The cholinergic medial septum-diagonal band (MSDB) projections to the hippocampus regulate effort-based motivation and spatial working memory, but the role of presynaptic cannabinoid receptor type 1 (CB1R) in modulating these processes remains unclear. We hypothesized that deleting CB1Rs selectively in MSDB cholinergic terminals projecting to the CA1 hippocampus (cKO) would enhance motivation and cognition by disinhibiting acetylcholine (ACh) release. To test this, we employed a retrograde viral strategy to delete CB1Rs in cholinergic terminals and combined chemogenetics (Gq-DREADDs) with local antagonism of muscarinic (mAChRs) and nicotinic (nAChRs) receptors to dissect circuit-specific mechanisms. Fiber photometry was integrated with behavioral assays to track real-time ACh (ACh sensor) and endocannabinoid (eCB sensor) signaling. The cKO mice exhibited enhanced effort-based motivation (increased Pmax, breakpoint) and spatial working memory (increased alternations). These phenotypes were replicated using a chemogenetic approach to activate MSDB cholinergic projections and abolished by intrahippocampal mAChR/nAChR antagonism, indicating both receptor subtypes critically mediate motivational outcomes. Photometry revealed that ACh signaling encodes reward-related behaviors, with (i) anticipatory decreases preceding reward delivery, and (ii) a post-reward transient increase followed by a prolonged suppression below baseline. The duration of post-reward suppression correlated with diminishing reward demand and was attenuated in cKO mice. Similarly, latency to lever press and hippocampal ACh were inversely correlated, with elevated ACh corresponding to shorter latencies. Lastly, preliminary photometry recordings of eCB signaling revealed a transient increase post-reward, temporally overlapping with ACh suppression. This eCB signal lengthened as reward demand decreased, implicating eCBs in feedback regulation of cholinergic tone. These findings establish CB1R in MSDB cholinergic terminals as a key regulator of hippocampal ACh release, while also linking eCB-ACh signaling to motivated behavior. The distinct temporal dynamics of ACh and eCB signaling suggest a mechanism by which these systems dynamically adjust reward-seeking behaviors based on effort-outcome associations. These results advance our understanding of how neuromodulatory systems interact to shape cognitive and motivational states, with implications for disorders marked by cholinergic dysfunction.