Life and Death of Immature Neurons in the Juvenile and Adult Primate Amygdala

In recent years, a large population of immature neurons has been documented in the paralaminar nucleus of the primate amygdala. A substantial fraction of these immature neurons differentiate into mature neurons during postnatal development or following selective lesion of the hippocampus. Notwithstanding a growing number of studies on the origin and fate of these immature neurons, fundamental questions about the life and death of these neurons remain. Here, we briefly summarize what is currently known about the immature neurons present in the primate ventral amygdala during development and in adulthood, as well as following selective hippocampal lesions. We provide evidence confirming that the distribution of immature neurons extends to the anterior portions of the entorhinal cortex and layer II of the perirhinal cortex. We also provide novel arguments derived from stereological estimates of the number of mature and immature neurons, which support the view that the migration of immature neurons from the lateral ventricle accompanies neuronal maturation in the primate amygdala at all ages. Finally, we propose and discuss the hypothesis that increased migration and maturation of neurons in the amygdala following hippocampal dysfunction may be linked to behavioral alterations associated with certain neurodevelopmental disorders.

133Bipolar ablation of refractory ventricular arrhythmias originating from the close proximity of His bundle

Introduction Biophysics of bipolar radiofrequency catheter ablation (Bi-RFCA) suggest more condensed and selective lesion formation when compared to conventional-unipolar approach. Whether more selective Bi-RFCA can result in safe and effective ablation of arrhythmic substrates in close proximity of His bundle has not been investigated so far. Purpose To determine feasibility and effectiveness of Bi-RFCA in His bundle area. Methods Consecutive patients after failed unipolar ablation for symptomatic premature ventricular complexes (PVC) or ventricular tachycardia (VT) originating from the vincity of His bundle underwent Bi-RFCA. Results We ultimately enrolled 8 patients (2 females, age 60 ± 15 years) to undergo Bi-RFCA of PVC/VT. Previous pharmacological treatment consisting of at least one antiarrhythmic drug and conventional catheter ablation failed in all. Bi-RFCA using open-irrigated and non-irrigated ablation catheters (AC) was delivered from two earliest PVC/VT activation sites located in the vincity of His bundle (Figure, panels A-B). A total number of 93 bipolar applications were delivered (mean bipolar RF time 508 ± 565s, mean power 35 ± 13W, mean impedance 163 ± 18Ω). Transient conduction disturbances occurred in 2 patients and were associated with mechanical compression of conduction system. No persistent conduction disturbances occurred. Bipolar RFCA led to acute elimination of PVC/VT in 6 (75%) patients. Follow up lasted 11 ± 5 months: two patients underwent repeat procedure using dual-irrigated Bi-RFCA, there was no VT recurrence and 72% PVC burden reduction was achieved (16200 ± 11600 pre-ablation vs 4500 ± 6200 post-ablation PVC/day, p = 0,035) (Figure, panel C). Conclusion Bi-RFCA performed in proximity of His bundle can be safe and effective in majority of patients. Abstract Figure. Bipolar ablation of parahisian PVC/VT

Using loss- and gain-of-function approaches to target amygdala-projecting serotonergic neurons in the dorsal raphe nucleus that enhance anxiety-related and conditioned fear behaviors

Background: The central serotonergic system originating from the dorsal raphe nucleus (DR) plays a critical role in anxiety and trauma-related disorders such as posttraumatic stress disorder. Although many studies have investigated the role of serotonin (5-HT) within pro-fear brain regions such as the amygdala, the majority of these studies have utilized non-selective pharmacological approaches or poorly understood lesioning techniques which limit their interpretation. Aim: Here we investigated the role of amygdala-projecting 5-HT neurons in the DR in innate anxiety and conditioned fear behaviors. Methods: To achieve this goal, we utilized (1) selective lesion of 5-HT neurons projecting to the amygdala with saporin toxin conjugated to anti-serotonin transporter (SERT) injected into the amygdala, and (2) optogenetic excitation of amygdala-projecting DR cell bodies with a combination of a retrogradely transported canine adenovirus-expressing Cre-recombinase injected into the amygdala and a Cre-dependent-channelrhodopsin injected into the DR. Results: While saporin treatment lesioned both local amygdalar 5-HT fibers and neurons in the DR as well as reduced conditioned fear behavior, optical activation of amygdala-projecting DR neurons enhanced anxious behavior and conditioned fear response. Conclusion: Collectively, these studies support the hypothesis that amygdala-projecting 5-HT neurons in the DR represent an anxiety and fear-on network.

