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EEG and the anterior thalamic nucleus
Published in Hans O Lüders, Deep Brain Stimulation and Epilepsy, 2020
The principal objective of evoking the recruiting rhythm in the operating room was to verify placement of electrodes in the AN. After being driven into the lateral ventricle by a servo-controlled device attached to a stereotaxic frame, the first tissue encountered from which single units may be recorded should be the AN. Ventral and medial to AN is the dorsal medial nucleus of the thalamus (DM) and ventrally, the ventral anterior (VA) nucleus. It is unclear if electrode position can be determined within the AN solely from the recruiting response since these other nuclei appear to be capable of generating a similar response. There is some suggestion that it may be possible to distinguish AN from DM by single unit recording (see Figure 14.1), however, this has not been demonstrated. If electrode placement is too shallow or lateral to AN, placing contacts within the ventricle, no recruiting response should be elicited. In all three study patients, post-operative MRI identified whether contacts of the DBS electrode were within the AN on each side. These results were compared to intra-operative evoked recruiting responses for each patient.
Geometric Transformations in the Visual-Motor Interface for Saccades
Published in Michael Fetter, Thomas Haslwanter, Hubert Misslisch, Douglas Tweed, Three-Dimensional Kinematics of Eye, Head and Limb Movements, 2020
This choice of a plant model is important for the upstream visuomotor transformation because it defines the motor information content of its inputs. For example, if the position-dependent tilts for Listing’s law are implemented downstream, then reticular formation burst neurons encode not angular velocity, but rate-of-position change (the time derivative of position). In other words, the burst neurons would normally encode a vector parallel to Listing’s plane, rather than the actual axis of rotation. This appears to be consistent with recent single unit recording studies (Hepp et al., 1994) and inactivation studies of burst neurons (Crawford and Vilis, unpublished observations). Furthermore, unlike angular velocity, this signal can be input directly into a neural integrator, which is consistent with the patterns of ocular drift observed during failure of the torsional and vertical integrators (Crawford et al., 1991; Crawford, 1994). Finally, we can drive this system with a three-dimensional version of displacement feedback (Jürgens et al., 1981), in which each of the three components of rate-of-position change (i.e. at the burst neurons) is driven by an instantaneous motor error signal that corresponds to the difference between the corresponding component of “initial motor error” and the time integral of the burst neuron output (cumulative change in eye position).
Using the in vitro Hippocampal Slice as a Model to Teach Methods in Neurophysiology
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
When we first started teaching a course in methods in neurophysiology, we used a variety of biological preparations depending on the objectives of a particular laboratory exercise. Although the students benefited from learning about different model systems, much of their time was spent mastering new dissection techniques. One of the preparations that we used in the early classes, the in vitro hippocampal slice, seemed like it might be an appropriate model for most of the techniques and principles that we were trying to illustrate. Thus, the next time we taught the class, we attempted to use this single preparation to achieve all or the majority of the objectives of the course. The topics covered in the class included the following: Instrumentation for neurophysiologyStimulation of neuronal tissueField potential recordingSingle-unit recordingIntracellular recording
Photoaversion in inherited retinal diseases: clinical phenotypes, biological basis, and qualitative and quantitative assessment
Published in Ophthalmic Genetics, 2022
Serena Zaman, Thomas Kane, Mohamed Katta, Michalis Georgiou, Michel Michaelides
Second, Noseda et al. identified dura sensitive neurons by means of single unit recording and neural tract tracing in the rat. These trigeminovascular neurons were found to project across somatosensory, visual and associated visual cortices; and interestingly also found to receive input from ipRGCs (16). Maleki et al. identified similar projections in humans by means of MR tractography (46). Contralateral primary somatosensory cortex, while considered part of the trigeminal nociceptive pathway, was not found to be activated in the study by Moulton et al.; postulated to be owing to a relatively low reported pain index by the patient when exposed to the light stimulus (3/10) (45). Perhaps primary somatosensory cortex recruitment is dependent upon a certain threshold being reached. There is evidence to suggest that summative spatial light exposure plays a role in eliciting PA (47). However, this group linked this to relative retinal photopigment density in different retinal quadrants (48). It is also possible that photophobia per se does not elicit certain observed responses and that instead downstream pathways are activated by resulting autonomic activity, e.g. lacrimation and increased involuntary blinking (45).
