit function. Our purpose here is to motivate the neuroscience and neurosurgical community to capitalize on the opportunities that this next decade will bring. -
Striatal and Midbrain Connectivity with the Hippocampus Selectively Boosts Memory for Contextual Novelty
HIPPOCAMPUS 25:1262–1273 (2015) Striatal and Midbrain Connectivity with the Hippocampus Selectively Boosts Memory for Contextual Novelty Alexandros Kafkas* and Daniela Montaldi ABSTRACT: The role of contextual expectation in processing familiar of the new information (Kakade and Dayan, 2002). and novel stimuli was investigated in a series of experiments combining eye The ability to discriminate potentially salient familiar tracking, functional magnetic resonance imaging, and behavioral methods. An experimental paradigm emphasizing either familiarity or novelty detec- and novel information, in a context abundant with tion at retrieval was used. The detection of unexpected familiar and novel old and new stimuli, becomes crucial for ensuring stimuli, which were characterized by lower probability, engaged activity in effective contextual learning. Efficient discrimination midbrain and striatal structures. Specifically, detecting unexpected novel may trigger an orienting response toward the new stimuli, relative to expected novel stimuli, produced greater activity in the unexpected information and may therefore enhance substantia nigra/ventral tegmental area (SN/VTA), whereas the detection of unexpected familiar, relative to expected, familiar stimuli, elicited activity memory formation (Tulving and Kroll, 1995). Indeed, in the striatum/globus pallidus (GP). An effective connectivity analysis the brain’s dopaminergic system, including striatal and showed greater functional coupling between these two seed areas (GP and midbrain structures, has been shown to respond to SN/VTA) and the hippocampus, for unexpected than for expected stimuli. reward anticipation and to prediction errors as well as Within this network of midbrain/striatal–hippocampal interactions two having an effect on memory formation (Adcock et al., pathways are apparent; the direct SN–hippocampal pathway sensitive to unexpected novelty and the perirhinal–GP–hippocampal pathway sensitive 2006; Wittmann et al., 2011). -
MR Findings in Patients with Subacute Necrotizing Encephalomyelopathy (Leigh Syndrome): Correlation with Biochemical Defect
379 MR Findings in Patients with Subacute Necrotizing Encephalomyelopathy (Leigh Syndrome): Correlation with Biochemical Defect 1 2 L. Medina · MR studies were correlated with biochemical results in nine children who presented 1 3 T. L. Chi · with lactic acidosis andjor abnormal MR findings in the basal ganglia. Neurologic D. C. DeVivo4 development was delayed in all nine children. Seven of these patients were diagnosed S. K. Hilal 1 as having subacute necrotizing encephalomyelopathy (SNE, or Leigh syndrome) on the basis of history, clinical findings, and biochemical studies; of the remaining two, one had congenital lactic acidosis and the other had familial bilateral striatal necrosis with no known biochemical correlate. Although the clinical presentation of these patients was similar, we found distinctive MR abnormalities in characteristic locations in the seven patients with SNE, with or without detectable specific mitochondrial enzyme deficiency in cultured skin fibroblast assays. In our case studies of SNE patients with detectable enzyme deficiency states, defects in pyruvate dehydrogenase complex and cytochrome c oxidase have been found. The MR finding of note in SNE is the remarkably symmetrical involvement, most frequently of the putamen. In our study, lesions were also commonly found in the globus pallidus and the caudate nucleus, but never in the absence of putamina! abnormalities. Other areas of involvement included the paraven tricular white matter, corpus callosum, substantia nigra, decussation of superior cere bellar peduncles, periaqueductal region, and brainstem. In patients who present with lactic acidosis and whose MR findings show symmetrical abnormalities in the brain, but with sparing of the putamen, the diagnosis of SNE is in doubt.