Articles by Amy C. Jongeling in JoVE
Investigating the Function of Deep Cortical and Subcortical Structures Using Stereotactic Electroencephalography: Lessons from the Anterior Cingulate Cortex Robert A. McGovern1,3, Tarini Ratneswaren4, Elliot H. Smith1,3, Jennifer F. Russo3, Amy C. Jongeling2,3, Lisa M. Bateman2,3, Catherine A. Schevon2,3, Neil A. Feldstein1,3, Guy M. McKhann, II1,3, Sameer Sheth1,3 1Department of Neurosurgery, Columbia University Medical Center, New York Presbyterian Hospital, 2Department of Neurology, Columbia University Medical Center, New York Presbyterian Hospital, 3Columbia University Medical Center, New York Presbyterian Hospital, 4School of Medicine, King's College London Stereotactic Electroencephalography (SEEG) is an operative technique used in epilepsy surgery to help localize seizure foci. It also affords a unique opportunity to investigate brain function. Here we describe how SEEG can be used to investigate cognitive processes in human subjects.
Other articles by Amy C. Jongeling on PubMed
Suitability of the Retrograde Tracer Dil for Electrophysiological Studies of Brainstem Neurons: Adverse Ramifications for G-protein Coupled Receptor Agonists Journal of Neuroscience Methods. Feb, 2007 | Pubmed ID: 17045656 Despite the acknowledged advantages of studying identified populations of neurons, few studies have convincingly established that fluorescent retrograde tracers do not alter the passive membrane properties, action potential characteristics, or effects of drugs on the labeled neurons. Whole-cell patch clamp recordings were made from spinally-projecting serotonergic neurons in the rostral ventromedial medulla (RVM) and spinally-projecting noradrenergic neurons in the locus coeruleus (LC) that were retrogradely labeled with 1,1'-dioactadecyl-3,3,3',3'-tetramethylindocarbodyanine perchlorate (Dil). The passive membrane and the action potential properties of Dil-labeled (0.2%) and non-labeled serotonergic neurons in the RVM did not differ. Similarly, the passive membrane and action potential properties of non-labeled noradrenergic LC neurons did not differ from neurons labeled with 0.2% or 5% Dil. Although the mu opioid receptor agonist [D-Ala(2)-NMePhe(4)-Gly-ol(5)]enkephalin (DAMGO) produced equivalent outward currents in non-labeled noradrenergic LC neurons and those labeled with 0.2% Dil, significantly smaller currents were recorded in LC neurons labeled with 5% Dil. Baclofen, a gamma-aminobutryic acid(B) receptor agonist, also produced smaller currents in RVM neurons labeled with 5% Dil compared to 0.2% Dil. These results indicate that 0.2% Dil is suitable for retrograde labeling of brainstem neurons in vivo for subsequent in vitro electrophysiological study. However, 5% Dil is likely to confound studies of the postsynaptic actions of G-protein coupled receptor ligands.
