Previous essays have used Pv (ventral pallidum) as part of the seek and avoidance circuit without exploring it in detail. For this essay, I’m revisiting Pv in more detail for two purposes: first, to check that the simulation’s seek and avoid model is compatible with scientific results about Pv, and second, to understand more on how those internal circuits work.

Timeouts are critical for the food-odor seek circuit to prevent the animal from getting stuck in a trap where it either can’t reach the food, or the food odor has no food. A timeout could simply disable seek and return to the default roaming random walk, or it could actively avoid the current area. When the seek times out, an active avoidance phase is more effective than returning to roaming, because the avoidance moves away from the current false cues and into a distant area more likely to have a new food source.

The simulation uses the basal ganglia as a timeout system, specifically Sv (ventral striatum) with Pv that’s interconnected with food-seek motivation based in H.l (lateral hypothalamus). The model uses Ado (adenosine) as a timeout neurotransmitter and S.d2 (striatum projection neuron with D2.i receptor) to signal the timeout. Essay 31 covered the adenosine-S.d2 system in more detail. Essentially, neural activity produces Ado from neurons and neighboring astrocytes. The Ado then activates A2a.s (adenosine G-s coupled receptors) on S.d2, which potentiates S.d2 and increases internal activity in an PKA (protein kinase A) activation chain. As Ado builds up over time, S.d2 activity increases until it triggers a switch from seek to avoid in Pv.

The above diagram shows how the current simulation model uses Sv/Pv as a timeout. H.l (lateral hypothalamus) is responsible for seek motivation based on odor input from Ob (olfactory bulb) and it drives roaming search to R1.a (anterior hindbrain motor region). The basal ganglia, represented by S.ot (olfactory tubercle, an olfactory region of Sv) and Pv serve as the timeout function. This essay aims to expand that simple model into a more accurate representation of the Sv/Pv timeout.

Seek and avoid

In neuroscience, seek and avoid are measured with RTPP (real-time place preference) and RTPA (real-time place avoidance) experiments, although these measurements are often interpreted as “valence” instead of actions. Circuits that produce RTPP could contribute to the seek action, and circuits that produced RTPA could produce avoidance. For example, Hb.lm (lateral habenula, medial part) produces RTPA when stimulated and RTPP when inhibited [Stamatakis et al 2016], and Sv, Pv, and H.l produce either RTPP or RTPA, depending on which neurons are stimulated. In Sv, S.d1 (striatum projection neuron with D1.s dopamine receptor) produces RTPP [Soares-Cunha et al 2020], [Tan et al 2024], while S.d2 produces RTPA [Bonnavion et al 2024], but only when stimulated for longer times [Soares-Cunha et al 2020]. Different regions of Sv have flipped seek and avoidance, between S.msh.d (medial shell of Sv, dorsal) and S.msh.v (medial shell of Sv, ventral) [Yao Y et al 2021]. In Pv, glutamate neurons produce RTPA and GABA neurons produce RTPP [Stephenson-Jones et al 2020], which matches H.l, where glutamate produces RTPA [Stamatakis et al 2016] and GABA produces RTPP [Jennings et al 2015], [Siemian et al 2021].

The above diagram shows a simplified timeout and avoid circuit. The blue arrows show the proposed timeout avoid path. The greyed arrows show related connectivity, which are either contextual or for other actions. For example, the H.l glutamate to Hb.lm avoidance is necessary for predator and toxin avoidance such as a looming response from OT (optic tectum) [Lecca et al 2017] or pain responses from R.pb.l (lateral parabrachium) [Phua et al 2021]. Although the H.l is RTPA and also uses Hb.lm as an avoidance action path, it seems less likely to be a seek-timeout path. Because the Sv, Pv, and H.l circuit is also an eating circuit, some of the locomotion is stopping to eat. Some of the Sv and Pv projections to H.l are eating circuits [Root et al 2015], and eating also inhibits Hb.lm avoidance [Hu H et al 2020] because the animal shouldn’t move away from its food.

Hb.lm is a key action node for avoidance, using V.rn (raphe nuclei) to drive avoidance. In zebrafish, this path is exclusively V.mr (median raphe) because the zebrafish Hb.lm only connects to V.mr [Agetsuma et al 2010]. In mammals, the target of Hb.lm is less clear cut because both V.mr and V.dr (dorsal raphe) receive Hb.lm output [Baker et al 2015] and could participate in avoidance.

