scholarly journals A thalamic reticular circuit for head direction cell tuning and spatial navigation

2019 ◽  
Author(s):  
Gil Vantomme ◽  
Zita Rovó ◽  
Romain Cardis ◽  
Elidie Béard ◽  
Georgia Katsioudi ◽  
...  
Keyword(s):  
Spatial Navigation ◽  
Sensory Information ◽  
Search Strategies ◽  
Retrosplenial Cortex ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Head Direction ◽  
Thalamic Nuclei

SummaryTo navigate in space, an animal must refer to sensory cues to orient and move. Circuit and synaptic mechanisms that integrate cues with internal head-direction (HD) signals remain, however, unclear. We identify an excitatory synaptic projection from the presubiculum (PreS) and the multisensory-associative retrosplenial cortex (RSC) to the anterodorsal thalamic reticular nucleus (TRN), so far classically implied in gating sensory information flow. In vitro, projections to TRN involved AMPA/NMDA-type glutamate receptors that initiated TRN cell burst discharge and feedforward inhibition of anterior thalamic nuclei. In vivo, chemogenetic anterodorsal TRN inhibition modulated PreS/RSC-induced anterior thalamic firing dynamics, broadened the tuning of thalamic HD cells, and led to preferential use of allo-over egocentric search strategies in the Morris water maze. TRN-dependent thalamic inhibition is thus an integral part of limbic navigational circuits wherein it coordinates external sensory and internal HD signals to regulate the choice of search strategies during spatial navigation.

scholarly journals Corticothalamic gating of population auditory thalamocortical transmission in mouse

2019 ◽  
Author(s):  
Baher A. Ibrahim ◽  
Caitlin Murphy ◽  
Guido Muscioni ◽  
Aynaz Taheri ◽  
Georgiy Yudintsev ◽  
...  
Keyword(s):  
Receptive Field ◽  
Auditory Cortex ◽  
Cortical Neurons ◽  
Feedback Inhibition ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Linear Filter ◽  
Sensory Stimuli

AbstractSince the discovery of the receptive field, scientists have tracked receptive field structure to gain insights about mechanisms of sensory processing. At the level of the thalamus and cortex, this linear filter approach has been challenged by findings that populations of cortical neurons respond in a stereotyped fashion to sensory stimuli. Here, we elucidate a possible mechanism by which gating of cortical representations occurs. All-or-none population responses (here called “ON” and “OFF” responses) were observed in vivo and in vitro in the mouse auditory cortex at near-threshold acoustic or electrical stimulation. ON-responses were associated with previously-described UP states in the auditory cortex. OFF-responses in the cortex were only eliminated by blocking GABAergic inhibition in the thalamus. Opto- and chemogenetic silencing of NTSR-positive corticothalamic layer 6 (CTL6) neurons as well as the pharmacological blocking of the thalamic reticular nucleus (TRN) retrieved the missing cortical responses, suggesting that the corticothalamic feedback inhibition via TRN controls the gating of thalamocortical activity. Moreover, the oscillation of the pre-stimulus activity of corticothalamic cells predicted the cortical ON vs. OFF responses, suggesting that underlying cortical oscillation controls thalamocortical gating. These data suggest that the thalamus may recruit cortical ensembles rather than linearly encoding ascending stimuli and that corticothalamic projections play a key role in selecting cortical ensembles for activation.

scholarly journals Analysis of the Neuron Dynamics in Thalamic Reticular Nucleus by a Reduced Model

2021 ◽  
Vol 15 ◽  
Author(s):  
Chaoming Wang ◽  
Shangyang Li ◽  
Si Wu
Keyword(s):  
Bifurcation Analysis ◽  
Neuron Model ◽  
Salient Feature ◽  
Thalamic Reticular Nucleus ◽  
Reduced Model ◽  
Reticular Nucleus ◽  
Variable Model ◽  
Dynamical Mechanism

Strategically located between the thalamus and the cortex, the inhibitory thalamic reticular nucleus (TRN) is a hub to regulate selective attention during wakefulness and control the thalamic and cortical oscillations during sleep. A salient feature of TRN neurons contributing to these functions is their characteristic firing patterns, ranging in a continuum from tonic spiking to bursting spiking. However, the dynamical mechanism under these firing behaviors is not well understood. In this study, by applying a reduction method to a full conductance-based neuron model, we construct a reduced three-variable model to investigate the dynamics of TRN neurons. We show that the reduced model can effectively reproduce the spiking patterns of TRN neurons as observed in vivo and in vitro experiments, and meanwhile allow us to perform bifurcation analysis of the spiking dynamics. Specifically, we demonstrate that the rebound bursting of a TRN neuron is a type of “fold/homo-clinic” bifurcation, and the tonic spiking is the fold cycle bifurcation. Further one-parameter bifurcation analysis reveals that the transition between these discharge patterns can be controlled by the external current. We expect that this reduced neuron model will help us to further study the complicated dynamics and functions of the TRN network.

