Enhancing GABAergic Tone in the Rostral Nucleus of the Solitary Tract Reconfigures Sensorimotor Neural Activity.

Recent work has shown that most cells in the rostral, gustatory portion of the nucleus tractus solitarius (rNTS) in awake, freely licking rats show lick-related firing. However, the relationship between taste-related and lick-related activity in rNTS remains unclear. Here, we tested whether GABA-derived inhibitory activity regulates the balance of lick- and taste-driven neuronal activity.

Heterogeneity of neuronal responses in the nucleus of the solitary tract suggests sensorimotor integration in the neural code for taste.

Theories of neural coding in the taste system typically rely exclusively on data gleaned from taste-responsive cells. However, even in the nucleus tractus solitarius (NTS), the first stage of central processing, neurons with taste selectivity coexist with neurons whose activity is linked to motor behavior related to ingestion. We recorded from a large ( n = 324) sample of NTS neurons recorded in awake rats, examining both their taste selectivity and the association of their activity with licking.

Spontaneous Changes in Taste Sensitivity of Single Units Recorded over Consecutive Days in the Brainstem of the Awake Rat.

A neuron's sensitivity profile is fundamental to functional classification of cell types, and underlies theories of sensory coding. Here we show that gustatory neurons in the nucleus of the solitary tract (NTS) and parabrachial nucleus of the pons (PbN) of awake rats spontaneously change their tuning properties across days. Rats were surgically implanted with a chronic microwire assembly into the NTS or PbN.

Taste coding of complex naturalistic taste stimuli and traditional taste stimuli in the parabrachial pons of the awake, freely licking rat.

Several studies have shown that taste-responsive cells in the brainstem taste nuclei of rodents respond to sensory qualities other than gustation. Such data suggest that cells in the classical gustatory brainstem may be better tuned to respond to stimuli that engage multiple sensory modalities than to stimuli that are purely gustatory. Here, we test this idea by recording the electrophysiological responses to complex, naturalistic stimuli in single neurons in the parabrachial pons (PbN, the second neural relay in the central gustatory pathway) in awake, freely licking rats.

Abrupt onset of mutations in a developmentally regulated gene during terminal differentiation of post-mitotic photoreceptor neurons in mice.

For sensitive detection of rare gene repair events in terminally differentiated photoreceptors, we generated a knockin mouse model by replacing one mouse rhodopsin allele with a form of the human rhodopsin gene that causes a severe, early-onset form of retinitis pigmentosa. The human gene contains a premature stop codon at position 344 (Q344X), cDNA encoding the enhanced green fluorescent protein (EGFP) at its 3' end, and a modified 5' untranslated region to reduce translation rate so that the mutant protein does not induce retinal degeneration. Mutations that eliminate the stop codon express a human rhodopsin-EGFP fusion protein (hRho-GFP), which can be readily detected by fluorescence microscopy.

Biochemical analysis of a rhodopsin photoactivatable GFP fusion as a model of G-protein coupled receptor transport.

Rhodopsin is trafficked to the rod outer segment of vertebrate rod cells with high fidelity. When rhodopsin transport is disrupted retinal photoreceptors apoptose, resulting in the blinding disease autosomal dominant retinitis pigmentosa. Herein, we introduce rhodopsin-photoactivatable GFP-1D4 (rhodopsin-paGFP-1D4) for the purposes of monitoring rhodopsin transport in living cells.