Pv as a heterogenous area

In this model, Pv is a key decision node. It receives seek-driving input from H.l and A.bl (basolateral amygdala) [Giardino et al 2018], [Heinsbroek et al 2020] and decision and timeout information from S.ot. Pv is defined by the projection of Sv, specifically using tac1 (tachykinin 1 for substance-p neurotransmitter), which S.d1 neurons exhibit. However, the neuron types and origins are heterogenous [Ottenheimer et al 2024], and derive from neighboring regions. In part, Pv derives from Po.l (lateral preoptic area) and H.l neuron types, in part it derives from P.bst (bed nucleus of the stria terminalis, extended amygdala), in part it derives from Pd (global pallidus external) [Ottenheimer et al 2024], and it has some functionality more similar to P.bf (basal forebrain), including ACh (acetylcholine) attention projections.

The above diagram shows some of the difficulty by categorizing Pv functions by its output projections. Pv ACh (acetylcholine) projections particularly to A.bl to sustain attention, such as enabling odor seek [Kim R et al 2024], which is a P.bf function. Separate Pv glutamate and GABA projections to Hb.lm produce RTPP and RTPA [Stephenson-Jones et al 2020], which matches theH.l and Po.l function. Projections to H.l are more complex, producing wake [Luo YJ et al 2023] and eating [Palmer et al 2024]. Pv has choice-related output to Vta (ventral tegmentum) [Faget et al 2018], [Palmer et al 2024], which drives seek but is not motivational. Pv also has similar connections to the basal ganglia, similar to the S.d (dorsal striatum) and Pd (dorsal pallidum aka globus pallidus external) connections to H.stn (subthalamic nucleus), Snr (substantia nigra pars reticulata) and P.epn (entopeduncular nucleus aka globus pallidus internal) [Root et al 2015]. However, those Pd-like circuits are restricted to a particular part of Pv.dl (dorsolateral Pv). Finally, like Pd, Pv has “arkypallidal” feedback connections to Sv [Vachez et al 2021].

Decision: selection and commitment

Decision can be decomposed into a selection function and a commitment function. Selection chooses between competing options, such as left or right. Commitment ensures that the selection follows through and is not immediately distracted. Commitment is more important because without commitment, a selection isn’t a decision, while a random selection or a first-arriving selection is a workable decision. In a WTA (winner-take-all) process, the key part is the “take-all” part. Random take-all would also work. The commitment function needs a lockout function (“take-all”) but also a timeout function,e ach of which may be separate circuits.

The above diagram shows a possible functional decomposition for Pv and decision-making. The Pv to Vta projection is important for the selection process [Palmer et al 2024]. More speculatively, the Pv feedback connection to Pv could provide a lockout function by inhibiting new selections through Sv. A similar circuit may exist in H.sth, which also projects directly to S.d [Williams 2024]. The Pv to Hb.lm projection is more clearly established as an avoidance pathway [Faget et al 2018].

One neuron, two functions

Although selection isn’t the focus of the essay, some learning theory results and some neuroscience measurements show that single S.d2 neurons are possibly serving opposite roles: selecting an action, but then opposing that same action [Hodge and Yttri 2025], [Soares-Cunha et al 2020], or terminating the current activity [Tecuapetla et al 2016]. In the classical model of basal ganglia selection, S.d1 and S.d2 are oppositional: S.d1 promotes an action and S.d2 either opposes the action or promotes an opposite action [Bariselli et al 2019]. In the learning model where DA (dopamine) serves as a teaching signal, DA enhances selected actions when successful and suppresses unsuccessful actions. However, some scientists argue that this learning model doesn’t work for S.d2 if S.d1 and S.d2 are selection with no other function [Lindsey et al 2025]. Some proposals to rescue the learning models include sustaining S.d2 activity after selection [Lindsey et al 2025]

Some prominent results show both S.d1 and S.d2 selecting the winning option [Cui G et al 2013], not opposing each other. However, studies consistently show the stimulating S.d1 makes contralateral turns but stimulating S.d2 makes ipsilateral turns [Conde-Berriozabal et al 2025], which is clearly oppositional. Possibly resolving this conflict, stimulating S.d2 shows a short 1s period of inhibiting Pv and exciting Vta while longer 2s stimulation excites Pv and inhibits Vta [Soares-Cunha et al 2020]. Another study shows short 350ms S.d2 as not producing RTPA, but 2s long S.d2 stimulus does produce RTPA [Hodge and Yttri 2025].

