{"id":{"repo_id":"potsdam-diss","oai_identifier":"oai:kobv.de-opus4-uni-potsdam:39660"},"canonical_url":"https://search.dev.ndltd.org/etd/potsdam-diss/oai:kobv.de-opus4-uni-potsdam:39660","repository":{"repo_id":"potsdam-diss","name":"Universität Potsdam - Diss","base_url":"https://publishup.uni-potsdam.de/opus4-ubp/oai"},"display":{"title":"Arc expression in the parabrachial nucleus following taste stimulation","abstract":"Researchers have made many approaches to study the complexities of the mammalian taste system; however molecular mechanisms of taste processing in the early structures of the central taste pathway remain unclear. More recently the Arc catFISH (cellular compartment analysis of temporal activity by fluorescent in situ hybridisation) method has been used in our lab to study neural activation following taste stimulation in the first central structure in the taste pathway, the nucleus of the solitary tract. This method uses the immediate early gene Arc as a neural activity marker to identify taste-responsive neurons. Arc plays a critical role in memory formation and is necessary for conditioned taste aversion memory formation. In the nucleus of the solitary tract only bitter taste stimulation resulted in increased Arc expression, however this did not occur following stimulation with tastants of any other taste quality. The primary target for gustatory NTS neurons is the parabrachial nucleus (PbN) and, like Arc, the PbN plays an important role in conditioned taste aversion learning. The aim of this thesis is to investigate Arc expression in the PbN following taste stimulation to elucidate the molecular identity and function of Arc expressing, taste- responsive neurons. Naïve and taste-conditioned mice were stimulated with tastants from each of the five basic taste qualities (sweet, salty, sour, umami, and bitter), with additional bitter compounds included for comparison. The expression patterns of Arc and marker genes were analysed using in situ hybridisation (ISH). The Arc catFISH method was used to observe taste-responsive neurons following each taste stimulation. A double fluorescent in situ hybridisation protocol was then established to investigate possible neuropeptide genes involved in neural responses to taste stimulation. The results showed that bitter taste stimulation induces increased Arc expression in the PbN in naïve mice. This was not true for other taste qualities. In mice conditioned to find an umami tastant aversive, subsequent umami taste stimulation resulted in an increase in Arc expression similar to that seen in bitter-stimulated mice. Taste-responsive Arc expression was denser in the lateral PbN than the medial PbN. In mice that received two temporally separated taste stimulations, each stimulation time-point showed a distinct population of Arc-expressing neurons, with only a small population (10 – 18 %) of neurons responding to both stimulations. This suggests that either each stimulation event activates a different population of neurons, or that Arc is marking something other than simple cellular activation, such as long-term cellular changes that do not occur twice within a 25 minute time frame. Investigation using the newly established double-FISH protocol revealed that, of the bitter-responsive Arc expressing neuron population: 16 % co-expressed calcitonin RNA; 17 % co-expressed glucagon-like peptide 1 receptor RNA; 17 % co-expressed hypocretin receptor 1 RNA; 9 % co-expressed gastrin-releasing peptide RNA; and 20 % co-expressed neurotensin RNA. This co-expression with multiple different neuropeptides suggests that bitter-activated Arc expression mediates multiple neural responses to the taste event, such as taste aversion learning, suppression of food intake, increased heart rate, and involves multiple brain structures such as the lateral hypothalamus, amygdala, bed nucleus of the stria terminalis, and the thalamus. The increase in Arc-expression suggests that bitter taste stimulation, and