Unconditioned oromotor taste reactivity elicited by sucrose and quinine is unaffected by extensive bilateral damage to the gustatory zone of the insular cortex in rats

Abstract

Rats display stereotypical oromotor and somatic responses to small volumes of intraorally infused taste solutions. These behaviors, known as taste reactivity, are categorized by their association with ingestion or rejection and are thought to reflect the palatability of the stimulus. Because supracollicular decerebrate rats display normal taste reactivity responses, it would appear that forebrain structures are not necessary for generating them. However, because moving the plane of transection rostrally, or damaging or manipulating specific ventral forebrain sites disrupts normal taste reactivity behavior, lesions of the gustatory cortex, a region that has been suggested to be involved with palatability processing, may do the same. In the current study, rats received two injections of either ibotenic acid (N=12) or vehicle (N=8), targeting the conventionally defined gustatory cortex in each hemisphere, and were implanted with intraoral cannulae. Following recovery, their responses to intraoral infusions (0.23 ml in 1 min) of dH20, sucrose (1.0M and 0.1M), and quinine hydrochloride (3 mM and 0.3 mM) were video recorded. Analysis of brains with sufficient bilateral lesions (N=10) revealed that, on average, approximately 94% of the gustatory cortex was destroyed. These extensive bilateral lesions had no significant effect on taste reactivity; the numbers of ingestive and aversive responses to sucrose and quinine were similar between groups. Though these findings do not rule out involvement of the gustatory cortex in palatability processing, they make evident that the region of insular cortex destroyed is not necessary for the normal expression of unconditioned affective behavioral responses to taste stimuli.

Chemospecific deficits in taste sensitivity following bilateral or right hemispheric gustatory cortex lesions in rats

“…Even in brief access taste tests, which minimize the contribution of postingestive events associated with intake measures, rats with lesions placed centrally in GC display normal concentration‐dependent licking responses during very short duration trials of sucrose and quinine (Hashimoto & Spector, 2014). These results are consistent with the finding that rats with large lesions in GC display normal unconditioned oromotor and somatic responses to small volumes of sucrose and quinine infused directly into the oral cavity (King, Hashimoto, Blonde, & Spector, 2015), a behavioral assay referred to as taste reactivity (see Grill & Norgren, 1978).…”

“…In summary, in the rat, the GC is necessary for normal taste detection of some taste compounds but not all. It appears to be unnecessary for the maintenance of normal affective responsiveness to preferred and avoided stimuli as measured by intake and preference tests (Braun et al, 1982; Dunn & Everitt, 1988; Benjamin & Pfaffmann, 1955; but see Benjamin & Akert, 1959), brief access assays (Hashimoto & Spector, 2014), and taste reactivity (King et al, 2015). An intact GC, specifically the posterior portion, is necessary for the normal acquisition and expression of a CTA (see Schier et al, 2014; Schier et al, 2016).…”

Opioid and orexin hedonic hotspots in rat orbitofrontal cortex and insula

“…However, damage to those higher structures would produce loss of hierarchical control but not loss of original functions remaining in lower structures. These considerations may help explain why cortical lesions of the hedonic hotspot/coldspot sites identified here have generally failed to impair measures of food reward (12,14,61,64). Similarly, human patients with extensive damage to OFC and insula appear to remain capable of normal hedonic reactions to many pleasant versus unpleasant stimuli (9,10).…”

Behavioral analyses of taste function and ingestion in rodent models

“…For the last several years, we have been exploring the consequences of extensive bilateral lesions in the conventionally defined gustatory cortex of the rat [70–73]. Lindsey Schier, a current postdoc and Koji Hashimoto, a prior postdoc, along with Ginger Blonde and my graduate student Michelle Bales helped develop a new lesion mapping system to quantify the size, position, and bilateral symmetry of insular cortex lesions (Figure 12) [71].…”