S.d2 neurons produce both GABA and the opioid enkephalin as neurotransmitters [Dai KZ et al 2022]. GABA is a fast neurotransmitter on the order of 3-5ms and only requires electrical AP (action potentials). Enkephalin is a much slower neuropeptide and is released when internal Ca2+ (calcium) and PKA (protein kinase A) levels have risen [Konradi et al 2023], [Hook et al 2008]. PKA levels rise in response to G-s protein coupled receptors like A2a.s (adenosine G-s coupled receptor). Enkephalin requires both action potentials and PKA, likely triggered by A2a.s. This A2a.s PKA signaling needs to overcome D2.i, which inhibits the PKA pathway. Technically, D2.i inhibits AC (adenylyl cyclase), which prevents cAMP accumulation, which prevents PKA. One result of this longer chain is that enkephalin signaling is much slower than GABA and is modulated by other neurotransmitters like DA and Ado.

This dual transmitter system means that a short stimulus might release GABA, while a longer stimulus would release enkephalin. In addition, S.d2 axons contain DOR.i (δ-opioid inhibitory receptor), which can self-inhibit its own GABA release [Steiner and Gerfen 1998]. The longer enkephalin path may disable the faster GABA path. Prolonged S.d2 stimulation produces RTPA and requires active DOR.i in Pv [Soares-Cunha et al 2020]. A similar oppositional fast vs slow transmitter system exists in the H.l to Vta connection, where GABA provides fast inhibition but a slower neurotensin neurotransmitter excites [Patterson et al 2015].

The above diagram shows hypothetical fast and slow multiplexing circuit with GABA driving the fast selection path and enkephalin driving the slow avoidance path. The fast S.d2 GABA path disinhibits Vta by inhibiting a tonically active Pv GABA interneuron. The slow S.d2 enkephalin path inhibits a distinct tonically active Pv GABA interneuron, which disinhibits the Pv glutamate to Hb.lm avoidance path, and re-inhibits Vta DA. Re-inhibition of Vta DA serves as a lockout of subsequence decisions. Disinhibition of the Hb.lm avoidance enables timeout avoidance. With this temporal multiplexing system, a single S.d2 neuron can serve all three decision functions: selection, lockout, and timeout.

Pv glutamate inputs vs tonic activity

The most prominent Pv inputs from Sv are inhibitory, which raises the question: what are they inhibiting? Either it is inhibiting an excitatory input or it’s inhibiting tonically active neurons. So, the glutamate inputs have an outsized importance because without glutamate or tonic activity, the inhibition has nothing to work against.

In studying the Pv projection to Hb.lm, [Stephenson-Jones et al 2020] inhibited glutamate and GABA neurons to explore the tonic behavior. Inhibiting glutamate did not produce an effect, either RTPP or RTPA, and inhibiting GABA also did not produce an effect. This result suggests that the Pv output neurons are not tonically active, either from their own activity or other internal Pv activity. Without tonic activity, glutamate inputs are necessary to drive output.

The major glutamate inputs are from A.bl, H.l, and H.stn, but the H.stn input is specific to the Pd-like area in Pv.dl [Root et al 2015], so for the purpose of this essay I’m assuming H.stn is restricted to a specific Pv subarea with dorsal basal ganglia function and does not apply to the rest of Pv.

The above diagram shows an hypothetical circuit using H.l.ox (orexin neurons of H.l) as a food search signal that drives both roaming random walk and directed, targeted seek. When the animal is not seeking food because it’s sated or eating, H.l.ox is silent, which unpowers the circuit. My choice of H.l.ox as a glutamate source is hypothetical. H.l has at least 17 glutamate populations [Wang Y et al 2021], including one that implements SLR (subthalamic locomotor region) [Ji C et al 2024], some that project to Hb.lm directly for aversion [Lecca et al 2017], as well as eating-related neurons, and H.l.ox.

I’ve used the enkephalin output from S.d2 because the Hb.lm is the avoidance circuit. The enkephalins receptor DOR.i (δ-opioid receptor) is coupled to inhibitory G-protein and acts primarily presynaptically but does act postsynaptically in Pv [Neuhofer and Kalivas 2023], [Rysztak and Jutkiewicz 2020]. In Pv, stimulating DOR.i inhibits 24% of Pv neurons and excites 13% [Root et al 215]. In an alternative circuit, the S.d2 enkephalin-triggered DOR.i receptor is presynaptic on the glutamate input to Pv.g. Without that glutamate input, the Pv.g neuron is inhibited, which disinhibits the Pv.glu path.