The Architect Who Lost the Ability to Imagine: The Cerebral Basis of Visual Imagery

While the loss of mental imagery following brain lesions was first described more than a century ago, the key cerebral areas involved remain elusive. Here we report neuropsychological data from an architect (PL518) who lost his ability for visual imagery following a bilateral posterior cerebral artery (PCA) stroke. We compare his profile to three other patients with bilateral PCA stroke and another architect with a large PCA lesion confined to the right hemisphere. We also compare structural images of their lesions, aiming to delineate cerebral areas selectively lesioned in acquired aphantasia. When comparing the neuropsychological profile and structural magnetic resonance imaging (MRI) for the aphantasic architect PL518 to patients with either a comparable background (an architect) or bilateral PCA lesions, we find: (1) there is a large overlap of cognitive deficits between patients, with the very notable exception of aphantasia which only occurs in PL518, and (2) there is large overlap of the patients’ lesions. The only areas of selective lesion in PL518 is a small patch in the left fusiform gyrus as well as part of the right lingual gyrus. We suggest that these areas, and perhaps in particular the region in the left fusiform gyrus, play an important role in the cerebral network involved in visual imagery.

Meningioma in cervical spinal cord segment 6 of a dog – a case report

Meningiomas in dogs occur more commonly in the brain than in the cranial spinal cord. Intramedullary spinal cord tumours in dogs are described infrequently and present a diagnostic and therapeutic challenge. A nine-year-old Beagle dog was referred because of tetraparesis of a 20-day duration. The neurological signs were suggestive of a selective lesion involving the cervical spinal cord. Sagittal T2-weighted magnetic resonance imaging of the cervical vertebral column revealed a ventral, well-circumscribed mass within the vertebral canal at the level of cervical segment 6 (C6). A primary neoplasia was considered as probable differential diagnosis. The mass was removed by cervical laminectomy, durotomy and gentle dissections. On the basis of histological and immunohistochemical findings, a diagnosis of transitional meningioma (grade I) was made. Treatment of the meningioma with surgery resulted in a complete recovery, the dog was able to walk 21 days after surgery and had normal walk two months after presentation. Clinicopathologic and treatment data of cranial intraspinal meningiomas have been reported sporadically, but a segment 6 location was not thoroughly described before.

Selective lesion of the hippocampus increases the differentiation of immature neurons in the monkey amygdala

A large population of immature neurons is present in the ventromedial portion of the adult primate amygdala, a region that receives substantial direct projections from the hippocampal formation. Here, we show the effects of neonatal (n = 8) and adult (n = 6) hippocampal lesions on the populations of mature and immature neurons in the paralaminar, lateral, and basal nuclei of the adult monkey amygdala. Compared with unoperated controls (n = 7), the number of mature neurons was about 70% higher in the paralaminar nucleus of neonate- and adult-lesioned monkeys, and 40% higher in the lateral and basal nuclei of neonate-lesioned monkeys. The number of immature neurons in the paralaminar nucleus was 40% higher in neonate-lesioned monkeys and 30% lower in adult-lesioned monkeys. Similar changes in neuron numbers were also found in two monkeys with nonexperimental, selective, bilateral hippocampal damage. These changes in neuron numbers following hippocampal lesions appear to reflect the differentiation of immature neurons present in the paralaminar nucleus. After adult lesions, the differentiation of immature neurons was essentially restricted to the paralaminar nucleus and was associated with a decrease in the population of immature neurons. In contrast, after neonatal lesions, the differentiation of immature neurons involved the paralaminar, lateral, and basal nuclei. It was associated with an increase in the population of immature neurons in the paralaminar nucleus. Such lesion-induced neuronal plasticity sheds new light on potential mechanisms that may facilitate functional recovery following focal brain injury.