scholarly journals Selective Loss and Selective Sparing of Neurons in the Thalamic Reticular Nucleus following Human Cardiac Arrest

1993 ◽  
Vol 13 (4) ◽  
pp. 558-567 ◽  
Author(s):  
Douglas T. Ross ◽  
David I. Graham
Keyword(s):  
Cardiac Arrest ◽  
Heart Surgery ◽  
Neuronal Damage ◽  
Open Heart Surgery ◽  
Thalamic Reticular Nucleus ◽  
Global Cerebral Ischemia ◽  
Reticular Nucleus ◽  
Thalamic Nuclei ◽  
Attentional Processing ◽  
Thalamic Relay Nuclei

Neurons in the portion of the human thalamic reticular nucleus (RT) associated with the prefrontal cortex and mediodorsal thalamic nuclei were found to be selectively vulnerable to ischemic neuronal damage following relatively short (≤5-min) duration cardiac arrest. In contrast, selective sparing of these RT neurons occurred in cases with longer (>10-min) duration of arrest that was sufficient to produce extensive ischemic neuronal damage throughout the cerebral cortex and thalamic relay nuclei. The selective degeneration of RT neurons appears to require the sustained activity of corticothalamic or thalamocortical projections to the RT following the ischemic insult. Loss of RT neurons associated with the frontal cortex and mediodorsal thalamus may be the biological basis of some types of persisting cognitive deficits in attentional processing experienced by patients following cardiac arrest, open heart surgery, or other forms of brief global cerebral ischemia.

High Responsiveness and Direction Sensitivity of Neurons in the Rat Thalamic Reticular Nucleus to Vibrissa Deflections

2000 ◽  
Vol 83 (5) ◽  
pp. 2791-2801 ◽  
Author(s):  
Jed A. Hartings ◽  
Simona Temereanca ◽  
Daniel J. Simons
Keyword(s):  
Sensory Information ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Directional Sensitivity ◽  
Starting Position ◽  
Baseline Activity ◽  
High Responsiveness ◽  
Direction Of Movement ◽  
Mystacial Vibrissae ◽  
Direction Sensitivity

The thalamic reticular nucleus (Rt) is strategically positioned to integrate descending and ascending signals in the control of sensorimotor and other thalamocortical activity. Its prominent role in the generation of sleep spindles notwithstanding, relatively little is known of Rt function in regulating interactions with the sensory environment. We recorded and compared the responses of individual Rt and thalamocortical neurons in the ventroposterior medial (VPm) nucleus of the rat to controlled deflections of mystacial vibrissae. Transient Rt responses to the onset (on) and offset (off) of vibrissa deflection are larger and longer in duration than those of VPm and of all other populations studied in the whisker/barrel pathway. Magnitudes of on and off responses in Rt were negatively correlated with immediately preceding activities, suggesting a contribution of low-threshold T-type Ca2+ channels. Rt neurons also respond with high tonic firing rates during sustained vibrissa deflections. By comparison, VPm neurons are less likely to respond tonically and are more likely to exhibit tonic suppression. Rt and VPm populations are similar to each other, however, in that they retain properties of directional sensitivity established in primary afferent neurons. In both populations neurons are selective for deflection angle and exhibit directional consistency, responding best to a particular direction of movement regardless of the starting position of the vibrissal hair. These findings suggest a role for Rt in the processing of detailed sensory information. Temporally, Rt may function to limit the duration of stimulus-evoked VPm responses and to focus them on rapid vibrissa perturbations. Moreover, by regulating the baseline activity of VPm neurons, Rt may indirectly enhance the response selectivity of layer IV barrel neurons to synchronous VPm firing.

Oscillatory synaptic interactions between ventroposterior and reticular neurons in mouse thalamus in vitro

1994 ◽  
Vol 72 (4) ◽  
pp. 1993-2003 ◽  
Author(s):  
R. A. Warren ◽  
A. Agmon ◽  
E. G. Jones
Keyword(s):  
Receptor Antagonist ◽  
Gabab Receptor ◽  
Initial Response ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Excitatory Postsynaptic Potential ◽  
Postsynaptic Potential ◽  
Synaptic Interactions ◽  
Gabaa Receptor Antagonist

1. The thalamic reticular nucleus (RTN) has reciprocal connections with relay neurons in the dorsal thalamus. We used whole cell recording in a mouse in vitro slice preparation maintained at room temperature to study the synaptic interactions between the RTN and the ventroposterior thalamic nucleus (VP) during evoked low-frequency oscillations. 2. After a single electrical stimulus of the internal capsule, postsynaptic potentials (PSPs) were recorded in all VP and RTN neurons. In 76% of slices, there was an initial response followed by recurrent PSPs lasting for up to 8 s and with a frequency of approximately 2 Hz in both the VP and RTN. 3. In RTN neurons the initial response consisted of a fast excitatory postsynaptic potential (EPSP) that generated a burst of action potentials. Recurrent PSPs consisted of barrages of EPSPs that often reached burst threshold. The structure of subthreshold EPSP barrages in RTN neurons suggested that they were generated by bursting VP neurons. 4. In VP neurons the stimulus usually evoked a small EPSP followed by a large inhibitory postsynaptic potential (IPSP) that was often followed by a rebound burst. This initial response was often followed by a series of recurrent IPSPs presumably generated by RTN bursts, because intrinsic inhibitory neurons are absent in rodent VP. 5. IPSPs in VP neurons and recurrent EPSPs in RTN neurons were completely abolished by application of a gamma-aminobutyric acid-A (GABAA) receptor antagonist. A GABAB receptor antagonist produced no or little change in either the initial or recurrent response. 6. Recurrent IPSPs in VP neurons were abolished by glutamate receptor antagonists before the initial IPSP, which always remained stimulus dependent. 7. The dependency of recurring IPSPs in VP and recurring EPSPs in RTN upon GABA-mediated inhibition and excitatory amino acid-mediated excitation, plus the character of recurring EPSPs in the RTN strongly suggest that the recurring events were generated through reverse-reciprocal synaptic interactions between VP and RTN neurons. These synaptic interactions most likely play an important role in thalamic oscillations in behavior.

scholarly journals Developmental switch in the polarity of experience-dependent synaptic changes in layer 6 of mouse visual cortex

2011 ◽  
Vol 106 (5) ◽  
pp. 2499-2505 ◽  
Author(s):  
Emily Petrus ◽  
Terence T. Anguh ◽  
Huy Pho ◽  
Angela Lee ◽  
Nicholas Gammon ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Pyramidal Neurons ◽  
Light Exposure ◽  
Visual Deprivation ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Excitatory Synapses ◽  
Thalamic Nuclei ◽  
Developmental Age

Layer 6 (L6) of primary sensory cortices is distinct from other layers in that it provides a major cortical input to primary sensory thalamic nuclei. L6 pyramidal neurons in the primary visual cortex (V1) send projections to the lateral geniculate nucleus (LGN), as well as to the thalamic reticular nucleus and higher order thalamic nuclei. Although L6 neurons are proposed to modulate the activity of thalamic relay neurons, how sensory experience regulates L6 neurons is largely unknown. Several days of visual deprivation homeostatically adjusts excitatory synapses in L4 and L2/3 of V1 depending on the developmental age. For instance, L4 exhibits an early critical period during which visual deprivation homeostatically scales up excitatory synaptic transmission. On the other hand, homeostatic changes in L2/3 excitatory synapses are delayed and persist into adulthood. In the present study we examined how visual deprivation affects excitatory synapses on L6 pyramidal neurons. We found that L6 pyramidal neurons homeostatically increase the strength of excitatory synapses following 2 days of dark exposure (DE), which was readily reversed by 1 day of light exposure. This effect was restricted to an early critical period, similar to that reported for L4 neurons. However, at a later developmental age, a longer duration of DE (1 wk) decreased the strength of excitatory synapses, which reversed to normal levels with light exposure. These changes are opposite to what is predicted from the homeostatic plasticity theory. Our results suggest that L6 neurons differentially adjust their excitatory synaptic strength to visual deprivation depending on the age of the animals.