Unfortunately, the exact details of the circuits aren’t known yet. It seems reasonable to assume that the S.d1 RTPP path opposes the S.d2 RTPA path using peptides or opioids instead of GABA, but S.d1 produces two additional outputs: the opioid dynorphin with its inhibitory KOR.i (κ-opioid receptor) and the peptide SP (substance P) with its excretory NK1.q (neurokinin 1 with PLC/PKC path). Like enkephalin’s DOR.i receptor, dynorphin’s KOR.i is primarily presynaptic. The above diagram shows three hypothetical circuits, but other more complicated possible circuits exist, including using more tonically active inhibitory GABA interneurons. In particular, S.d1 and S.d2 have auto-receptors for dynorphin and enkephalin respectively, which inhibits their own release of the opioids. Dynorphin is known to self-inhibit S.d1 neurons in Pv [Steiner and Gerfen 1998], which may be its main function. Although I’ve focused on S.d1 and S.d2 neurotransmitters for the slow circuit, another possibility is that a distinct internal Pv mechanism drives the slow avoidance circuit, independent of S.d2 enkephalin and S.d2 dynorphin or SP.

A.bl glutamate

I used H.l.ox as the source of glutamate above, but A.bl is also an important source of glutamate, and inhibiting A.bl can turn odor seek into avoid [Kim R et al 2024], which is exactly the situation here. A.bl is a cortical area, which means it’s more complicated, but has the advantage of supporting sustained, working-memory output. A.bl receives olfactory input from Ob and O.pir (piriform cortex) and outputs glutamate to Pv and to Sv. A.bl has both seek and avoid outputs with distinct projections [Sniffen et al 2024]. A.bl is necessary for conflicting seek and threat, but disabling A.bl does not prevent seek [Hernández-Jaramillo et al 2024]. In addition A.bl receives ACh input from Pv [Root et al 2015]. For this circuit, I’m using the A.bl seek output to serve the same function as H.l did in the previous description. Without A.bl seek input, the seek collapses and turns to avoidance [Kim R et al 2024].

The ACh input from Pv to A.bl is important to sustaining attention. ACh acts on m1.q (ACh metabotropic G-q coupled receptor) in the A.bl PY (pyramidal) neurons [Unal et al 2015]. Activating m1.q turns the PY neurons into a sustained excitation with an ADP (after-depolarization potential) after receiving both ACh and an AP (action potential) [Unal et al 2015]. ADP turns the PY neuron into an Up state for 7-10 seconds, meaning it’s more easily activated by inputs than its base state. Essentially, ACh converts A.bl firing into working memory or sustained attention.

The Pv ACh neuron inputs include H.l, Sv, and Sa (central amygdala) and P.bst (bed nucleus of the stria terminalis, external amygdala) [Schlingloff et al 2025]. This ACh modulation gives another opportunity to control seek to an odor target. An initial odor detection on the order of 500ms might only trigger sustained seek if ACh is activated by a food-seek drive from H.l and not suppressed by Sv, Sa, or P.bst. Working memory or sustained attention for the odor would require food motivation and an absence of habituation.

Simulation

The main seek path is almost entirely disconnected from the Pv timeout circuitry discussed in the essay. The main seek path is a short, fast path from Ob to V.pt (posterior tuberculum) to MLR (midbrain locomotor region) to R5.rs (mid-hindbrain reticulospinal turning area), represented by Ob to MidSeek to HindMove.

An earlier simulation model used S.d as a timeout for an OT orientation circuit, but the S.d lacks the direct avoidance action that Sv has with Hb.lm. However, the Pv and Hb.lm circuit is almost entirely disconnected from the V.pt-MLR, which means that the Pv modulation is quite convoluted.

In the avoid circuit, HbAvoid is the key avoidance node, which PvSeek uses for avoidance. An avoidance action needs to stop ongoing action, and to enable a reversal of the current seek direction. In the simulation, MidSeek can reverse its direction if it received an avoid signal. However, I don’t know if any midbrain circuit can reverse direction with an external modulating signal. The most plausible path is from V.mr as the main target of Hb.lm.

If this seek to avoid reversal circuit does exist, it might exist in OT, which does handle both seek and avoid, is used for general left vs right decisions, and receives V.rn input. But for the sake of this essay, I’m avoiding the complexity of revisiting OT and instead assuming that MidSeek can reverse direction on its own.