umami taste stimulation in umami-averse animals, may result in an enhanced state of Arc- dependent synaptic plasticity in the PbN, allowing animals to form taste-relevant memories to these aversive compounds more readily. The results investigating neuropeptide RNA co- expression suggest the amygdala, bed nucleus of the stria terminalis, and thalamus as possible targets for bitter-responsive Arc-expressing PbN neurons.","abstract_html":"Researchers have made many approaches to study the complexities of the mammalian taste system; however molecular mechanisms of taste processing in the early structures of the central taste pathway remain unclear. More recently the Arc catFISH (cellular compartment analysis of temporal activity by fluorescent in situ hybridisation) method has been used in our lab to study neural activation following taste stimulation in the first central structure in the taste pathway, the nucleus of the solitary tract. This method uses the immediate early gene Arc as a neural activity marker to identify taste-responsive neurons. Arc plays a critical role in memory formation and is necessary for conditioned taste aversion memory formation. In the nucleus of the solitary tract only bitter taste stimulation resulted in increased Arc expression, however this did not occur following stimulation with tastants of any other taste quality. The primary target for gustatory NTS neurons is the parabrachial nucleus (PbN) and, like Arc, the PbN plays an important role in conditioned taste aversion learning. The aim of this thesis is to investigate Arc expression in the PbN following taste stimulation to elucidate the molecular identity and function of Arc expressing, taste- responsive neurons. Naïve and taste-conditioned mice were stimulated with tastants from each of the five basic taste qualities (sweet, salty, sour, umami, and bitter), with additional bitter compounds included for comparison. The expression patterns of Arc and marker genes were analysed using in situ hybridisation (ISH). The Arc catFISH method was used to observe taste-responsive neurons following each taste stimulation. A double fluorescent in situ hybridisation protocol was then established to investigate possible neuropeptide genes involved in neural responses to taste stimulation. The results showed that bitter taste stimulation induces increased Arc expression in the PbN in naïve mice. This was not true for other taste qualities. In mice conditioned to find an umami tastant aversive, subsequent umami taste stimulation resulted in an increase in Arc expression similar to that seen in bitter-stimulated mice. Taste-responsive Arc expression was denser in the lateral PbN than the medial PbN. In mice that received two temporally separated taste stimulations, each stimulation time-point showed a distinct population of Arc-expressing neurons, with only a small population (10 – 18 %) of neurons responding to both stimulations. This suggests that either each stimulation event activates a different population of neurons, or that Arc is marking something other than simple cellular activation, such as long-term cellular changes that do not occur twice within a 25 minute time frame. Investigation using the newly established double-FISH protocol revealed that, of the bitter-responsive Arc expressing neuron population: 16 % co-expressed calcitonin RNA; 17 % co-expressed glucagon-like peptide 1 receptor RNA; 17 % co-expressed hypocretin receptor 1 RNA; 9 % co-expressed gastrin-releasing peptide RNA; and 20 % co-expressed neurotensin RNA. This co-expression with multiple different neuropeptides suggests that bitter-activated Arc expression mediates multiple neural responses to the taste event, such as taste aversion learning, suppression of food intake, increased heart rate, and involves multiple brain structures such as the lateral hypothalamus, amygdala, bed nucleus of the stria terminalis, and the thalamus. The increase in Arc-expression suggests that bitter taste stimulation, and umami taste stimulation in umami-averse animals, may result in an enhanced state of Arc- dependent synaptic plasticity in the PbN, allowing animals to form taste-relevant memories to these aversive compounds more readily. The results investigating neuropeptide RNA co- expression suggest the amygdala, bed nucleus of the stria terminalis, and thalamus as possible targets for bitter-responsive Arc-expressing PbN neurons.","abstract_has_math":false,"creators":["Tyree, Susan"],"institution":"Universität Potsdam","degree_name":null,"degree_level":"thesis.doctoral","degree_discipline":null,"degree_department":null,"school":null,"contributors":["Meyerhof, Wolfgang","Warschburger, Petra"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2017,"date_issued":"2017-05-29","date_published":"2017-05-29","updated_at":"2026-07-24T03:52:02Z","subjects":["taste processing","Geschmackssystems","parabrachial nucleus","Nucleus parabrachialis"],"languages":[],"rights":["CC-BY-NC - Namensnennung, nicht kommerziell 4.0 International"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://publishup.uni-potsdam.de/frontdoor/index/index/docId/39660","outbound_label":"Repository record","outbound_source":"source_url"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Meyerhof, Wolfgang","Warschburger, Petra"]},{"key":"dc:creator","label":"Author","values":["Tyree, Susan"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:publisher","label":"Institution","values":["Universität Potsdam"]},{"key":"dc:type","label":"Dc Type","values":["doctoralThesis"]},{"key":"thesis:degree_level","label":"Degree Level","values":["thesis.doctoral"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["Universität Potsdam"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["taste processing","Geschmackssystems","parabrachial nucleus","Nucleus parabrachialis"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["CC-BY-NC - Namensnennung, nicht kommerziell 4.0 International"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Researchers have made many approaches to study the complexities of the mammalian taste system; however molecular mechanisms of taste processing in the early structures of the central taste pathway remain unclear. More recently the Arc catFISH (cellular compartment analysis of temporal activity by fluorescent in situ hybridisation) method has been used in our lab to study neural activation following taste stimulation in the first central structure in the taste pathway, the nucleus of the solitary tract. This method uses the immediate early gene Arc as a neural activity marker to identify taste-responsive neurons. Arc plays a critical role in memory formation and is necessary for conditioned taste aversion memory formation. In the nucleus of the solitary tract only bitter taste stimulation resulted in increased Arc expression, however this did not occur following stimulation with tastants of any other taste quality. The primary target for gustatory NTS neurons is the parabrachial nucleus (PbN) and, like Arc, the PbN plays an important role in conditioned taste aversion learning. The aim of this thesis is to investigate Arc expression in the PbN following taste stimulation to elucidate the molecular identity and function of Arc expressing, taste- responsive neurons. Naïve and taste-conditioned mice were stimulated with tastants from each of the five basic taste qualities (sweet, salty, sour, umami, and bitter), with additional bitter compounds included for comparison. The expression patterns of Arc and marker genes were analysed using in situ hybridisation (ISH). The Arc catFISH method was used to observe taste-responsive neurons following each taste stimulation. A double fluorescent in situ hybridisation protocol was then established to investigate possible neuropeptide genes involved in neural responses to taste stimulation. The results showed that bitter taste stimulation induces increased Arc expression in the PbN in naïve mice. This was not true for other taste qualities. In mice conditioned to find an umami tastant aversive, subsequent umami taste stimulation resulted in an increase in Arc expression similar to that seen in bitter-stimulated mice. Taste-responsive Arc expression was denser in the lateral PbN than the medial PbN. In mice that received two temporally separated taste stimulations, each stimulation time-point showed a distinct population of Arc-expressing neurons, with only a small population (10 – 18 %) of neurons responding to both stimulations. This suggests that either each stimulation event activates a different population of neurons, or that Arc is marking something other than simple cellular activation, such as long-term cellular changes that do not occur twice within a 25 minute time frame. Investigation using the newly established double-FISH protocol revealed that, of the bitter-responsive Arc expressing neuron population: 16 % co-expressed calcitonin RNA; 17 % co-expressed glucagon-like peptide 1 receptor RNA; 17 % co-expressed hypocretin receptor 1 RNA; 9 % co-expressed gastrin-releasing peptide RNA; and 20 % co-expressed neurotensin RNA. This co-expression with multiple different neuropeptides suggests that bitter-activated Arc expression mediates multiple neural responses to the taste event, such as taste aversion learning, suppression of food intake, increased heart rate, and involves multiple brain structures such as the lateral hypothalamus, amygdala, bed nucleus of the stria terminalis, and the thalamus. The increase in Arc-expression suggests that bitter taste stimulation, and umami taste stimulation in umami-averse animals, may result in an enhanced state of Arc- dependent synaptic plasticity in the PbN, allowing animals to form taste-relevant memories to these aversive compounds more readily. The results investigating neuropeptide RNA co- expression suggest the amygdala, bed nucleus of the stria terminalis, and thalamus as possible targets for bitter-responsive Arc-expressing PbN neurons.","Trotz vielfältiger experimenteller Ansätze, die Komplexität des Geschmackssystems der Säugetiere zu erforschen, bleiben viele molekulare Mechanismen der Geschmacksverarbeitung in den frühen Strukturen der zentralen Geschmacksbahn unklar. Kürzlich wurde in unserem Labor die Arc catFISH-Methode (cellular compartment analysis of temporal activity by fluorescent in situ hybridisation) angewandt, um die neuronale Aktivierung nach Geschmacksstimulation in der ersten zentralnervösen Struktur der Geschmacksbahn, dem Nucleus tractus solitarii (NTS) zu untersuchen. Diese Methode nutzt das Immediate-early-Gen Arc als neuronalen Aktivitätsmarker, um geschmacksverarbeitende Neurone zu identifizieren. Arc spielt eine wichtige Rolle bei der Gedächtnisbildung und ist notwendig für die Ausprägung konditionierter Geschmacksaversionen. Im NTS führten nur Bitterstimuli zu einer erhöhten Arc- Expression, jedoch nicht Stimuli der anderen Geschmacksqualitäten. Das primäre Projektionsziel für geschmacksverarbeitende NTS-Neurone ist der Nucleus parabrachialis (PbN). Wie Arc, spielt dieser eine wichtige Rolle bei der Ausbildung konditionierter Geschmacksaversionen. Das Ziel dieser Arbeit ist, die Expression von Arc im PbN nach Geschmacksstimulation zu untersuchen, um die molekulare Identität der Arc- exprimierenden, geschmacksverarbeitenden Neurone aufzuklären. Naive und konditionierte Mäuse wurden mit Geschmacksstoffen der fünf Geschmacksqualitäten (süß, salzig, sauer, umami und bitter) stimuliert, wobei zum Vergleich mehrere Bitterstoffe verwendet wurden. Die Expression von Arc und ausgewählter Markergene wurde per In- situ-Hybridisierung (ISH) analysiert. Die Arc catFISH-Methode wurde eingesetzt, um geschmacksverarbeitende Neuronen zu untersuchen, die durch den jeweiligen Geschmacksstimulus aktiviert wurden. Ein Fluoreszenz-in-situ-Hybridisierungs-Protokoll (FISH) mit zwei RNA-Sonden wurde etabliert, um den Einfluss von Neuropeptiden in der neuronalen Verarbeitung von Geschmacksinformation zu untersuchen. Die Ergebnisse zeigen, dass in unkonditionierten Mäusen nur Bitterstimuli zu einer erhöhten Arc-Expression im PbN führen, nicht jedoch Stimuli anderer Geschmacksqualitäten. Bei Mäusen, die konditioniert wurden, einen Umami-Stimulus zu vermeiden, führt die nachfolgende Stimulation mit diesem Geschmacksstoff zu einer erhöhten Arc-Expression, die der in bitterstimulierten Mäusen vergleichbar ist. Die geschmacksinduzierte Arc-Expression ist im lateralen PbN stärker konzentriert als im medialen PbN. Bei Mäusen, die im Abstand von 25 min zwei Geschmackstimulationen erhielten, führt jede der Stimulationen zu einer Erregung eigenen Population von Arc- exprimierenden Neuronen. Nur ein geringer Anteil (10 - 18 %) reagiert auf beide Stimuli. Dies deutet darauf hin, dass entweder jeder Stimulationsvorgang eine eigene Neuronenpopulation aktiviert oder dass Arc nicht als einfacher Aktivitätsmarker zu verstehen ist, sondern vielmehr als Marker für längerfristige neuronale Veränderungen, die nicht zweimal innerhalb des 25-minütigen Zeitrahmens des Experiments auftreten. Die Ergebnisse des neu etablierten Doppel-FISH-Protokolls zeigen, dass von den Neuronen mit Arc-Expression nach Bitterstimulation: 16 % Calcitonin-RNA koexprimieren; 17 % Glucagon-like-peptide-1-receptor-RNA koexprimieren; 17 % Hypocretin-receptor-1-RNA koexprimieren; 9 % Gastrin-releasing-peptide-RNA koexprimieren; und 20 % Neurotensin-RNA koexprimieren. Diese Koexpression mit verschiedenen Neuropeptiden deutet darauf hin, dass die bitterinduzierte Arc-Expression an verschiedenen neuralen Prozessen beteiligt ist, die durch Geschmacksstimulation hervorgerufen werden. Darunter sind das Erlernen von Geschmacksaversion, reduzierte Nahrungsaufnahme und gesteigerte Herzfrequenz. Außerdem deutet dies darauf hin, dass an diesen Prozessen mehrere V Hirnstrukturen, wie lateraler Hypothalamus, Amygdala, Nucleus interstitialis striae terminalis und Thalamus beteiligt sind. Die erhöhte Arc-Expression deutet darauf hin, dass Stimulation mit Bitterstoffen und die Stimulation mit einem Umami-Stimulus bei umami vermeidenden Tieren zu einer erhöhten Arc-abhängigen neuronalen Plastizität führt. Dies könnte den Tieren ermöglichen, geschmacksbezogene Erinnerungen bezüglich aversiver Stimuli zu formen. Die Ergebnisse der Koexpression von Arc und Neuropeptiden legen die Amygdala, den Nucleus interstitialis striae terminalis und den Thalamus als mögliche Projektionsziele der Arc- exprimierenden PbN-Neurone nahe."]},{"key":"dc:format.medium","label":"Dc Format Medium","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Arc expression in the parabrachial nucleus following taste stimulation","Arc-Expression im Nucleus parabrachialis nach Geschmacksstimulation"]}]}],"canonical_facts":{"dc:contributor":["Meyerhof, Wolfgang","Warschburger, Petra"],"dc:creator":["Tyree, Susan"],"dc:description.abstract":["Researchers have made many approaches to study the complexities of the mammalian taste system; however molecular mechanisms of taste processing in the early structures of the central taste pathway remain unclear. More recently the Arc catFISH (cellular compartment analysis of temporal activity by fluorescent in situ hybridisation) method has been used in our lab to study neural activation following taste stimulation in the first central structure in the taste pathway, the nucleus of the solitary tract. This method uses the immediate early gene Arc as a neural activity marker to identify taste-responsive neurons. Arc plays a critical role in memory formation and is necessary for conditioned taste aversion memory formation. In the nucleus of the solitary tract only bitter taste stimulation resulted in increased Arc expression, however this did not occur following stimulation with tastants of any other taste quality. The primary target for gustatory NTS neurons is the parabrachial nucleus (PbN) and, like Arc, the PbN plays an important role in conditioned taste aversion learning. The aim of this thesis is to investigate Arc expression in the PbN following taste stimulation to elucidate the molecular identity and function of Arc expressing, taste- responsive neurons. Naïve and taste-conditioned mice were stimulated with tastants from each of the five basic taste qualities (sweet, salty, sour, umami, and bitter), with additional bitter compounds included for comparison. The expression patterns of Arc and marker genes were analysed using in situ hybridisation (ISH). The Arc catFISH method was used to observe taste-responsive neurons following each taste stimulation. A double fluorescent in situ hybridisation protocol was then established to investigate possible neuropeptide genes involved in neural responses to taste stimulation. The results showed that bitter taste stimulation induces increased Arc expression in the PbN in naïve mice. This was not true for other taste qualities. In mice conditioned to find an umami tastant aversive, subsequent umami taste stimulation resulted in an increase in Arc expression similar to that seen in bitter-stimulated mice. Taste-responsive Arc expression was denser in the lateral PbN than the medial PbN. In mice that received two temporally separated taste stimulations, each stimulation time-point showed a distinct population of Arc-expressing neurons, with only a small population (10 – 18 %) of neurons responding to both stimulations. This suggests that either each stimulation event activates a different population of neurons, or that Arc is marking something other than simple cellular activation, such as long-term cellular changes that do not occur twice within a 25 minute time frame. Investigation using the newly established double-FISH protocol revealed that, of the bitter-responsive Arc expressing neuron population: 16 % co-expressed calcitonin RNA; 17 % co-expressed glucagon-like peptide 1 receptor RNA; 17 % co-expressed hypocretin receptor 1 RNA; 9 % co-expressed gastrin-releasing peptide RNA; and 20 % co-expressed neurotensin RNA. This co-expression with multiple different neuropeptides suggests that bitter-activated Arc expression mediates multiple neural responses to the taste event, such as taste aversion learning, suppression of food intake, increased heart rate, and involves multiple brain structures such as the lateral hypothalamus, amygdala, bed nucleus of the stria terminalis, and the thalamus. The increase in Arc-expression suggests that bitter taste stimulation, and umami taste stimulation in umami-averse animals, may result in an enhanced state of Arc- dependent synaptic plasticity in the PbN, allowing animals to form taste-relevant memories to these aversive compounds more readily. The results investigating neuropeptide RNA co- expression suggest the amygdala, bed nucleus of the stria terminalis, and thalamus as possible targets for bitter-responsive Arc-expressing PbN neurons.","Trotz vielfältiger experimenteller Ansätze, die Komplexität des Geschmackssystems der Säugetiere zu erforschen, bleiben viele molekulare Mechanismen der Geschmacksverarbeitung in den frühen Strukturen der zentralen Geschmacksbahn unklar. Kürzlich wurde in unserem Labor die Arc catFISH-Methode (cellular compartment analysis of temporal activity by fluorescent in situ hybridisation) angewandt, um die neuronale Aktivierung nach Geschmacksstimulation in der ersten zentralnervösen Struktur der Geschmacksbahn, dem Nucleus tractus solitarii (NTS) zu untersuchen. Diese Methode nutzt das Immediate-early-Gen Arc als neuronalen Aktivitätsmarker, um geschmacksverarbeitende Neurone zu identifizieren. Arc spielt eine wichtige Rolle bei der Gedächtnisbildung und ist notwendig für die Ausprägung konditionierter Geschmacksaversionen. Im NTS führten nur Bitterstimuli zu einer erhöhten Arc- Expression, jedoch nicht Stimuli der anderen Geschmacksqualitäten. Das primäre Projektionsziel für geschmacksverarbeitende NTS-Neurone ist der Nucleus parabrachialis (PbN). Wie Arc, spielt dieser eine wichtige Rolle bei der Ausbildung konditionierter Geschmacksaversionen. Das Ziel dieser Arbeit ist, die Expression von Arc im PbN nach Geschmacksstimulation zu untersuchen, um die molekulare Identität der Arc- exprimierenden, geschmacksverarbeitenden Neurone aufzuklären. Naive und konditionierte Mäuse wurden mit Geschmacksstoffen der fünf Geschmacksqualitäten (süß, salzig, sauer, umami und bitter) stimuliert, wobei zum Vergleich mehrere Bitterstoffe verwendet wurden. Die Expression von Arc und ausgewählter Markergene wurde per In- situ-Hybridisierung (ISH) analysiert. Die Arc catFISH-Methode wurde eingesetzt, um geschmacksverarbeitende Neuronen zu untersuchen, die durch den jeweiligen Geschmacksstimulus aktiviert wurden. Ein Fluoreszenz-in-situ-Hybridisierungs-Protokoll (FISH) mit zwei RNA-Sonden wurde etabliert, um den Einfluss von Neuropeptiden in der neuronalen Verarbeitung von Geschmacksinformation zu untersuchen. Die Ergebnisse zeigen, dass in unkonditionierten Mäusen nur Bitterstimuli zu einer erhöhten Arc-Expression im PbN führen, nicht jedoch Stimuli anderer Geschmacksqualitäten. Bei Mäusen, die konditioniert wurden, einen Umami-Stimulus zu vermeiden, führt die nachfolgende Stimulation mit diesem Geschmacksstoff zu einer erhöhten Arc-Expression, die der in bitterstimulierten Mäusen vergleichbar ist. Die geschmacksinduzierte Arc-Expression ist im lateralen PbN stärker konzentriert als im medialen PbN. Bei Mäusen, die im Abstand von 25 min zwei Geschmackstimulationen erhielten, führt jede der Stimulationen zu einer Erregung eigenen Population von Arc- exprimierenden Neuronen. Nur ein geringer Anteil (10 - 18 %) reagiert auf beide Stimuli. Dies deutet darauf hin, dass entweder jeder Stimulationsvorgang eine eigene Neuronenpopulation aktiviert oder dass Arc nicht als einfacher Aktivitätsmarker zu verstehen ist, sondern vielmehr als Marker für längerfristige neuronale Veränderungen, die nicht zweimal innerhalb des 25-minütigen Zeitrahmens des Experiments auftreten. Die Ergebnisse des neu etablierten Doppel-FISH-Protokolls zeigen, dass von den Neuronen mit Arc-Expression nach Bitterstimulation: 16 % Calcitonin-RNA koexprimieren; 17 % Glucagon-like-peptide-1-receptor-RNA koexprimieren; 17 % Hypocretin-receptor-1-RNA koexprimieren; 9 % Gastrin-releasing-peptide-RNA koexprimieren; und 20 % Neurotensin-RNA koexprimieren. Diese Koexpression mit verschiedenen Neuropeptiden deutet darauf hin, dass die bitterinduzierte Arc-Expression an verschiedenen neuralen Prozessen beteiligt ist, die durch Geschmacksstimulation hervorgerufen werden. Darunter sind das Erlernen von Geschmacksaversion, reduzierte Nahrungsaufnahme und gesteigerte Herzfrequenz. Außerdem deutet dies darauf hin, dass an diesen Prozessen mehrere V Hirnstrukturen, wie lateraler Hypothalamus, Amygdala, Nucleus interstitialis striae terminalis und Thalamus beteiligt sind. Die erhöhte Arc-Expression deutet darauf hin, dass Stimulation mit Bitterstoffen und die Stimulation mit einem Umami-Stimulus bei umami vermeidenden Tieren zu einer erhöhten Arc-abhängigen neuronalen Plastizität führt. Dies könnte den Tieren ermöglichen, geschmacksbezogene Erinnerungen bezüglich aversiver Stimuli zu formen. Die Ergebnisse der Koexpression von Arc und Neuropeptiden legen die Amygdala, den Nucleus interstitialis striae terminalis und den Thalamus als mögliche Projektionsziele der Arc- exprimierenden PbN-Neurone nahe."],"dc:format.medium":["application/pdf"],"dc:publisher":["Universität Potsdam"],"dc:rights":["CC-BY-NC - Namensnennung, nicht kommerziell 4.0 International"],"dc:subject":["taste processing","Geschmackssystems","parabrachial nucleus","Nucleus parabrachialis"],"dc:title":["Arc expression in the parabrachial nucleus following taste stimulation","Arc-Expression im Nucleus parabrachialis nach Geschmacksstimulation"],"dc:type":["doctoralThesis"],"thesis:degree_level":["thesis.doctoral"],"thesis:institution_name":["Universität Potsdam"]},"updated_at":"2026-07-24T03:52:02Z"}