Calcium-independent phospholipase A2 inhibitor produces an analgesic effect in a rat model of neuropathic pain by reducing central sensitization in the dorsal horn
Published in Neurological Research, 2021
Young Seob Gwak, Guanxing Chen, Salahadin Abdi, Hee Kee Kim
To evaluate the firing activity of the lumbar 4 and L5 wide dynamic range (WDR) neurons, in vivo extracellular, single–unit recording of the number of spikes per second was performed 1 week after L5 SNL (n = 13, 250–350 g) and sham (n = 6, 250-350 g) using a carbon–filled, glass microelectrode (0.4-0.8 MΩ, Kation Scientific) and Spike2 software (Cambridge Electronic Design). One week later, the firing rates of single WDR neurons in response to various mechanical stimuli – including hairy brushes, pressure from bulldog clamps, pinches from Serrefine clamps, and 5 different VFFs (1.4, 2, 6, 15, and 60 g) – were recorded [23,24]. It is well known that the use of brush, pressure, and pinch stimuli is a standard means of characterizing WDR neuronal types in vivo. In the present study, we also stimulated rats’ paws with VFFs to study rats’ neuropathic pain behaviors. All stimulations were applied for 10 seconds. The inter–stimulus interval was 20 seconds. Next, to determine the impact of BEL treatment on WDR firing activity, either 0.03 g BEL (n = 7, 250–350 g) or the vehicle (10% DMSO and 10% Tween 80 in olive oil; n = 6, 250-350 g) was applied on the surface of the spinal cord near the recording electrode 1 week after SNL. After BEL treatment, neuronal firing activity was recorded for 60 minutes. Spontaneous activity was recorded for 20 seconds without any stimulation.
High-fat diet attenuates morphine withdrawal effects on sensory-evoked locus coeruleus norepinephrine neural activity in male obese rats
Published in Nutritional Neuroscience, 2022
Xinyi Li, Chung-Yang Yeh, Nicholas T. Bello
The objective of these studies was to characterize the in vivo responses of the LC-NE system in rats subjected to obesogenic diet and weight gain and to determine the effects of obesity in altering LC-NE responses to morphine withdrawal. Inter-individual differences in susceptibility for the development of obesity are modeled in selectively-bred obese prone (OP) and obese resistant (OR) rats. In addition to body weight and metabolic differences, OP and OR rats also displayed differences in stress axis functions and OR rats showed higher secretion of corticotrophin-releasing hormone (CRH) and corticosterone (CORT) following high-fat feeding [15], but the difference in the LC response have not been examined. For the first set of experiments, we examined the effects of obesity by selective breeding (i.e. OP vs. OR), diet (i.e. high fat vs. low fat), and their interaction on LC neural responses. For these first set of experiments, we initially compared OP with OR and observed an interaction of obesity propensity and diet on signal-to-noise (evoked/tonic ratio). In addition, we further examined how diet and obesity would influence morphine withdrawal and weight loss. We did so by examining whether prolonged exposure to obesogenic diet alters LC-NE neural activity and attenuates LC responsivity to morphine withdrawal. We hypothesized obesity to decrease LC activity and attenuate morphine withdrawal-induced LC activation. In order to characterize the LC-NE neural responses to long-term dietary interventions that result in weight gain, we used in vivo single-unit recording under isoflurane anesthesia. While this in vivo preparation has its limitations, these methods allowed for the examination of sensory-evoked LC activity in older animal (>20 weeks old) with prolonged access to an obesogenic diet. To our knowledge, this is the first study to examine the LC-NE system role in mediating the neurobiological overlap between obesity and opioid withdrawal.