An alternative is more of a switchboard configuration, where avoidance disables the seek path and enables an odor avoidance path. In animals like the lamprey and fish, Ob directly drives Hb.m for odor chemotaxis, although that path does not exist for mammals, because hippocampus output drives their Hb.m. Using that switchboard model, Pv would use V.rn as the controller to switch between the V.pt seek circuit and the Hb.m odor avoidance chemotaxis. V.rn is essentially part of the Hb.m and R1.a motor circuit, and can project to essentially the entire brain the serotonin and non-serotonin projections.

Hysteresis

The simulation raised the problem of hysteresis again. This time partially because of its simplified PKA and enkephalin model. In this case, the simulation uses a single threshold for deciding to avoid, using PKA and enkephalin rising above a threshold. Unfortunately, when avoidance occurs, the simulation immediately decays the PKA, which drops it below the threshold, curtailing the avoidance and allowing the animal to reenter the failed odor plume. Because the simulation is a program, this problem could be easily fixed by adding a second threshold to disable avoidance, but how could Pv accomplish this hysteresis?

One solution could have Pv blocking any new decision to seek an odor. The S.d2 fast selection phase could be inhibited by low levels of enkephalin. When a new odor triggers S.d2, it would release some level of enkephalin because of the remaining PKA, which might be enough to block a new decision. An alternative solution could use the ACh to A.bl attention circuit. If the lower enkephalin level was still high enough to block ACh attention, it would block a new seek action. This A.bl solution would work especially well if A.bl habituates to an odor if it has no ACh.

References

Agetsuma M., Aizawa H., Aoki T., Nakayama R., M. Takahoko, M. Goto, T. Sassa, R. Amo, T. Shiraki, K. Kawakami, et al. The habenula is crucial for experience-dependent modification of fear responses in zebrafish Nat. Neurosci., 13 (2010), pp. 1354-1356

Baker PM, Mathis V, Lecourtier L, Simmons SC, Nugent FS, Hill S, Mizumori SJY. Lateral Habenula Beyond Avoidance: Roles in Stress, Memory, and Decision-Making With Implications for Psychiatric Disorders. Front Syst Neurosci. 2022 Mar 3;16:826475. 

Bariselli S, Fobbs WC, Creed MC, Kravitz AV. A competitive model for striatal action selection. Brain Res. 2019 Jun 15;1713:70-79. 

Bonnavion, P., Varin, C., Fakhfouri, G., Martinez Olondo, P., De Groote, A., Cornil, A., Lorenzo Lopez, R., Pozuelo Fernandez, E., Isingrini, E., Rainer, Q. and Xu, K., 2024. Striatal projection neurons coexpressing dopamine D1 and D2 receptors modulate the motor function of D1-and D2-SPNs. Nature neuroscience, 27(9), pp.1783-1793.

Conde-Berriozabal, S., Sitja-Roqueta, L., García-García, E., García-Gilabert, L., Sancho-Balsells, A., Fernandez-García, S., Rodriguez-Urgellés, E., Giralt, A., Castañé, A., Rodríguez, M.J. and Alberch, J., 2025. Differential impact of optogenetic stimulation of direct and indirect pathways from dorsolateral and dorsomedial striatum on motor symptoms in Huntington’s disease mice. Experimental Neurology, 383, p.114991.

Cui G, Jun SB, Jin X, Pham MD, Vogel SS, Lovinger DM, Costa RM. Concurrent activation of striatal direct and indirect pathways during action initiation. Nature. 2013 Feb 14;494(7436):238-42. 

Dai, K.Z., Choi, I.B., Levitt, R., Blegen, M.B., Kaplan, A.R., Matsui, A., Shin, J.H., Bocarsly, M.E., Simpson, E.H., Kellendonk, C. and Alvarez, V.A., 2022. Dopamine D2 receptors bidirectionally regulate striatal enkephalin expression: Implications for cocaine reward. Cell reports, 40(13).

Faget, L., Oriol, L., Lee, W.C., Zell, V., Sargent, C., Flores, A., Hollon, N.G., Ramanathan, D. and Hnasko, T.S., 2024. Ventral pallidum GABA and glutamate neurons drive approach and avoidance through distinct modulation of VTA cell types. Nature Communications, 15(1), p.4233.