Persistent Inflammatory Pain Decreases the Antinociceptive Effects of the Mu Opioid Receptor Agonist DAMGO in the Locus Coeruleus of Male Rats Neuropharmacology. May-Jun, 2009 | Pubmed ID: 19265713 Persistent inflammatory nociception increases levels of endogenous opioids with affinity for delta opioid receptors in the ventromedial medulla and enhances the antinociceptive effects of the mu opioid receptor (MOPr) agonist [D-Ala2, N-Me-Phe4, Gly5-ol]enkephalin (DAMGO) [Hurley, R.W., Hammond, D.L., 2001. Contribution of endogenous enkephalins to the enhanced analgesic effects of supraspinal mu opioid receptor agonists after inflammatory injury. J. Neurosci. 21, 2536-2545]. It also increases levels of endogenous opioids that act at MOPr elsewhere in the CNS [Zangen, A., Herzberg, U., Vogel, Z., Yadid, G., 1998. Nociceptive stimulus induces release of endogenous beta-endorphin in the rat brain. Neuroscience 85, 659-662]. This study tested the hypothesis that a sustained release of endogenous opioids leads to a downregulation of MOPr in the locus coeruleus (LC) and induces a state of endogenous opioid tolerance. Four days after injection of complete Freund's adjuvant (CFA) in the left hindpaw of the rat, both the magnitude and duration of the antinociception produced by microinjection of DAMGO in the right LC were reduced. Saturation isotherms demonstrated a 50% decrease in MOPr B(max) in homogenates of the LC from CFA-treated rats; K(d) was unchanged. Receptor autoradiography revealed that this decrease was bilateral. The decreased efficacy of DAMGO in CFA-treated rats most likely results from a decreased number of MOPr in the LC. Microinjection of the MOPr antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) in the LC did not exacerbate hyperalgesia in the ipsilateral hindpaw or produce hyperalgesia in the contralateral hindpaw of CFA-treated rats. The downregulation in MOPr is therefore unlikely to result from the induction of endogenous opioid tolerance in the LC. These results indicate that persistent inflammatory nociception alters the antinociceptive actions of MOPr agonists in the CNS by diverse mechanisms that are nucleus specific and likely to have different physiological implications.
Pearls and Oy-sters: Tuberculous Meningitis: Not a Diagnosis of Exclusion Neurology. Jan, 2013 | Pubmed ID: 23339213 A 21-year-old man presented to his local emergency department with 5 days of headache, which was dull, occipital, bilateral, nonthrobbing, and progressively worsening. It was associated with mild fever, photophobia, and neck pain and stiffness. He had no history of headache, chronic illness, recent vaccinations, cutaneous rash, cough, diarrhea, arthralgia, or myalgia. He was from Ecuador and had been living in the United States for less than 1 year. He had been incarcerated while in Ecuador. Sublingual temperature on admission was 102.6°F. Other vital signs were within normal limits. On physical examination, he appeared thin but not cachectic. He had meningismus and photophobia, but no papilledema and his mental status was alert and attentive. There were no focal neurologic deficits. CSF contained red blood cells: 24 × 10(3)/μL; white blood cells: 85/μL (lymphocytic predominant); protein: 128 mg/dL; and glucose: 48 mg/dL (CSF/serum glucose ratio = 0.53). CSF Gram stain and cultures, PPD test, and blood and urine cultures were all negative. CT scan of the head on day of admission was entirely normal. MRI without gadolinium contrast showed a single punctate T2 hyperintensity in the left frontal periventricular white matter. Chest radiograph was clear. He received empiric vancomycin, ceftriaxone, and acyclovir. Corticosteroids were not given. The patient did not improve with antibiotics and continued to be intermittently febrile. On day 5, he became abruptly more somnolent, then comatose, opening eyes only to pain, his pupils were 5 mm and reactive, he had intact brainstem reflexes, withdrawing both arms and legs. Emergent head CT showed development of hydrocephalus and a ventriculoperitoneal shunt was emergently placed. The neurologic examination did not improve after shunt placement, and repeat head CT showed increased hydrocephalus with bilateral cerebral infarcts. On day 11, he was transferred to Columbia University Medical Center for intensive care. He was febrile and comatose. He did not open his eyes to pain, pupils were 7 mm minimally reactive, brainstem reflexes were intact, and he exhibited extensor posturing to pain. Mannitol was given, corticosteroid therapy was started, and an extraventricular drain was placed. The next day, his right pupil was 8 mm and nonreactive. MRI showed diffuse contrast enhancement of the arachnoid, extensive infarction of basal ganglia, midbrain, and pons, and small ring-enhancing lesions in the cerebellum (figure 1, A-D). Repeat lumbar puncture showed red blood cells: 550 × 10(3)/μL; white blood cells: 250/μL (14% neutrophils, 80% lymphocytes, 6% monocytes); protein: 65 mg/dL; and glucose: