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Jongbloets, B. C.

Publications and source records attributed to Jongbloets, B. C..

3 recordsLinked to original sources

Neuronal architecture of the mouse insular cortex underlying its diverse functions

The insular cortex integrates interoceptive and exteroceptive information to mediate bodily homeostasis, emotion, learning, and potentially consciousness.1-4 However, the cellular and circuit substrates governing the insula and other associative cortices are poorly understood compared to primary cortices. Here, we quantify the dendritic morphology together with electrical properties, local inputs, and/or projections of 1,093 insular pyramidal neurons. These neurons are mapped onto a quantitative anatomical model of the insula based on a Nissl-staining coordinate framework. Using improved algorithms, we define 21 morphological, 12 electrical, and 9 input neuronal types, and identify several morphological and input types that are unique to the insula. Further, we find that morphological properties constrain and often predict inputs, electrical properties, or projection targets. Several morphological types are differentially distributed between the functionally distinct anterior and posterior insula, providing the substrates for a quantitative demarcation between the anterior and posterior insular subregions. Surprisingly, certain neuronal types receive intra-insular inputs originating far beyond canonical cortical columns. Functionally, these connections bridge a long-range thalamus-to-amygdalar circuit that potentially links sensory information to valence. Our work establishes a structure-and-function foundation for investigating the insular cortex.

neuroscience↗

Distinct in vivo dynamics of excitatory synapses onto cortical pyramidal neurons and inhibitory interneurons

Cortical function relies on the balanced activation of excitatory and inhibitory neurons. However, little is known about the organization and dynamics of shaft excitatory synapses onto cortical inhibitory interneurons, which cannot be easily identified morphologically. Here, we fluorescently visualize the excitatory postsynaptic marker PSD-95 at endogenous levels as a proxy for excitatory synapses onto layer 2/3 pyramidal neurons and parvalbumin-positive (PV+) inhibitory interneurons in the mouse barrel cortex. Longitudinal in vivo imaging reveals that, while synaptic weights in both neuronal types are log-normally distributed, synapses onto PV+ neurons are less heterogeneous and more stable. Markov-model analyses suggest that the synaptic weight distribution is set intrinsically by ongoing cell type-specific dynamics, and substantial changes are due to accumulated gradual changes. Synaptic weight dynamics are multiplicative, i.e., changes scale with weights, though PV+ synapses also exhibit an additive component. These results reveal that cell type-specific processes govern cortical synaptic strengths and dynamics.

neuroscience↗

Synapse-specific Opioid Modulation of Thalamo-cortico-striatal Circuits

The medial thalamus (MThal), anterior cingulate cortex (ACC) and striatum play important roles in affective-motivational pain processing and reward learning. Opioids affect both pain and reward through uncharacterized modulation of this circuitry. This study examined opioid actions on glutamate transmission between these brain regions in mouse. Mu-opioid receptor (MOR) agonists potently inhibited MThal inputs without affecting ACC inputs to individual striatal medium spiny neurons (MSNs). MOR activation also inhibited MThal inputs to the pyramidal neurons in the ACC. In contrast, delta-opioid receptor (DOR) agonists disinhibited ACC pyramidal neuron responses to MThal inputs by suppressing local feed-forward GABA signaling from parvalbumin-positive interneurons. As a result, DOR activation in the ACC facilitated poly-synaptic (thalamo-cortico-striatal) excitation of MSNs by MThal inputs. These results suggest that opioid effects on pain and reward may be shaped by the relative selectivity of opioid drugs to the specific circuit components.

neuroscience↗