Giardino WJ, Eban-Rothschild A, Christoffel DJ, Li SB, Malenka RC, de Lecea L. Parallel circuits from the bed nuclei of stria terminalis to the lateral hypothalamus drive opposing emotional states. Nat Neurosci. 2018 Aug;21(8):1084-1095. 

Heinsbroek JA, Bobadilla AC, Dereschewitz E, Assali A, Chalhoub RM, Cowan CW, Kalivas PW. Opposing Regulation of Cocaine Seeking by Glutamate and GABA Neurons in the Ventral Pallidum. Cell Rep. 2020 Feb 11;30(6):2018-2027.e3.

Hernández-Jaramillo, A., Illescas-Huerta, E. and Sotres-Bayon, F., 2024. Ventral pallidum and amygdala cooperate to restrain reward approach under threat. Journal of Neuroscience, 44(23).

Hodge, A. and Yttri, E., 2025. Striatal modulation supports context-specific reinforcement and not action selection. Cell Reports, 44(8).

Hook, V., Toneff, T., Baylon, S. and Sei, C., 2008. Differential activation of enkephalin, galanin, somatostatin, NPY, and VIP neuropeptide production by stimulators of protein kinases A and C in neuroendocrine chromaffin cells. Neuropeptides, 42(5-6), pp.503-511.

Hu, H., Cui, Y. and Yang, Y., 2020. Circuits and functions of the lateral habenula in health and in disease. Nature Reviews Neuroscience, 21(5), pp.277-295.

Jennings JH, Ung RL, Resendez SL, Stamatakis AM, Taylor JG, Huang J, Veleta K, Kantak PA, Aita M, Shilling-Scrivo K, Ramakrishnan C, Deisseroth K, Otte S, Stuber GD. Visualizing hypothalamic network dynamics for appetitive and consummatory behaviors. Cell. 2015 Jan 29;160(3):516-27.

Ji, C., Zhang, Y., Lin, Z., Zhao, Z., Jiao, Z., Zheng, Z., Shi, X., Wang, X., Li, Z., Yu, S. and Qu, Y., 2024. Activation of hypothalamic-pontine-spinal pathway promotes locomotor initiation and functional recovery after spinal cord injury in mice. bioRxiv, pp.2024-11.

Kim, R., Ananth, M.R., Desai, N.S., Role, L.W. and Talmage, D.A., 2024. Distinct subpopulations of ventral pallidal cholinergic projection neurons encode valence of olfactory stimuli. Cell reports, 43(4).

Konradi, C., Macı́as, W., Dudman, J.T. and Carlson, R.R., 2003. Striatal proenkephalin gene induction: coordinated regulation by cyclic AMP and calcium pathways. Molecular brain research, 115(2), pp.157-161.

Lecca S, Meye FJ, Trusel M, Tchenio A, Harris J, Schwarz MK, Burdakov D, Georges F, Mameli M. Aversive stimuli drive hypothalamus-to-habenula excitation to promote escape behavior. Elife. 2017 Sep 5;6:e30697.

Lindsey JW, Markowitz J, Gillis WF, Datta SR, Litwin-Kumar A. Dynamics of striatal action selection and reinforcement learning. Elife. 2025 May 8;13:RP101747.

Luo, Y.J., Ge, J., Chen, Z.K., Liu, Z.L., Lazarus, M., Qu, W.M., Huang, Z.L. and Li, Y.D., 2023. Ventral pallidal glutamatergic neurons regulate wakefulness and emotion through separated projections. Iscience, 26(8).

Neuhofer, D. and Kalivas, P., 2023. Differential modulation of GABAergic and glutamatergic neurons in the ventral pallidum by GABA and neuropeptides. Eneuro, 10(7).

Ottenheimer, D.J., Simon, R.C., Burke, C.T., Bowen, A.J., Ferguson, S.M. and Stuber, G.D., 2024. Single-cell sequencing of rodent ventral pallidum reveals diverse neuronal subtypes with non-canonical interregional continuity. BioRxiv, pp.2024-03.

Palmer D, Cayton CA, Scott A, Lin I, Newell B, Paulson A, Weberg M, Richard JM. Ventral pallidum neurons projecting to the ventral tegmental area reinforce but do not invigorate reward-seeking behavior. Cell Rep. 2024 Jan 23;43(1):113669. 