The Amygdaloid Complex: Anatomy and Physiology

2003 ◽  
Vol 83 (3) ◽  
pp. 803-834 ◽  
Author(s):  
P. SAH ◽  
E. S. L. FABER ◽  
M. LOPEZ DE ARMENTIA ◽  
J. POWER
Keyword(s):  
Synaptic Plasticity ◽  
Sensory Information ◽  
Amygdaloid Complex ◽  
In Vivo Studies ◽  
Anatomy And Physiology ◽  
Efferent Connections ◽  
Complex Anatomy ◽  
Subcortical Regions

Sah, P., E. S. L. Faber, M. Lopez de Armentia, and J. Power. The Amygdaloid Complex: Anatomy and Physiology. Physiol Rev 83: 803–834, 2003; 10.1152/physrev.00002.2003.—A converging body of literature over the last 50 years has implicated the amygdala in assigning emotional significance or value to sensory information. In particular, the amygdala has been shown to be an essential component of the circuitry underlying fear-related responses. Disorders in the processing of fear-related information are likely to be the underlying cause of some anxiety disorders in humans such as posttraumatic stress. The amygdaloid complex is a group of more than 10 nuclei that are located in the midtemporal lobe. These nuclei can be distinguished both on cytoarchitectonic and connectional grounds. Anatomical tract tracing studies have shown that these nuclei have extensive intranuclear and internuclear connections. The afferent and efferent connections of the amygdala have also been mapped in detail, showing that the amygdaloid complex has extensive connections with cortical and subcortical regions. Analysis of fear conditioning in rats has suggested that long-term synaptic plasticity of inputs to the amygdala underlies the acquisition and perhaps storage of the fear memory. In agreement with this proposal, synaptic plasticity has been demonstrated at synapses in the amygdala in both in vitro and in vivo studies. In this review, we examine the anatomical and physiological substrates proposed to underlie amygdala function.

scholarly journals 0028 GABAA Receptors Of The Thalamic Reticular Nucleus Regulate Sleep Spindles: An In Vivo Investigation By CRISPR-cas9 Genetic Abscission

SLEEP ◽  
2018 ◽  
Vol 41 (suppl_1) ◽  
pp. A12-A12
Author(s):  
D S Uygun ◽  
C Yang ◽  
H Miwa ◽  
J T McKenna ◽  
J M McNally ◽  
...  
Keyword(s):  
Gabaa Receptors ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Sleep Spindles

scholarly journals Corticothalamic Inhibition in the Thalamic Reticular Nucleus

2004 ◽  
Vol 91 (2) ◽  
pp. 759-766 ◽  
Author(s):  
Liming Zhang ◽  
Edward G. Jones
Keyword(s):  
Barrel Cortex ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Receptor Antagonists ◽  
Experimental Conditions ◽  
Inhibitory Network ◽  
Corticothalamic Projection ◽  
Substantial Network ◽  
Layer Vi

Mutual inhibition between the GABAergic cells of the thalamic reticular nucleus (RTN) is important in regulating oscillations in the thalamocortical network, promoting those in the spindle range of frequencies over those at lower frequencies. Excitatory inputs to the RTN from the cerebral cortex are numerically large and particularly powerful in inducing spindles. However, the extent to which corticothalamic influences can engage the inhibitory network of the RTN has not been fully explored. Focal electrical stimulation of layer VI in the barrel cortex of the mouse thalamocortical slice in vitro resulted in prominent di- or polysynaptic inhibitory postsynaptic currents (IPSCs) in RTN cells under the experimental conditions used. The majority of cortically induced responses consisted of mixed PSCs in which the inhibitory component predominated or of large IPSCs alone, implying inhibition of neighboring cells by other, cortically excited RTN cells. Within the mixed PSCs, fixed and variable latency components could commonly be identified. IPSCs could be blocked by application of ionotropic glutamate receptor antagonists or of GABAA receptor antagonists, also indicating their dependence on corticothalamic excitation triggering disynaptic or polysynaptic inhibition. Spontaneous GABAA receptor-dependent IPSCs were routinely observed in the RTN and, taken together with the results of cortical stimulation, indicate the existence of a substantial network of intrareticular inhibitory connections that can be effectively recruited by the corticothalamic system. These results suggest activation of cortical excitatory inputs triggers the propagation of inhibitory currents within the RTN and support the view that activation of the RTN from the somatosensory cortex, although focused by the topography of the corticothalamic projection, is capable of disynaptically engaging the whole inhibitory network of the RTN, by local and probably by reentrant GABAA receptor–based synapses, thus spreading the corticothalamic influence throughout the RTN.

Sign in / Sign up

Export Citation Format

Share Document