Patterson CM, Wong JM, Leinninger GM, Allison MB, Mabrouk OS, Kasper CL, Gonzalez IE, Mackenzie A, Jones JC, Kennedy RT, Myers MG Jr. Ventral tegmental area neurotensin signaling links the lateral hypothalamus to locomotor activity and striatal dopamine efflux in male mice. Endocrinology. 2015 May;156(5):1692-700. 

Phua SC, Tan YL, Kok AMY, Senol E, Chiam CJH, Lee CY, Peng Y, Lim ATJ, Mohammad H, Lim JX, Fu Y. A distinct parabrachial-to-lateral hypothalamus circuit for motivational suppression of feeding by nociception. Sci Adv. 2021 May 7;7(19):eabe4323. 

Root DH, Melendez RI, Zaborszky L, Napier TC. The ventral pallidum: Subregion-specific functional anatomy and roles in motivated behaviors. Prog Neurobiol. 2015 Jul;130:29-70. 

Rysztak, L.G. and Jutkiewicz, E.M., 2022. The role of enkephalinergic systems in substance use disorders. Frontiers in Systems Neuroscience, 16, p.932546.

Schlingloff, D., Szabó, Í., Gulyás, É., Király, B., Kispál, R., Stephenson-Jones, M. and Hangya, B., 2025. Most ventral pallidal cholinergic neurons are cortically projecting bursting basal forebrain cholinergic neurons. bioRxiv, pp.2025-02.

Siemian JN, Arenivar MA, Sarsfield S, Aponte Y. Hypothalamic control of interoceptive hunger. Curr Biol. 2021 Sep 13;31(17):3797-3809.e5.

Soares-Cunha C, de Vasconcelos NAP, Coimbra B, Domingues AV, Silva JM, Loureiro-Campos E, Gaspar R, Sotiropoulos I, Sousa N, Rodrigues AJ. Nucleus accumbens medium spiny neurons subtypes signal both reward and aversion. Mol Psychiatry. 2020 Dec;25(12):3241-3255. 

Stamatakis AM, Van Swieten M, Basiri ML, Blair GA, Kantak P, Stuber GD. Lateral Hypothalamic Area Glutamatergic Neurons and Their Projections to the Lateral Habenula Regulate Feeding and Reward. J Neurosci. 2016 Jan 13;36(2):302-11. 

Steiner, H. and Gerfen, C.R., 1998. Role of dynorphin and enkephalin in the regulation of striatal output pathways and behavior. Experimental brain research, 123(1), pp.60-76.

Stephenson-Jones M, Bravo-Rivera C, Ahrens S, Furlan A, Xiao X, Fernandes-Henriques C, Li B. Opposing Contributions of GABAergic and Glutamatergic Ventral Pallidal Neurons to Motivational Behaviors. Neuron. 2020 Mar 4;105(5):921-933.e5. 

Tan, B., Browne, C.J., Nöbauer, T., Vaziri, A., Friedman, J.M. and Nestler, E.J., 2024. Drugs of abuse hijack a mesolimbic pathway that processes homeostatic need. Science, 384(6693), p.eadk6742.

Tecuapetla F, Jin X, Lima SQ, Costa RM. Complementary Contributions of Striatal Projection Pathways to Action Initiation and Execution. Cell. 2016 Jul 28;166(3):703-715. 

Unal, C.T., Pare, D. and Zaborszky, L., 2015. Impact of basal forebrain cholinergic inputs on basolateral amygdala neurons. Journal of Neuroscience, 35(2), pp.853-863.

Vachez YM, Tooley JR, Abiraman K, Matikainen-Ankney B, Casey E, Earnest T, Ramos LM, Silberberg H, Godynyuk E, Uddin O, Marconi L, Le Pichon CE, Creed MC. Ventral arkypallidal neurons inhibit accumbal firing to promote reward consumption. Nat Neurosci. 2021 Mar;24(3):379-390.

Wang Q, Sun RY, Hu JX, Sun YH, Li CY, Huang H, Wang H, Li XM. Hypothalamic-hindbrain circuit for consumption-induced fear regulation. Nat Commun. 2024 Sep 4;15(1):7728.

Williams, M., 2024. Study of the network involving the subthalamic nucleus in various measures of motivation in rats (Doctoral dissertation, Aix-marseille université).

Yao Y, Gao G, Liu K, Shi X, Cheng M, Xiong Y, Song S. Projections from D2 Neurons in Different Subregions of Nucleus Accumbens Shell to Ventral Pallidum Play Distinct Roles in Reward and Aversion. Neurosci Bull. 2021 May;37(5):623-640.